Nuclear Activity Research Articles

Helium plasma operations on ASDEX Upgrade and JET in support of the non-nuclear phases of ITER

For its initial operational phase, ITER has until recently considered using non-nuclear hydrogen (H) or helium (He) plasmas to keep nuclear activation at low levels. To this end, the Tokamak Exploitation Task Force of the EUROfusion Consortium carried out dedicated experimental campaigns in He on the ASDEX Upgrade (AUG) and JET tokamaks in 2022, with particular emphasis put on the ELMy H-mode operation and plasma-wall interaction processes as well as comparison to H or deuterium (D) plasmas. Both in pure He and mixed He + H plasmas, H-mode operation could be reached but more effort was needed to obtain a stable plasma scenario than in H or D. Even if the power threshold for the LH transition was lower in He, entering the type-I ELMy regime appeared to require equally much or even more heating power than in H. Suppression of ELMs by resonant magnetic perturbations was studied on AUG but was only possible in plasmas with a He content below 19%; the reason for this unexpected behaviour remains still unclear and various theoretical approaches are being pursued to properly understand the physics behind ELM suppression. The erosion rates of tungsten (W) plasma-facing components were an order of magnitude larger than what has been reported in hydrogenic plasmas, which can be attributed to the prominent role of He2+ ions in the plasma. For the first time, the formation of nanoscale structures (W fuzz) was unambiguously demonstrated in H-mode He plasmas on AUG. However, no direct evidence of fuzz creation on JET was obtained despite the main conditions for its occurrence being met. The reason could be a delicate balance between W erosion by ELMs, competition between the growth and annealing of the fuzz, and coverage of the surface with co-deposits.

Stress-Related Roles of Exosomes and Exosomal miRNAs in Common Neuropsychiatric Disorders.

Exosomes, natural nanovesicles that contain a cargo of biologically active molecules such as lipids, proteins, and nucleic acids, are released from cells to the extracellular environment. They then act as autocrine, paracrine, or endocrine mediators of communication between cells by delivering their cargo into recipient cells and causing downstream effects. Exosomes are greatly enriched in miRNAs, which are small non-coding RNAs that act both as cytoplasmic post-transcriptional repression agents, modulating the translation of mRNAs into proteins, as well as nuclear transcriptional gene activators. Neuronal exosomal miRNAs have important physiologic functions in the central nervous system (CNS), including cell-to-cell communication, synaptic plasticity, and neurogenesis, as well as modulating stress and inflammatory responses. Stress-induced changes in exosomal functions include effects on neurogenesis and neuroinflammation, which can lead to the appearance of various neuropsychiatric disorders such as schizophrenia, major depression, bipolar disorder, and Alzheimer's and Huntington's diseases. The current knowledge regarding the roles of exosomes in the pathophysiology of common mental disorders is discussed in this review.

Large-Scale Screening of Per- and Polyfluoroalkyl Substance Binding Interactions and Their Mixtures with Nuclear Receptors.

Despite their significant impact, comprehensive screenings and detailed analyses of per- and polyfluoroalkyl substance (PFAS) binding strengths at the orthosteric and allosteric sites of NRs are currently lacking. This study addresses this gap by focusing on the binding interaction analysis of both common and uncommon PFAS with the nuclear receptors (NRs) vitamin D receptor (VDR), peroxisome proliferator-activated receptor gamma (PPARγ), pregnane X receptor (PXR), and estrogen receptor alpha (ERα). Advanced docking simulations were used to screen 9507 PFAS chemicals at the orthosteric and allosteric sites of PPARγ, PXR, VDR, and ERα. All receptors exhibited strong binding interactions at the orthosteric and allosteric site with a significant number of PFAS. We verified the accuracy of the docking protocol through multiple docking controls and validations. A mixture modeling analysis indicates that PFAS can bind in various combinations with themselves and endogenous ligands simultaneously, to disrupt the endocrine system and cause carcinogenic responses. These findings reveal that PFAS can interfere with nuclear receptor activity by displacing endogenous or native ligands by binding to the orthosteric and allosteric sites. The purpose of this study is to explore the mechanisms through which PFAS exert their endocrine-disrupting effects, potentially leading to more targeted therapeutic strategies. Importantly, this study is the first to explore the binding of PFAS at allosteric sites and to model PFAS mixtures at nuclear receptors. Given the high concentration and persistence of PFAS in humans, this study further emphasizes the urgent need for further research into the carcinogenic mechanisms of PFAS and the development of therapeutic strategies that target nuclear receptors.

Cleavage of protein kinase c δ by caspase-3 mediates proinflammatory cytokine-induced apoptosis in pancreatic islets

In type 1 diabetes (T1D), autoreactive immune cells infiltrate the pancreas and secrete pro-inflammatory cytokines that initiate cell death in insulin producing islet β-cells. Protein kinase C δ (PKCδ) plays a role in mediating cytokine-induced β-cell death; however, the exact mechanisms are not well understood. To address this, we utilized an inducible β-cell specific PKCδ KO mouse as well as a small peptide inhibitor of PKCδ. We identified a role for PKCδ in mediating cytokine-induced β-cell death and have shown that inhibiting PKCδ protects pancreatic β-cells from cytokine-induced apoptosis in both mouse and human islets. We determined that cytokines induced nuclear translocation and activity of PKCδ and that caspase-3 cleavage of PKCδ may be required for cytokine-mediated islet apoptosis. Further, cytokine activated PKCδ increases activity both of pro-apoptotic Bax with acute treatment and JNK with prolonged treatment. Overall, our results suggest that PKCδ mediates cytokine-induced apoptosis via nuclear translocation, cleavage by caspase-3, and upregulation of pro-apoptotic signaling in pancreatic β-cells. Combined with the protective effects of PKCδ inhibition with δV1-1, the results of this study will aid in the development of novel therapies to prevent or delay β-cell death and preserve β-cell function in T1D.

High energy resolution CsPbBr3 alpha particle detector with a full-customized readout application specific integrated circuit

α particles must be monitored to be managed as radioactive diagnostic agents or nuclear activity indicators. The new generation of perovskite detectors suffer from limited energy resolution, which affects spectroscopy and imaging applications. Here, we report that the solution-grown CsPbBr3 crystal exhibits a low and stable dark current (34.6 nA·cm−2 at 200 V) by thinning the as-grown crystal to decrease the high concentration CsPb2Br5 phase near the surface. The introduction of the Schottky electrode for the CsPbBr3 detector further reduces the dark current and improves the high-temperature stability. An energy resolution of 6.9% is achieved with the commercial electronic system, while the effects of air scattering and absorption are investigated. Moreover, 1.1% energy resolution is recognized by a full-customized readout application-specific integrated circuit without any additional signal processing, which matches well with the given parameters of the CsPbBr3 detector by reducing the parasitic capacitance and electronic noise.

Developmental neurotoxicity of PFOA exposure on hiPSC-derived cortical neurons

PFOA is a legacy Per- and Polyfluorinated Substances (PFAS), a group of chemicals widely used in various industrial applications and consumer products. Although there has been a voluntary phase out of PFOA since 2005, it is still widely detected in various water supplies. A growing body of evidence suggests an association between PFOA exposure, particularly during developmental stages, with increased risks of neurodegenerative diseases (NDs). The neurotoxic mechanism of developmental PFOA exposure, however, remains poorly understood. Utilizing human induced-pluripotent stem cell (hiPSC)-derived cortical neurons, we investigated the effect of PFOA exposure prior to differentiation and assessed changes in neuronal characteristics, transcriptome, and neurodegeneration markers mimicking a Developmental Origin of Health and Disease (DoHAD) paradigm. Exposure to PFOA before neuron differentiation resulted in persistent alterations in nuclear morphology, neuronal network, and calcium activity. RNA sequencing analysis further revealed transcriptomic changes aligning with Alzheimer’s Disease (AD) after PFOA exposure. These observations were further corroborated by alterations in tau phosphorylation markers, the presence of fibrillar tau, an increase in liquid droplets, and a decrease in RNA translational efficiency characterized using a battery of biochemical assays. Taken together, our results revealed persistent deficits of key neuronal characteristics induced by pre-differentiation PFOA exposure, suggesting impairments in several AD-related pathways that can together contribute to the elevation of AD risk after pre-differentiation PFOA exposure.

High-fat diet modulates bile acid composition and gut microbiota, affecting severe cholangitis and cirrhotic change in murine primary biliary cholangitis

Increasing evidence suggests that, in addition to a loss of tolerance, bile acid (BA) modulates the natural history of primary biliary cholangitis (PBC). We focused on the impacts of dietary changes on the immunopathology of PBC, along with alterations in BA composition and gut microbiota. In this study, we have taken advantage of our unique PBC model, a Cyp2c70/Cyp2a12 double knockout (DKO), which includes a human-like BA composition, and develops progressive cholangitis following immunization with the PDC-E2 mimic, 2-octynoic acid (2OA). We compared the effects of a ten-week high-fat diet (HFD) (60 % kcal from fat) and a normal diet (ND) on 2OA-treated DKO mice. Importantly, we report that 2OA-treated DKO mice fed HFD had significantly exacerbated cholangitis, leading to cirrhosis, with increased hepatic expression of Th1 cytokines/chemokines and hepatic fibrotic markers. Serum lithocholic acid (LCA) levels and the ratio of chenodeoxycholic acid (CDCA)-derived BAs to cholic acid-derived BAs were significantly increased by HFD. This was also associated with downregulated expression of key regulators of BA synthesis, including Cyp8b1, Cyp3a11, and Sult2a1. In addition, there were increases in the relative abundances of Acetatifactor and Lactococcus and decreases in Desulfovibrio and Lachnospiraceae_NK4A136_group, which corresponded to the abundances of CDCA and LCA. In conclusion, HFD and HFD-induced alterations in the gut microbiota modulate BA composition and nuclear receptor activation, leading to cirrhotic change in this murine PBC model. These findings have significant implications for understanding the progression of human PBC.

Structural evolution and electronic properties of anionic plutonium-doped oxygen clusters

Plutonium oxides are important in actinide chemistry and nuclear industry activities, and the demand and interest in enriching knowledge of plutonium chemistry is growing increasingly significant. However, unlike uranium oxide clusters, few studies related to the geometry and bonding properties of anionic plutonium oxide clusters have been reported. Here we explored the geometries, photoelectron spectra, and electronic properties of anionic plutonium oxide clusters by means of unbiased structural searches coupled with density-functional theory (DFT). The results show that the PuO6− cluster with a high D2h symmetry formed by a linear O-Pu-O plutonyl unit with two O2 units exhibits excellent stability. In addition, the HOMO–LUMO gap value of PuO6− cluster are 4.35 eV and 3.41 eV for the α- and β-orbitals, respectively, as well as the vertical detachment energy (VDE) of 4.20 eV. In the analysis of molecular orbitals and adaptive natural density partitioning in oxygen-rich systems, the σ bonds between plutonium atom and oxygen ligands, primarily from the Pu-5f and O-2p orbitals, are responsible for the goodish stability of PuO6− cluster. We hope that the current work can enrich the geometrical configuration of plutonium oxide oxygen clusters and provide reference information for the subsequent research work.

Active fraction of Polyrhachis vicina (Rogers) inhibits osteoclastogenesis by targeting Trim38 mediated proteasomal degradation of TRAF6

BackgroundReactive Oxygen Species (ROS) is a key factor in the pathogenesis of osteoporosis (OP) primarily characterized by excessive osteoclast activity. Active fraction of Polyrhachis vicina Rogers (AFPR) exerts antioxidant effects and possesses extensive promising therapeutic effects in various conditions, however, its function in osteoclastogenesis and OP is unknown. PurposeThe aim of this study is to elucidate the cellular and molecular mechanisms of AFPR in OP. Study design and methodsCCK8 assay was used to evaluate the cell viability under AFPR treatment. TRAcP staining, podosome belts staining and bone resorption were used to test the effect of AFPR on osteoclastogenesis. Immunofluorescence staining was used to observe the effect of AFPR on ROS production. si-RNA transfection, coimmunoprecipitation and Western-blot were used to clarify the underlying mechanisms. Further, an ovariectomy (OVX) -induced OP mice model was used to identify the effect of AFPR on bone loss using Micro-CT scanning and histological examination. ResultsIn the present study, AFPR inhibited osteoclast differentiation and bone resorption induced by nuclear factor-κB receptor activator (NF-κB) ligand (RANKL) in dose-/ time-dependent with no cytotoxicity. Meanwhile, AFPR decreased RANKL-mediated ROS levels and enhanced ROS scavenging enzymes. Mechanistically, AFPR promoted proteasomal degradation of TRAF6 by significantly upregulating its K48-linked ubiquitination, subsequently inhibiting NFATc1 activity. We further observed that tripartite motif protein 38 (TRIM38) could mediate the ubiquitination of TRAF6 in response to RANKL. Moreover, TRIM38 could negatively regulate the RANKL pathway by binding to TRAF6 and promoting K48-linked polyubiquitination. In addition, TRIM38 deficiency rescued the inhibition of AFPR on ROS and NFATc1 activity and osteoclastogenesis. In line with these results, AFPR reduced OP caused by OVX through ameliorating osteoclastogenesis. ConclusionAFPR alleviates ovariectomized-induced bone loss via suppressing ROS and NFATc1 by targeting Trim38 mediated proteasomal degradation of TRAF6. The research offers innovative perspectives on AFPR's suppressive impact in vivo OVX mouse model and in vitro, and clarifies the fundamental mechanism.

Decoding Cesium-137: a Deep Learning Approach to Environmental Prediction

The study delves into the significant environmental threat posed by cesium-137, a byproduct of nuclear mishaps, industrial activities, and past weapons tests. The persistence of cesium-137 disrupts ecosystems by contaminating soil and water, which subsequently affects human health through the food chain. Traditional monitoring techniques like gamma spectroscopy and soil sampling face challenges such as variability and the intensive use of resources. The paper introduces deep learning, a branch of artificial intelligence, as a revolutionary method for environmental monitoring. By utilizing extensive datasets, deep learning predicts the spread of cesium-137, thus enhancing our understanding and management of its impact. The application of predictive models based on deep learning in various environmental domains demonstrates their potential for analyzing cesium-137 pollution.

Rhizoma Zedoariae Inhibits G-CSF-Induced MDSCs-like Differentiation of THP-1 Cells

Objective: Rhizoma Zedoariae is widely used in the treatment of solid tumors in China, but there has been no deep research on its role in the formation of timmunosuppressive environments mediated by myeloid-derived suppressor cells (MDSCs) in breast cancer. This research aims to investigate the effect of Rhizoma Zedoariae extract and its active compounds curcumin and germacrone on MDSCs-like differentiation by a novel Granulocyte colony-stimulating factor (G-CSF) induced THP-1 cell model. Methods: THP-1 cells were treated with Rhizoma Zedoariae extract and its active compounds (curcumin, germacrone, curcumol, curcumenol, and curdione) at different concentrations (0.01, 0.1, 0.3, 1, 10, 30, 100, and 300 μg/mL), followed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to detect the changes of cell viability in THP-1. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was performed to quantify the mRNA expression levels of transforming growth factor-β (TGF-β), Interleukin-10 (IL-10), Interleukin-6 (IL-6), Janus kinase 1 (JAK1), nuclear factor kappa-B (NF-κB), signal transducer and activator of transcription 3 (STAT3) and arginase-1 (ARG-1), to detected the differentiation of THP-1 into MDSCs-like cells. Results: G-CSF can induce the cell viability and MDSCs-like differentiation of THP-1 cells. Rhizoma Zedoariae extract (0.1, 1, 10, 30, 100, 300 μg/mL), germacrone (0.1, 1, 10, 30, 100, 300 μg/mL) and curcumin (0.01, 0.1, 1, 10, 30, 100 μg/mL) exerted obvious inhibitory effects (>70%) on THP-1 cell viability. G-CSF increased the ARG-1 and IL-10 mRNA levels. Rhizoma Zedoariae extract in 100 μg/mL decreased the ARG-1 and IL-10 mRNA levels. Furthermore, Rhizoma Zedoariae extract in 300 μg/mL also significantly decreased the mRNA expressions of JAK1 and STAT3 (p < 0.001). Conclusion: Rhizoma Zedoariae extract maybe inhibit G-CSF-induced MDSCs-like differentiation of THP-1 through the STAT3 pathway. The active compound that exerts this effect may be germacrone and curcumin.

Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation.

Nuclear actin-based movements support DNA double-strand break (DSB) repair. However, molecular determinants that promote filamentous actin (F-actin) formation on the damaged chromatin remain undefined. Here we describe the DYRK1A kinase as a nuclear activity that promotes local F-actin assembly to support DSB mobility and repair, accomplished in part by its targeting of actin nucleator spire homolog 1 (Spir1). Indeed, perturbing DYRK1A-dependent phosphorylation of S482 mis-regulated Spir1 accumulation at damaged-modified chromatin, and led to compromised DSB-associated actin polymerization and attenuated DNA repair. Our findings uncover a role of the DYRK1A-Spir1 axis in nuclear actin dynamics during early DSB responses, and highlight the intricate details of nuclear cytoskeletal network in DSB repair and genome stability maintenance.

DNA hypomethylation in wood frog liver under anoxia and dehydration stresses

Wood frogs are freeze-tolerant vertebrates that can endure weeks to months frozen during the winter without breathing and with as much as 65% of total body water frozen as extracellular ice. Underlying tolerances of anoxia and of cellular dehydration support whole body freezing. One pro-survival mechanism employed by these frogs is epigenetic modifications via DNA hypomethylation processes facilitating transcriptional repression or activation. These processes involve proteins such as DNA Methyltransferases (DNMTs), Methyl Binding Domain proteins (MBDs), Ten-Eleven Translocases (TETs), and Thymine Deglycosylase (TDG). The present study evaluates the responses of these proteins to dehydration and anoxia stresses in wood frog liver. DNMT relative protein expression was reduced in liver, but nuclear DNMT activity did not change significantly under anoxia stress. By contrast, liver DNMTs and nuclear DNMT activity were upregulated under dehydration stress. These stress-specific differences were speculated to arise from Post-Translational Modifications (PTMs). DNMT3A and DNMT3B showed increased relative protein expression during recovery from dehydration and anoxia. Further, MBD1 was elevated during both conditions suggesting transcriptional repression. TET proteins showed varying responses to anoxia likely due to the absence of oxygen, a main substrate required by TETs. Similarly, TDG, an enzyme that corrects DNA damage, was downregulated under anoxia potentially due to lower levels of reactive oxygen species that damage DNA, but levels returned to normal during reperfusion of oxygen. Our results indicate differential stress-specific responses that indicate the need for more research in the DNA hypomethylation mechanisms employed by the wood frog during stress.

Anthropocene 129I Record in the Yellow Sea Sediments and Its Indication for River-Delivered Radioactive Pollution to Marginal Seas.

As the number of coastal nuclear facilities rapidly increases and the wastewater from the Fukushima Nuclear Plant has been discharged into the Pacific Ocean, the nuclear environmental safety of China's marginal seas is gaining increased attention along with the heightened potential risk of nuclear accidents. However, insufficient work limits our understanding of the impact of human nuclear activities on the Yellow Sea (YS) and the assessment of their environmental process. This study first reports the 129I and 127I records of posthuman nuclear activities in the two YS sediments. Source identification of anthropogenic 129I reveals that, in addition to the gaseous 129I release and re-emission of oceanic 129I discharged from the European Nuclear Fuel Reprocessing Plants (NFRPs), the Chinese nuclear weapons testing fallout along with the global fallout is an additional 129I input for the continental shelf of the YS. The 129I/127I atomic ratios in the North YS (NYS) sediment are significantly higher than those in the other adjacent coastal areas, attributed to the significant riverine input of particulate 129I by the Yellow River. Furthermore, we found a remarkable 129I latitudinal disparity in the sediments than those in the seawaters in the various China seas, revealing that sediments in China's marginal seas already received a huge anthropogenic 129I from terrigenous sources via rivers and thus became a significant sink of anthropogenic 129I. This study broadens an insight into the potential impacts of terrigenous anthropogenic pollution on the Chinese coastal marine radioactive ecosystem.

A study of interacting galaxies from the Arp-Madore catalog. Triggering of star formation and nuclear activity

We present Gemini Multi-Object Spectrograph (GMOS) spectroscopic observations of 95 galaxies from the Arp Madore (1987) catalog of peculiar galaxies. These galaxies have been selected because they appear to be in pairs and small groups. These observations have enabled us to confirm that 60 galaxies are indeed interacting systems. For the confirmed interacting sample, we have built a matched control sample of isolated galaxies. We present an analysis of the stellar populations and nuclear activity in the interacting galaxies and compare them with the isolated galaxies. We find a median light (mass) fraction of 55<!PCT!> (10<!PCT!>) in the interacting galaxies coming from stellar populations younger than 2 Gyr and 28<!PCT!> (3<!PCT!>) in the case of the isolated galaxies. More than half of the interacting galaxies are dominated by this young stellar population, while in the isolated ones most of the light comes from older stellar populations. We used a combination of diagnostic diagrams (BPTs and WHAN) to classify the main ionization mechanisms of the gas. The interacting galaxies in our sample consistently show a higher fraction of active galactic nuclei (AGN) relative to the control sample, which ranges between 1.6 and 4 depending on the combination of diagnostic diagrams employed to classify the galaxies and the number of galaxies considered. Our study provides further observational evidence that interactions drive star formation and nuclear activity in galaxies and can have a significant impact on galaxy evolution.

Median nerve electrical stimulation improves traumatic brain injury by reducing TACR1 to inhibit nuclear factor-κB and CCL7 activation in microglia.

The existing report elucidates that median nerve electrical stimulation (MNS) plays a role in treating traumatic brain injury (TBI). Herein, we explored the mechanism of MNS in TBI. A TBI-induced coma model (skull was hit by a cylindrical impact hammer) was established in adult Sprague-Dawley rats. Microglia were isolated from newborn Sprague-Dawley rats and was injured by lipopolysaccharide (LPS; 10 ng/mL). Consciousness was assessed by sensory and motor functions. Brain tissue morphology was detected using hematoxylin-eosin staining assay. Ionized calcium binding adapter molecule 1, NeuN and tachykinin receptor 1 (TACR1) level were detected by immunohistochemical assay. Levels of pro-inflammatory and anti-inflammatory factors were measured by enzyme linked immune sorbent assay (ELISA). Levels of TACR1, C-C motif chemokine 7 (CCL7), phosphorylation (p)-P65 and P65 were assessed by quantitative real time polymerase chain reaction (qRT-PCR) and western blot. M1 markers (inducible nitric oxide synthase and CD86) and M2 markers (arginase-1 (Arg1) and chitinase 3-like 3 (YM1)) of microglia as well as the transfection efficiency of short hairpin TACR1 (shTACR1) were assessed by qRT-PCR. Immunofluorescence and flow cytometry assay were used to detect microglia morphology and neuron apoptosis. MNS reduced neuron injury and microglia activation in the TBI-induced rat coma model. MNS reversed the effects of TBI on levels of inflammation-related factors, M1/M2 microglia markers, TACR1, p-P65/P65 and CCL7 in rats. shTACR1 reversed the effects of LPS on inflammation-related factors, M1/M2 microglia markers, microglia activation, neuron apoptosis, p-P65/P65 value and CCL7 level. Our results revealed that MNS improved TBI by reducing TACR1 to inhibit nuclear factor-κB (NF-κB) and CCL7 activation in microglia.

Assessment of the Performance of the Dose Calibrator Used in Radioactivity Measurement

Aims: This study aimed to evaluate the principal technical characteristics of a well-type gas-filled ionization chamber dose calibrator used in measuring radiopharmaceutical activity, namely accuracy, repeatability, and linearity. Furthermore, this work also explored the correlation between the device’s response and the position and volume of the radiopharmaceutical I-131. Materials and Methods: Experimental measurements were conducted on the ATOMLAB 500 dose calibrator using NIST traceable Cs-137 source to determine the accuracy and repeatability. For the linearity test, the Tc-99m solution produced at the Dalat Nuclear Research Institute, Vietnam was utilized to examine the performance of the device over a wide measurement range. Effects resulting from different volumes and measuring positions were also determined by experiments and Monte Carlo simulations. Results: Based on acceptance test results, it is revealed that the dose calibrator’s characteristics comply with international standards, where the deviations of accuracy, repeatability, and linearity are all lower than 1.0%. The response of the dose calibrator to different measuring positions and volumes was well controlled. To rectify the discrepancy in the response to the changes in solution volume, correction functions were proposed. Conclusions: It is concluded that the dose calibrator is suitable for radioactivity quantification and adheres to standards recommended by international organizations for nuclear medicine activities. The outcome of this work will serve as the foundation for establishing a standard for I-131 radiopharmaceuticals’ radioactivity in Vietnam.

Tailoring Microbial Amino Acid Metabolism in Fermented Foods to Enhance Nuclear Receptor Activity and Regulate Experimental Colitis Severity

Tailoring Microbial Amino Acid Metabolism in Fermented Foods to Enhance Nuclear Receptor Activity and Regulate Experimental Colitis Severity

Nuclear ATP-citrate lyase regulates chromatin-dependent activation and maintenance of the myofibroblast gene program

Differentiation of cardiac fibroblasts to myofibroblasts is necessary for matrix remodeling and fibrosis in heart failure. We previously reported that mitochondrial calcium signaling drives α-ketoglutarate-dependent histone demethylation, promoting myofibroblast formation. Here we investigate the role of ATP-citrate lyase (ACLY), a key enzyme for acetyl-CoA biosynthesis, in histone acetylation regulating myofibroblast fate and persistence in cardiac fibrosis. We show that inactivation of ACLY prevents myofibroblast differentiation and reverses myofibroblasts towards quiescence. Genetic deletion of Acly in post-activated myofibroblasts prevents fibrosis and preserves cardiac function in pressure-overload heart failure. TGFβ stimulation enhances ACLY nuclear localization and ACLY–SMAD2/3 interaction, and increases H3K27ac at fibrotic gene loci. Pharmacological inhibition of ACLY or forced nuclear expression of a dominant-negative ACLY mutant prevents myofibroblast formation and H3K27ac. Our data indicate that nuclear ACLY activity is necessary for myofibroblast differentiation and persistence by maintaining histone acetylation at TGFβ-induced myofibroblast genes. These findings provide targets to prevent and reverse pathological fibrosis.

Uranium quantification in radioactive waste drums using In-Situ Object Counting System (ISOCS) for safeguards purposes

For the peaceful use of nuclear energy, materials, and technology, various methods have been developed for safeguards purposes. Among them, the In-Situ Object Counting System has demonstrated its usefulness and reliability in various nuclear material verification activities, due to its capability of operating without standard materials. In the present study, the performance of In-Situ Object Counting System for uranium quantification was evaluated using an experimental drum at KEPCO NF as well as low-level radioactive waste drums at the Korea Radioactive Waste Agency. The results showed that In-Situ Object Counting System could quantify uranium in radioactive waste drums, with a relative error ranging from −1 to −67 % compared with destructive assay results. This study also examined, using the Monte Carlo N-particle transport 6.2 code, the factors that affect uncertainty in uranium quantification: geometrical conditions, spectrum quality, heterogeneity, and the self-shielding effect. These findings could prove useful in efforts to optimize the In-Situ Object Counting System as a tool for nuclear material verification in the safeguards context.