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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 1,045 records · Page 58
All sourcesNASA NTRSDOE OSTI
DOE OSTI2016

TGF-β1 accelerates the DNA damage response in epithelial cells via Smad signaling

The evidence suggests that transforming growth factor-beta (TGF-β) regulates the DNA-damage response (DDR) upon irradiation, and we previously reported that TGF-β1 induced DNA ligase IV (Lig4) expression and enhanced the nonhomologous end-joining repair pathway in irradiated cells. In the present study, we investigated the effects of TGF-β1 on the irradiation-induced DDRs of A431 and HaCaT cells. Cells were pretreated with or without TGF-β1 and irradiated. At 30 min post-irradiation, DDRs were detected by immunoblotting of phospho-ATM, phospho-Chk2, and the presence of histone foci (γH2AX). The levels of all three factors were similar right after irradiation regardless of TGF-β1 pretreatment. However, they soon thereafter exhibited downregulation in TGF-β1-pretreated cells, indicating the acceleration of the DDR. Treatment with a TGF-β type I receptor inhibitor (SB431542) or transfections with siRNAs against Smad2/3 or DNA ligase IV (Lig4) reversed this acceleration of the DDR. Furthermore, the frequency of irradiation-induced apoptosis was decreased by TGF-β1 pretreatment in vivo, but this effect was abrogated by SB431542. These results collectively suggest that TGF-β1 could enhance cell survival by accelerating the DDR via Smad signaling and Lig4 expression. -- Highlights: •TGF-β1 pretreatment accelerates γ-radiation-induced DNA damage response. •TGF-β1-accelerated DNA damage response is dependent on Smad signaling and DNA Ligase IV. •TGF-β1 pretreatment protects epithelial cells from γ-radiation in vivo.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Antibiotic tigecycline enhances cisplatin activity against human hepatocellular carcinoma through inducing mitochondrial dysfunction and oxidative damage

Targeting mitochondrial metabolism has been recently demonstrated to be a promising therapeutic strategy for the treatment of various cancer. In this work, we demonstrate that antibiotic tigecycline is selectively against hepatocellular carcinoma (HCC) through inducing mitochondrial dysfunction and oxidative damage. Tigecycline is more effective in inhibiting proliferation and inducing apoptosis of HCC than normal liver cells. Importantly, tigecycline significantly enhances the inhibitory effects of chemotherapeutic drug cisplatin in HCC in vitro and in vivo. Mechanistically, tigecycline specifically inhibits mitochondrial translation as shown by the decreased protein levels of Cox-1 and -2 but not Cox-4 or Grp78, and increased mRNA levels of Cox-1 and -2 but not Cox-4 in HCC cells exposed to tigecycline. In addition, tigecycline significantly induces mitochondrial dysfunction in HCC cells via decreasing mitochondrial membrane potential, complex I and IV activities, mitochondrial respiration and ATP levels. Tigecycline also increases levels of mitochondrial superoxide, hydrogen peroxide and ROS levels. Consistent with oxidative stress, oxidative damage on DNA, protein and lipid are also observed in tigecycline-treated cells. Importantly, antioxidant N-acetyl-L-cysteine (NAC) reverses the effects of tigecycline, suggesting that oxidative stress is required for the action of tigecycline in HCC cells. We further show that HCC cells have higher level of mitochondrial biogenesis than normal liver cells which might explain the different sensitivity to tigecycline between HCC and normal liver cells. Our work is the first to demonstrate that tigecycline is a promising candidate for HCC treatment and highlight the therapeutic value of targeting mitochondrial metabolism in HCC. - Highlights: • Tigecycline selectively targets HCC in vitro and in vivo. • Tigecycline enhances HCC cell response to chemotherapeutic drug. • Tigecycline inhibits mitochondrial translation and functions in HCC cells. • Tigecycline induces oxidative stress and damage in HCC cells. • Mitochondrial biogenesis and respiration is higher in HCC than normal liver cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Ku70 inhibits gemcitabine-induced DNA damage and pancreatic cancer cell apoptosis

The current study focused on the role of Ku70, a DNA-dependent protein kinase (DNA-PK) complex protein, in pancreatic cancer cell resistance to gemcitabine. In both established cell lines (Mia-PaCa-2 and PANC-1) and primary human pancreatic cancer cells, shRNA/siRNA-mediated knockdown of Ku70 significantly sensitized gemcitabine-induced cell death and proliferation inhibition. Meanwhile, gemcitabine-induced DNA damage and subsequent pancreatic cancer cell apoptosis were also potentiated with Ku70 knockdown. On the other hand, exogenous overexpression of Ku70 in Mia-PaCa-2 cells suppressed gemcitabine-induced DNA damage and subsequent cell apoptosis. In a severe combined immune deficient (SCID) mice Mia-PaCa-2 xenograft model, gemcitabine-induced anti-tumor activity was remarkably pontificated when combined with Ku70 shRNA knockdown in the xenografts. The results of this preclinical study imply that Ku70 might be a primary resistance factor of gemcitabine, and Ku70 silence could significantly chemo-sensitize gemcitabine in pancreatic cancer cells. - Highlights: • Ku70 knockdown sensitizes gemcitabine-induced killing of pancreatic cancer cells. • Ku70 knockdown facilitates gemcitabine-induced DNA damage and cell apoptosis. • Ku70 overexpression deceases gemcitabine's sensitivity in pancreatic cancer cells. • Ku70 knockdown sensitizes gemcitabine-induced anti-tumor activity in vivo.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2024

Zircon-to-reidite phase transition enhanced by minor radiation damage: Implications for hypervelocity impacts

Reidite, a high-pressure phase of zircon, is increasingly identified at terrestrial impact sites. Despite its growing recognition, the potential applications for estimating minimum impact pressure face impediments due to existing discrepancies in the condition of zircon-reidite transformation, controversial models governing the transformation mechanism, and unclear effects of pre-existing radiation damage on reidite formation. Here, we show enhanced reidite formation by synchrotron X-ray diffraction, Raman spectroscopy, and transmission electron microscopy analyses of zircon grains that have experienced different alpha-decay doses from U and Th impurities and subsequent pressurization in diamond anvil cells. Below ~1 × 10 18 α-decay events/g, the α-decay-induced isolated point defects in the still crystalline zircon facilitate the minor atomic readjustments required for reidite formation. However, above this dose, the loss of long-range periodicity in severely damaged or even metamict zircon inhibits the transformation. The enhanced reidite formation by minor radiation damage coincides with the more common occurrence of reidite at impact sites for which the precursor zircon has a relatively lower alphadecay- event dose before the impact event. In addition, the detailed atomic-scale structures of twinned reidite provide unambiguous evidence for a characteristic internal stress-induced martensitic transition. Furthermore, these findings have important implications for interpreting the formation conditions of natural reidite due to the convergence of pressure from the static, shockwave, and natural reidite samples.

58 GEOSCIENCES↗
DOE OSTI2026

Predicting fracture behavior in single crystal nickel using a coupled crystal plasticity phase field damage approach

Understanding the fracture behavior of single crystal metals is critical for predicting material performance under mechanical loading. Here, in this study, we investigate the fracture characteristics of single crystal nickel tensile bars using a crystal plasticity coupled phase field damage (CP-PFD) model. Experimental tensile tests were conducted on 15 specimens spanning five crystallographic orientations and three thickness variants per orientation. The results revealed two distinct fracture modes: brittle fractures with 45-degree angled surfaces and ductile fractures characterized by significant necking. The CP-PFD model successfully replicated these fracture behaviors, demonstrating strong agreement with experimental observations. The model effectively predicted the strain at which necking and fracture occurred, as well as the orientation-dependent fracture mechanisms. By comparing experimental and simulated fracture surfaces, we establish the CP-PFD model as a robust tool for predicting single crystal behavior and damage evolution. This work provides insight into the microstructural dependence of fracture behavior and establishes a predictive framework for modeling orientation-dependent damage evolution in single-crystal nickel.

Crystal plasticity↗
DOE OSTI2024

The damage Mechanics challenge Results: Participant predictions compared with experiment

In this article, We present results from a recent exercise where participating organizations were asked to provide model-based blind predictions of damage evolution in 3D-printed geomaterial analogue test articles. Participants were provided with a range of data characterizing both the undamaged state (e.g., ultrasonic measurements) and damage evolution (e.g., 3-point bending, unconfined compression, and Brazilian testing) of the material. In this paper, we focus on comparisons between the participants’ predictions and the previously secret challenge problem experimental observations. We present valuable lessons learned for the application of numerical methods to deformation and failure in brittle-ductile materials. The exercise also enables us to identify which specific types of calibration data were of most utility to the participants in developing their predictions. Further, we identify additional data that would have been useful for participants to improve the confidence of their predictions. Consequently, this work improves our understanding of how to better characterize a material to enable more accurate prediction of damage and failure propagation in natural and engineered brittle-ductile materials.

36 MATERIALS SCIENCE↗
DOE OSTI2014

Thalidomide Ameliorates Inflammation and Vascular Injury but Aggravates Tubular Damage in the Irradiated Mouse Kidney

Purpose: The late side effects of kidney irradiation include vascular damage and fibrosis, which are promoted by an irradiation-induced inflammatory response. We therefore treated kidney-irradiated mice with the anti-inflammatory and angiogenesis-modulating drug thalidomide in an attempt to prevent the development of late normal tissue damage and radiation nephropathy in the mouse kidney. Methods and Materials: Kidneys of C57Bl/6 mice were irradiated with a single dose of 14 Gy. Starting from week 16 after irradiation, the mice were fed with thalidomide-containing chow (100 mg/kg body weight/day). Gene expression and kidney histology were analyzed at 40 weeks and blood samples at 10, 20, 30, and 40 weeks after irradiation. Results: Thalidomide improved the vascular structure and vessel perfusion after irradiation, associated with a normalization of pericyte coverage. The drug also reduced infiltration of inflammatory cells but could not suppress the development of fibrosis. Irradiation-induced changes in hematocrit and blood urea nitrogen levels were not rescued by thalidomide. Moreover, thalidomide worsened tubular damage after irradiation and also negatively affected basal tubular function. Conclusions: Thalidomide improved the inflammatory and vascular side effects of kidney irradiation but could not reverse tubular toxicity, which probably prevented preservation of kidney function.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2014

Targeting the Renin–Angiotensin System Combined With an Antioxidant Is Highly Effective in Mitigating Radiation-Induced Lung Damage

Purpose: To investigate the outcome of suppression of the renin angiotensin system using captopril combined with an antioxidant (Eukarion [EUK]-207) for mitigation of radiation-induced lung damage in rats. Methods and Materials: The thoracic cavity of female Sprague-Dawley rats was irradiated with a single dose of 11 Gy. Treatment with captopril at a dose of 40 mg/kg/d in drinking water and EUK-207 given by subcutaneous injection (8 mg/kg daily) was started 1 week after irradiation (PI) and continuing until 14 weeks PI. Breathing rate was monitored until the rats were killed at 32 weeks PI, when lung fibrosis was assessed by lung hydroxyproline content. Lung levels of the cytokine transforming growth factor-β1 and macrophage activation were analyzed by immunohistochemistry. Oxidative DNA damage was assessed by 8-hydroxy-2-deoxyguanosine levels, and lipid peroxidation was measured by a T-BARS assay. Results: The increase in breathing rate in the irradiated rats was significantly reduced by the drug treatments. The drug treatment also significantly decreased the hydroxyproline content, 8-hydroxy-2-deoxyguanosine and malondialdehyde levels, and levels of activated macrophages and the cytokine transforming growth factor-β1 at 32 weeks. Almost complete mitigation of these radiation effects was observed by combining captopril and EUK-207. Conclusion: Captopril and EUK-207 can provide mitigation of radiation-induced lung damage out to at least 32 weeks PI after treatment given 1-14 weeks PI. Overall the combination of captopril and EUK-207 was more effective than the individual drugs used alone.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Conditional Plasminogen Activator Inhibitor Type 1 Deletion in the Endothelial Compartment Has No Beneficial Effect on Radiation-Induced Whole-Lung Damage in Mice

Purpose: To investigate whether the endothelial pool of plasminogen activator inhibitor type 1 (PAI-1) plays a role in the development of radiation-induced lung damage, as previously demonstrated in the intestine. Methods and Materials: Human lung microvascular endothelial cells were exposed to 10 Gy irradiation so as to study their ability to acquire an “activated” phenotype. Mice in which the Cre-Lox strategy was used to produce PAI-1 deletion specifically in the endothelial compartment were exposed to 17 Gy whole-thorax irradiation and followed up for 2, 13, and 23 weeks after irradiation. Results: Human lung microvascular endothelial cells had an activated phenotype after radiation exposure, overexpressed PAI-1, and underwent endothelial-to-mesenchymal transition. In mice, knockout of PAI-1 in the endothelium had no beneficial effect on radiation-induced lung damage and showed a tendency to worsen acute lesions. Conclusions: As opposed to the intestine, the endothelial pool of PAI-1 does not play a determinant role in the development of radiation-induced lung damage. The therapeutic value of PAI-1 inhibition in lung radiation injury may be associated with other types of cells.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2024

A non-isothermal breakage-damage model for plastic-bonded granular materials incorporating temperature, pressure, and rate dependencies

Plastic-bonded granular materials (PBM) are widely used in industrial sectors, including building construction, abrasive applications, and defense applications such as plastic-bonded explosives. The mechanical behavior of PBM is highly nonlinear, irreversible, rate dependent, and temperature sensitive governed by various micromechanical attributions such as grain crushing and binder damage. This paper presents a thermodynamically consistent, microstructure-informed constitutive model to capture these characteristic behaviors of PBM. Key features of the model include a breakage internal variable to upscale the grain-scale information to the continuum level and to predict grain size evolution under mechanical loading. In addition, a damage internal state variable is introduced to account for the damage, deterioration, and debonding of the binder matrix upon loading. Temperature is taken as a fundamental external state variable to handle non-isothermal loading paths. The proposed model is able to capture with good accuracy several important aspects of the mechanical properties of PBM, such as pressure-dependent elasticity, pressure-dependent yield strength, brittle-to-ductile transition, temperature dependency, and rate dependency in the post-yielding regime. Furthermore, the model is validated against multiple published datasets obtained from confined and unconfined compression tests, covering various PBM compositions, confining pressures, temperatures, and strain rates.

Breakage↗
DOE OSTI2021

Bayesian calibration of a physics-based crystal plasticity and damage model

In this work, we present a model parameter calibration procedure for a physics-based crystal plasticity model. The calibration process utilizes a powerful statistics-based Bayesian calibration method. Calibration of the crystal plasticity parameters makes use of experimentally-measured data, i.e. compressive stress–strain response, from $\langle$100$\rangle$ and $\langle$123$\rangle$ single crystal copper dynamically loaded via Kolsky bar tests. The calibration of damage parameters is achieved using experimentally-measured free-surface velocity history data from plate impact test on $\langle$100$\rangle$ and $\langle$110$\rangle$ single crystal copper, which generates shock compression followed by dynamic tensile failure. A validation assessment is then carried out by comparing the calibrated model predictions and experimental measurements of the dynamic tensile damage generated in an impacted bicrystal copper plate. Lastly, a model-informed rationale for the experimentally-observed dependence of the spatial distribution of ductile damage (porosity) on crystallography is provided.

42 ENGINEERING↗
DOE OSTI2019

Damage mechanics modeling of the non-linear behavior of SiC/SiC ceramic matrix composite fuel cladding

A damage model is developed and validated with experimental data for the non-linear mechanical behavior of SiC/SiC composite materials in nuclear applications. The model extends a continuum damage mechanics formalism, where explicit property degradation and volumetric swelling as a result of neutron irradiation are additionally included. The model is shown to be validated with out-of-pile experiments, and then applied to off-normal and high-burnup operating conditions associated with loss of cooling and extended radiation exposure, respectively. Optimized operating conditions aimed at reducing the fuel temperature included variation of the thermal conductivity and initial fuel-cladding gap thermal resistance. The nonlinear response along with continuum micro-cracking damage predictions are obtained and compared to the behavior during normal operating conditions. Numerical implementation of the model is based on 3-D Finite Element solutions.

36 MATERIALS SCIENCE↗
DOE OSTI2021

Irradiation Damages of Structural Materials under Different Irradiation Environments

For the advancement and development of nuclear systems used in heavy irradiation environments such as fusion DEMO reactors, fission reactors, fast reactors, and accelerator driven target systems, it is necessary to fully understand the changes of mechanical properties and the other properties of the materials induced by irradiation and to clarify the synergistic effect of displacement damage and helium generation. In this study the mechanical property changes and microstructural development induce by displacement damage and helium production have been mainly examined in austenitic stainless steels, 316FR and type304, and ferritic/martensitic steel, HCM12A, irradiated at around 550oC in JRR-3M reactor and/or JOYO fast reactor. At 550°C, 316FR steel was superior to 304 steel in terms of the amount of ductility and strength with respect to irradiation resistance. It is noteworthy that at 550 °C as well as room temperature, the higher fracture strength of the 316FR steels is a remarkable result. It is found that helium atoms strongly influenced on creep lifetime of the irradiated austenitic stainless steel, 316FR. It was found that the ratio of creep rupture time is slightly lower than the lower limit of previous study’s Miyaji and co-workers in the region from 0.01 appm to 1 appm. It is also found that the lower limit of reduction ratio of creep rupture time (irradiation specimen to unirradiation one) does not decrease linearly with the helium production above 10 appm up to about 33 appm. dpa enhanced the reduction of creep lifetime. Recent R&D of high-energy accelerator driven target systems used under heavy irradiation environment is also introduced and discussed for high radiation resistance materials such as Ti alloys with very high number density of nano size precipitate, which have been studying under RaDIATE collaboration, from points of view of irradiation damage and materials development.

radiation damage, structural alloys, neutron irrad↗
DOE OSTI2023

The effect of secondary phases on microstructure and irradiation damage in an as-built additively manufactured 316 L stainless steel with a hafnium compositional gradient

Additive manufacturing (AM) or rapid prototyping has become a crucial tool for reducing both cost and time while increasing efficiency in qualifying structural materials for reactor use. In this study, directed energy deposition (DED) was used to develop an as-built 316 L stainless steel sample with three regions of increasing Hf-dopant to study the effects of Hf on the irradiation response of the material. Morphological and microstructural changes were analyzed before and after 2 MeV proton irradiation at 360 °C to a damage of 2.5 dpa at ~ 10 µm below the surface. The addition of Hf effectively suppressed radiation-induced damage (dislocation loops, radiation-induced segregation) due to enhanced point defect recombination. The radiation damage seen in the as-built sample was further compared to a thermo-mechanically treated counterpart of the same fabrication and irradiation parameters which was found to behave superiorly. In conclusion, the increased radiation resistance of this material may be attributed to the as-built microstructure, which includes undissolved Hf particles, delta ferrite grains and cellular sub-grain boundaries that can hinder defect motion.

316L Stainless Steel↗
DOE OSTI2025

Accurate and rapid acoustic damage characterization in complex structures using sparse sensor networks and deep learning models

Damage diagnosis in critical components is essential for ensuring the safety and reliability of operations across industries, spanning manufacturing, aerospace, and energy. Traditional acoustic nondestructive testing methods primarily focus on detecting defects through the direct scattering of single-mode incident waves from the damage, which limit their applicability to simple structures and small inspection areas. Our earlier research demonstrated that machine learning algorithms combined with sparse sensor networks can identify critical defect signatures even from multiply scattered, multi-mode acoustic signals, indicating the potential for improved defect inspection in complex, real-world structures. In this work, we demonstrate the successful implementation of this approach in a fixed sensor configuration to rapidly and accurately detect simulated defects in a geometrically complex, real-world structure, a brake rotor hub. Three different types of defects were physically simulated on the surface of the hub, and the collected data were used to train an autoencoder-based deep learning model. Two models were tested, one using single measurements and the other using multiple measurements taking advantage of the spatial distribution of the sensor network. After training, the multi-measurement model achieved 100 % accuracy in identifying, classifying, and locating unseen, unique damages. This work illustrates the potential of the proposed method for a wide range of industrial applications.

36 MATERIALS SCIENCE↗
DOE OSTI2021

Remediating neutron damage in large area planar Ge-DSSD with amorphous germanium contacts through annealing and pulse-height correction

Large area, position sensitive planar germanium detectors offer new opportunities in -ray spectroscopy. For in-beam studies remediating neutron damage is important. This work studied a mechanically cooled circular planar 9 × 1 cm wafer with orthogonal 16 × 16 amorphous germanium strip electrodes. Before neutron irradiation the wafer was heated in-cryostat to above 373 K for more than 24 h in order to test the robustness of the contacts and the mechanical cooler. No deterioration in performance was observed. The detector was then exposed to controlled doses of 2.2 MeV neutrons, produced from the 7 Li(p,n) 7 Be reaction until substantial damage was observed. Averaged over the surface of the wafer, a flux of 1.9(1) x 10 9 n/cm 2 was delivered. The detector then survived thermal cycling and 350 K (~77°C) annealing for 70 h which substantially reduced hole trapping. pulse-height correction is investigated to further mitigate the neutron damage. Higher temperature annealing at 365 K was not successful.

73 NUCLEAR PHYSICS AND RADIATION PHYSICS↗
DOE OSTI2023

Multi-fidelity physics-informed machine learning for probabilistic damage diagnosis

Machine learning (ML) models are gaining popularity in structural health monitoring (SHM) because of their ability to learn the complex relationship between damage and sensor data. However, the lack of sufficient experimental data for structures with different degrees of damage is a key problem in training ML models for SHM. This problem can be alleviated by using physics-based models to generate the required training data to build physics-informed ML (PIML) models for SHM. However, it takes significant computational effort to perform enough high-fidelity simulations of the diagnostic test. It is thus desirable to know whether the available computational resource budget should be expended on numerous low-fidelity physics simulations, or a small number of high-fidelity simulations, or their combination. In this paper, we investigate this aspect of generating adequate training data for PIML, by constructing multi-fidelity PIML models. We evaluate the performance of several PIML models, trained with different amounts of low-fidelity and high-fidelity data, in locating hidden cracks in concrete structures using a nonlinear dynamics-based diagnosis technique. Here, we find that high-fidelity physics simulations that do not cover the (test and damage) parameter space do not improve the performance of diagnostic PIML models built using data from many low-fidelity physics simulations.

42 ENGINEERING↗
DOE OSTI2014

Inhibition of autophagy enhances DNA damage-induced apoptosis by disrupting CHK1-dependent S phase arrest

DNA damage has been shown to induce autophagy, but the role of autophagy in the DNA damage response and cell fate is not fully understood. BO-1012, a bifunctional alkylating derivative of 3a-aza-cyclopenta[a]indene, is a potent DNA interstrand cross-linking agent with anticancer activity. In this study, BO-1012 was found to reduce DNA synthesis, inhibit S phase progression, and induce phosphorylation of histone H2AX on serine 139 (γH2AX) exclusively in S phase cells. Both CHK1 and CHK2 were phosphorylated in response to BO-1012 treatment, but only depletion of CHK1, but not CHK2, impaired BO-1012-induced S phase arrest and facilitated the entry of γH2AX-positive cells into G2 phase. CHK1 depletion also significantly enhanced BO-1012-induced cell death and apoptosis. These results indicate that BO-1012-induced S phase arrest is a CHK1-dependent pro-survival response. BO-1012 also resulted in marked induction of acidic vesicular organelle (AVO) formation and microtubule-associated protein 1 light chain 3 (LC3) processing and redistribution, features characteristic of autophagy. Depletion of ATG7 or co-treatment of cells with BO-1012 and either 3-methyladenine or bafilomycin A1, two inhibitors of autophagy, not only reduced CHK1 phosphorylation and disrupted S phase arrest, but also increased cleavage of caspase-9 and PARP, and cell death. These results suggest that cells initiate S phase arrest and autophagy as pro-survival responses to BO-1012-induced DNA damage, and that suppression of autophagy enhances BO-1012-induced apoptosis via disruption of CHK1-dependent S phase arrest. - Highlights: • Autophagy inhibitors enhanced the cytotoxicity of a DNA alkylating agent, BO-1012. • BO-1012-induced S phase arrest was a CHK1-dependent pro-survival response. • Autophagy inhibition enhanced BO-1012 cytotoxicity via disrupting the S phase arrest.

60 APPLIED LIFE SCIENCES↗