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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 1,063 records · Page 59
All sourcesNASA NTRSDOE OSTI
DOE OSTI2014

The TWEAK–Fn14 dyad is involved in age-associated pathological changes in skeletal muscle

Highlights: • The levels of TWEAK receptor Fn14 are increased in skeletal muscle during aging. • Deletion of Fn14 attenuates age-associated skeletal muscle fiber atrophy. • Deletion of Fn14 inhibits proteolysis in skeletal muscle during aging. • TWEAK–Fn14 signaling activates transcription factor NF-κB in aging skeletal muscle. • TWEAK–Fn14 dyad is involved in age-associated fibrosis in skeletal muscle. - Abstract: Progressive loss of skeletal muscle mass and strength (sarcopenia) is a major clinical problem in the elderly. Recently, proinflammatory cytokine TWEAK and its receptor Fn14 were identified as key mediators of muscle wasting in various catabolic states. However, the role of the TWEAK–Fn14 pathway in pathological changes in skeletal muscle during aging remains unknown. In this study, we demonstrate that the levels of Fn14 are increased in skeletal muscle of 18-month old (aged) mice compared with adult mice. Genetic ablation of Fn14 significantly increased the levels of specific muscle proteins and blunted the age-associated fiber atrophy in mice. While gene expression of two prominent muscle-specific E3 ubiquitin ligases MAFBx and MuRF1 remained comparable, levels of ubiquitinated proteins and the expression of autophagy-related molecule Atg12 were significantly reduced in Fn14-knockout (KO) mice compared with wild-type mice during aging. Ablation of Fn14 significantly diminished the DNA-binding activity of transcription factor nuclear factor-kappa B (NF-κB), gene expression of various inflammatory molecules, and interstitial fibrosis in skeletal muscle of aged mice. Collectively, our study suggests that the TWEAK–Fn14 signaling axis contributes to age-associated muscle atrophy and fibrosis potentially through its local activation of proteolytic systems and inflammatory pathways.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Telmisartan, a possible PPAR-δ agonist, reduces TNF-α-stimulated VEGF-C production by inhibiting the p38MAPK/HSP27 pathway in human proximal renal tubular cells

Highlights: • TNF-α increased VEGF-C expression by enhancing phosphorylation of p38MAPK and HSP27. • Telmisartan decreased TNF-α-stimulated expression of VEGF-C. • Telmisartan suppressed TNF-α-induced phosphorylation of p38MAPK and HSP27. • Telmisartan activated endogenous PPAR-δ protein. • Telmisartan suppressed p38MAPK phosphorylation in a PPAR-δ-dependent manner. - Abstract: Vascular endothelial growth factor-C (VEGF-C) is a main inducer of inflammation-associated lymphangiogenesis in various inflammatory disorders including chronic progressive kidney diseases, for which angiotensin II receptor type 1 blockers (ARBs) are widely used as the main treatment. Although proximal renal tubular cells may affect the formation of lymphatic vessels in the interstitial area by producing VEGF-C, the molecular mechanisms of VEGF-C production and its manipulation by ARB have not yet been examined in human proximal renal tubular epithelial cells (HPTECs). In the present study, TNF-α dose-dependently induced the production of VEGF-C in HPTECs. The TNF-α-induced production of VEGF-C was mediated by the phosphorylation of p38MAPK and HSP27, but not by that of ERK or NFkB. Telmisartan, an ARB that can activate the peroxisome proliferator-activated receptor (PPAR), served as a PPAR-δ activator and reduced the TNF-α-stimulated production of VEGF-C. This reduction was partially attributed to a PPAR-δ-dependent decrease in p38MAPK phosphorylation. Our results indicate that TNF-α induced the production of VEGF-C in HPTECs by activating p38MAPK/HSP27, and this was partially inhibited by telmisartan in a PPAR-δ dependent manner. These results provide a novel insight into inflammation-associated lymphangiogenesis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Astragaloside IV suppresses transforming growth factor-β1 induced fibrosis of cultured mouse renal fibroblasts via inhibition of the MAPK and NF-κB signaling pathways

Renal fibrosis, a progressive process characterized by the accumulation of extracellular matrix (ECM) leading to organ dysfunction, is a characteristic of chronic kidney diseases. Among fibrogenic factors known to regulate the renal fibrotic process, transforming growth factor-β (TGF-β) plays a central role. In the present study, we examined the effect of Astragaloside IV (AS-IV), a component of the traditional Chinese medicinal plant Astragalus membranaceus, on the processes associated with renal fibrosis in cultured mouse renal fibroblasts treated with TGF-β1. RT-PCR, western blotting, immunofluorescence staining and collagen assays showed that AS-IV suppressed TGF-β1 induced fibroblast proliferation, transdifferentiation, and ECM production in a dose-dependent manner. Examination of the underlying mechanisms showed that the effect of AS-IV on the inhibition of fibroblast differentiation and ECM formation were mediated by its modulation of the activity of the MAPK and NF-κB signaling pathways. Taken together, our results indicate that AS-IV alleviates renal interstitial fibrosis via a mechanism involving the MAPK and NF-κB signaling pathways and demonstrate the therapeutic potential of AS-IV for the treatment of chronic kidney diseases. - Highlights: • AS-IV suppressed TGF-β1 induced renal fibroblast proliferation. • AS-IV suppressed TGF-β1 induced renal fibroblast transdifferentiation. • AS-IV suppressed TGF-β1 induced ECM production. • AS-IV alleviates renal fibrosis via the MAPK and NF-κB signaling pathways.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

High inorganic phosphate causes DNMT1 phosphorylation and subsequent fibrotic fibroblast activation

Phosphate is an essential constituent of critical cellular functions including energy metabolism, nucleic acid synthesis and phosphorylation-dependent cell signaling. Increased plasma phosphate levels are an independent risk factor for lowered life-expectancy as well as for heart and kidney failure. Nevertheless, direct cellular effects of elevated phosphate concentrations within the microenvironment are poorly understood and have been largely neglected in favor of phosphor-regulatory hormones. Because interstitial fibrosis is the common determinant of chronic progressive kidney disease, and because fibroblasts are major mediators of fibrogenesis, we here explored the effect of high extracellular phosphate levels on renal fibroblasts. We demonstrate that high inorganic phosphate directly induces fibrotic fibroblast activation associated with increased proliferative activity, increased expression of α-smooth muscle actin and increased synthesis of type I collagen. We further demonstrate that such fibroblast activation is dependent on phosphate influx, aberrant phosphorylation of DNA methyltransferase DNMT1 and aberrant CpG island promoter methylation. In summary, our studies demonstrate that elevated phosphate concentrations induce pro-fibrotic fibroblast activation independent of phospho-regulatory hormones. - Highlights: • We exposed human kidney fibroblasts to media containing 1 mM or 3 mM phosphate. • Increased phosphate influx causes phosphorylation of DNA methyltransferase Dnmt1. • Phosphorylated Dnmt1 causes promoter methylation and transcriptional silencing of RASAL1. • Depletion of RASAL1 causes increased intrinsic Ras-GTP activity and fibroblast activation. • Inorganic phosphate causes fibroblast activation independent of phospho-regulatory hormones.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Matrilin-2 regulates proliferation, apoptosis and cell cycle during radiation-induced injury in HPAEpiC cell

Radiation pulmonary injury is related to the accumulation of extracellular matrix proteins in the alveolar interstitial space. Matrilin-2 as a component of extracellular filamentous networks, present higher level in the lung tissue from irradiated mice and irradiated pulmonary epithelial cell line, HPAEpiC cells. Knockdown of endogenous matrilin-2 prevents the apoptosis of HPAEpiC cell induced by the irradiation injury. Consistently, over-expression of matrilin-2 reduced the proliferation and induced apoptosis of HPAEpiC cells. Matrilin-2 promotes the expression of p21 via increasing the transcriptional activity of p53, by which induces the G1 phase arresting in HPAEpiC cells. In summary, matrilin-2, increased by irradiation, reduced the proliferation and induces apoptosis of pulmonary epithelial cells via p53/p21 pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Activation of nuclear β-catenin/c-Myc axis promotes oxidative stress injury in streptozotocin-induced diabetic cardiomyopathy

Myocardial oxidative stress injury plays a crucial role in the pathogenesis of diabetic cardiomyopathy (DCM). Wnt/β-catenin signaling has been reported to involve in various heart diseases. However, the underlying mechanism associated with β-catenin in DCM remains elusive. This study intended to explore the effect of β-catenin on oxidative damage of DCM by establishing streptozotocin (STZ)-induced diabetic mouse model and hydrogen peroxide (H{sub 2}O{sub 2})-treated myocardial cell model. Cardiac oxidative stress in DCM was detected by measurements of lipid peroxidation and anti-oxidative enzyme activities as well as DHE staining. Nuclear β-catenin activity and oxidative damage degree were measured by western blotting, qPCR, MTT assay and TUNEL staining. Cardiac function and morphology were evaluated by echocardiography and histopathology. Under diabetic oxidative stress or H{sub 2}O{sub 2} stimulation, nuclear β-catenin accumulation upregulated downstream c-Myc and further facilitated DNA damage and p53-mediated apoptosis as well as cell viability reduction, followed by phenotypic changes of cardiac dysfunction, interstitial fibrosis deposition and myocardial atrophy. Conversely, through directly inhibiting nuclear β-catenin/c-Myc axis, not only did siRNA knockdown of β-catenin or c-Myc attenuate cell injury in H{sub 2}O{sub 2}-stimulated cardiomyocytes, but also diabetic cardiac-specific β-catenin-knockout mice displayed the same prevention of heart injury as insulin-treated diabetic mice. The present study demonstrated that activated nuclear β-catenin/c-Myc axis was responsible for oxidative cardiac impairment of DCM. Therefore, repressing functional nuclear β-catenin may provide a hopeful therapeutic strategy for DCM. - Highlights: • Nuclear β-catenin/c-Myc axis is activated in H{sub 2}O{sub 2}-treated cardiomyocytes. • Knockdown of β-catenin or c-Myc relieves H{sub 2}O{sub 2}-caused cardiomyocyte injury. • Nuclear β-catenin/c-Myc axis is activated in diabetic cardiomyopathy (DCM). • Cardiac deletion of β-catenin abates oxidative injury of DCM via inhibiting c-Myc.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Preservation of rat hearts in subfreezing temperature isochoric conditions to – 8 °C and 78 MPa

Highlights: • A novel method of low-temperature organ preservation is tested using rat hearts. • Isochoric systems allow ice-free preservation at temperatures well below freezing. • Conventional heart preservation employs on-ice storage in atmospheric conditions. • Histological quality is improved in hearts preserved in a −4 °C isochoric system. Isochoric (constant volume) preservation at subfreezing temperatures is being investigated as a novel method for preserving cells and organs. This study is a first initial effort to evaluate the efficacy of this method for heart preservation, and to provide a preliminary outline of appropriate preservation parameters. To establish a baseline for further studies, rat hearts were preserved in a University of Wisconsin (UW) intracellular solution for one hour under isochoric conditions at: 0 °C (atmospheric pressure - 0.1 MPa), - 4 °C (41 MPa), - 6 °C (60 MPa) and – 8 °C (78 MPa). The viability of the heart was evaluated using Langendorff perfusion and histological examination. The physiological performance of hearts preserved at – 4 °C (41 MPa) was comparable to that of a heart preserved on ice at atmospheric pressure, with no statistically significant difference in histological injury score. However, hearts preserved at −4 °C displayed substantially reduced interstitial edema compared to hearts preserved by conventional hypothermic preservation in UW on ice at atmospheric pressure, suggesting significant protection from increased vascular permeability following preservation. Hearts preserved at – 6 °C (60 MPa) suffered injury from cellular swelling and extensive edema, and at – 8 °C (78 MPa) hearts experienced significant morphological disruption. To the best of our knowledge, this is the first publication showing that a mammalian organ can survive low subfreezing temperatures without the use of a cryoprotective additive. Lowering the preservation temperature reduces metabolism and improves preservation quality, and these results suggest that improvements in preservation are possible at subzero temperatures with low to moderate pressures observed at −4 °C. Notably, tissue damage was observed at lower temperatures (−6 °C or below) accompanying further elevation of pressure associated with isochoric preservation that may prove detrimental. Therefore, subfreezing temperature isochoric preservation protocols should optimize, a combination of temperature and pressure that will minimize the negative effects of elevated pressure while retaining the beneficial effect of lower temperatures and reduced metabolism.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Suppression of Elp2 prevents renal fibrosis and inflammation induced by unilateral ureter obstruction (UUO) via inactivating Stat3-regulated TGF-β1 and NF-κB pathways

Highlights: • Elp2 knockout attenuates fibrotic progression in a UUO mouse model. • Elp2 deficiency reduces tubulointerstitial inflammation in the UUO model. • Elp2 knockdown ameliorates TGF-β1-induced fibrosis and LPS-triggered inflammation in mTECs through regulating STAT3. Renal fibrosis and inflammation are common underlying processes of progressive kidney diseases. Elongator protein 2 (Elp2), identical to signal transducer and activator of transcription-3 (STAT-3)-interacting protein-1 (Stip1), is a component of the Elongator complex that regulates RNA polymerase II. Elp2 regulates STAT-3 activation to control various cellular processes. The mechanisms of Elp2 prevention in renal interstitial fibrosis and inflammation remain unknown. In the study, Elp2 transgenic knockout (KO) and wild type (WT) mice were employed to investigate the effects of Elp2 on renal fibrosis and inflammation development after unilateral ureter obstruction (UUO) surgery. The results indicted that Elp2 was significantly expressed in renal tissues of WT/UUO mice. Elp2-KO mice exhibited attenuated histological changes of kidney, as well as collagen and fibrosis accumulation. Lower expressions of transforming growth factor (TGF)-β1, α-smooth muscle actin (α-SMA), fibronectin, vimentin, and phospho-Smad2/3 were observed in kidney of Elp2-KO mice than that of WT mice after UUO. Elp2-KO mice showed less inflammation, as evidenced by the decrease of circulating or renal pro-inflammatory cytokines, as well as the reduction of phospho-nuclear factor (NF)-κB. Additionally, Elp2-KO apparently led to a decrease in phospho-STAT3 in kidney of UUO mice. In vitro, we found that TGF-β1- and LPS-induced fibrosis and inflammation were abrogated by Elp2 knockdown, which were intriguingly abolished by activating STAT3 phosphorylation using its activator of colivelin (Col). Together, our findings supplied that Elp2 might be a potential therapeutic target to prevent the progression of renal fibrosis and inflammation.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Bisphenol A-elicited miR-146a-5p impairs murine testicular steroidogenesis through negative regulation of Mta3 signaling

The epigenetic effects on expression of non-coding RNAs (e.g. microRNAs) of environmental toxin bisphenol A (BPA) have extended our understanding of the etiology of human reproductive disorders including hypospermatogenesis and androgen deficiency. BPA-induced miR-146a-5p is a potent regulator of endocrine and immune homeostasis, but its role in testis remain unexplored. We show here that in murine testis, miR-146a-5p was exclusively expressed in interstitial Leydig cells (LCs). This expression was significantly induced by BPA exposure. Consequently, the elevated miR-146a-5p exacerbated the deleterious effects of BPA on testicular steroidogenesis. Mechanistically, miR-146a-5p repressed the expression of Mta3, a pivotal chromatin remodeling transcription factor recently involved in controlling the steroidogenic activity, via directly targeting its 3′UTR. This repression thereafter rendered LCs more sensitive to BPA-elicited inhibitory effects. Conversely, ectopic expression of hMTA3 successfully rescued miR-146a-5p-elicited inhibitory effects on testicular steroidogenesis in BPA-challenged LCs. Taken together, the available data provide novel evidence that deregulation of testicular miR-146a-5p/Mta3 cascade mediates, at least in part, the steroidogenic dysfunction caused by BPA exposure.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Administration of ubiquitin-activating enzyme UBA1 inhibitor PYR-41 attenuates angiotensin II-induced cardiac remodeling in mice

Highlights: • Ang II induces UBA1 expression. • PYR-41 inhibits cardiac remodeling. • PYR-41 stabilizes PTEN. Pathological cardiac hypertrophy is the main risk factor for heart diseases. The ubiquitin-proteasome system (UPS) is the major intracellular protein degradation system involved in the development of cardiac hypertrophic remodeling. Ubiquitin-activating enzyme E1, a key component of the UPS, catalyzes the first step in ubiquitin conjugation to mark cellular proteins for degradation via proteasome. However, the functional role of E1 (UBA1) in regulation of hypertrophic remodeling in angiotensin II (Ang II)-infused mice remains unknown. In this study, male wild-type mice were treated with UBA1 inhibitor PYR-41 at two doses of 5 and 10 mg and infused with Ang II (1000 ng/kg/min) for 14 days. Systolic blood pressure was detected by using tail-cuff system. Cardiac function was assessed by echocardiography. Hypertrophic remodeling was analyzed examined by histological examinations. The expressions of genes and proteins were detected by quantitative real-time PCR and immunoblotting analysis. After 14 days, Ang II infusion significantly increased UBA1 expression at both mRNA and protein levels in the hearts. Furthermore, Ang II-infused mice showed a significant increase in systolic blood pressure compensatory cardiac function, hypertrophy, interstitial fibrosis, inflammation and oxidative stress compared with saline-treated controls, whereas these effects were dose-dependently attenuated in PYR-41-treated mice. These beneficial actions were associated mainly with inhibition of PTEN degradation and multiple downstream mediators (AKT, ERK1/2, STAT3, TGF-β/Smad2/3 and NF-kB(p65)). In conclusion, these results indicate that inhibition of UBA1 suppresses Ang II-induced hypertrophic remodeling, and suggest that administration of low dose PYR-41 may be a new potential therapeutic approach for treating hypertensive heart diseases.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2026

Extending SLUSCHI for Automated Diffusion Calculations

We present an extension of the SLUSCHI package (Solid and Liquid in Ultra Small Coexistence with Hovering Interfaces) to enable automated diffusion calculations from first-principles molecular dynamics. While the original SLUSCHI workflow was designed for melting temperature estimation via solid-liquid coexistence, we adapt its input and output handling to isolate the volume search stage and generate one production trajectory suitable for diffusion analysis. Post-processing tools parse VASP outputs, compute mean-square displacements (MSD), and extract tracer diffusivities using the Einstein relation with robust error estimates through block averaging. Diagnostic plots, including MSD curves, running slopes, and velocity autocorrelations, are produced automatically to help identify diffusive regimes. The method has been validated through representative case studies: self-diffusion in Al-Cu liquid alloys, sublattice melting in Li7La3Zr2O12 and Er2O3, interstitial oxygen transport in bcc and fcc Fe, and oxygen diffusivity in Fe-O liquids with variable Si and Al contents. Viscosity and diffusivity are linked through the Stokes-Einstein relation, with composition dependence assessed via simple linear mixing. This capability broadens SLUSCHI from melting-point predictions to transport property evaluation, enabling high-throughput, fully first-principles datasets of diffusion coefficients and viscosities across metals and oxides.

36 MATERIALS SCIENCE↗
DOE OSTI2018

Formation of carbon nanostructures in nuclear graphite under high-temperature in situ electron-irradiation

Defect evolution in nuclear graphite has been studied in real time using high-temperature in situ transmission electron microscopy. In situ electron-irradiation was conducted at 800 °C on a 200 kV transmission electron microscope with a dose rate, given in terms of displacements per atom per second, of approximately 1.46 × 10 –3 dpa/s. Defect domains consisting of ordered arrangements of pentagons, hexagons, and heptagons exist intrinsically in nuclear graphite and in addition are readily produced via electron-irradiation; however, at elevated temperatures these defect domains undergo atomic rearrangements resulting in the formation of carbon nanostructures via curling and closure of the basal planes. The formation of fullerenes and other structures due to thermal annealing or high-temperature electron-irradiation has been observed in disordered regions of the microstructure and interstitially between basal planes. Furthermore, these defect structures result in localized swelling and expansion of crystallites along the c axis; thus, it is proposed as one of the many atomic mechanisms involved in the dimensional change of nuclear graphite subjected to high-temperature irradiation.

36 MATERIALS SCIENCE↗
DOE OSTI2019

Experimental evidence for ‘buckle, ruck and tuck’ in neutron irradiated graphite

The current mainstream theory for radiation-induced dimensional change of nuclear graphite is based on the notion that interstitially displaced carbon atoms will coalesce into dislocation loops (i.e., additional basal planes). This standard atomic-displacement model has been challenged by theories based on first principles calculations. Furthermore, the so-called ‘ruck and tuck’ of basal planes has been proposed as an alternative mechanism to explain the observed c-axis expansion under irradiation; however, no such defects have been observed experimentally so far. In this study, the first experimental evidence for the presence of a ‘ruck and tuck’ defect in high-temperature neutron-irradiated nuclear graphite is introduced.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Vacancy-driven variations in the phonon density of states of fast neutron irradiated nuclear graphite

Research examining radiation damage and its effects in graphite began in the 1940’s during the development of moderated nuclear reactors. Interest in this topic is expanding because of emerging applications associated with fullerenes and carbon nanostructures as well as its long-standing use as a fission moderator. In this work, we report the measurements of the full phonon density of states of irradiated nuclear graphite using inelastic neutron scattering experiments at room temperature. The samples were previously exposed to different levels of neutron doses and irradiation temperatures. The phonon density of states of perfect and defected graphite supercells including different configurations of vacancies and interstitials were calculated using first-principles direct method. Despite high neutron irradiation doses, the scattering measurements show that the induced damage is localized, and the layered structure is preserved. In conclusion, a comparison of the measured phonon densities of states of irradiated samples with those calculated of defected supercells indicates that the main changes observed are mainly attributed to formation of vacancies.

36 MATERIALS SCIENCE↗
DOE OSTI2022

Defect formation and bending properties in graphite under He atom implantation investigated by molecular dynamics method

The formation and evolution of radiation defects and their effects on bending property of a single graphite under low energy helium atom implantation have been studied at atomic scale through molecular dynamics simulations. Various simple interstitial and vacancy defects are observed during the implantation process, which is a function of incident energy and cross section of helium-carbon interaction. Large defects are observed after continuous helium atom implantations. The effects of incident energy on the density, size and distribution of defects are analyzed in detail. Furthermore, the kinetic evolution process of radiation defects at different annealing temperatures have also been simulated, including the migration, aggregation, transformation, coalescence, and self-healing. Here, the large defect clusters, crossing several carbon layers, have been confirmed to be the primary reasons that affect the bending property of graphite. All these results provide a new understanding for further applications of graphite in nuclear reactors.

Atomic implantation↗
DOE OSTI2013

Evaporation — a key mechanism for the thaumasite form of sulfate attack

Understanding the mechanisms leading to chemical attack on concrete is crucial in order to prevent damage of concrete structures. To date, most studies on sulfate attack and thaumasite formation are based on empirical approaches, as the identification of associated reaction mechanisms and paths is known to be highly complex. In this study, sulfate damaged concrete from Austrian tunnels was investigated by mineralogical, chemical and isotope methods to identify the reactions which caused intense concrete alteration. Major, minor and trace elemental contents as well as isotope ratios of local ground water (GW), drainage water (DW) and interstitial solutions (IS), extracted from damaged concrete material, were analyzed. Locally occurring GW contained 3 to 545 mg L{sup −1} of SO{sub 4} and is thus regarded as slightly aggressive to concrete in accordance to standard specifications (e.g. DIN EN 206-1). The concrete linings and drainage systems of the studied tunnels, however, have partly suffered from intensive sulfate attack. Heavily damaged concrete consisted mainly of thaumasite, secondary calcite, gypsum, and relicts of aggregates. Surprisingly, the concentrations of dissolved ions were extremely enriched in the IS with up to 30,000 and 12,000 mg L{sup −1} of SO{sub 4} and Cl, respectively. Analyses of aqueous ions with a highly conservative behavior, e.g. K, Rb and Li, as well as {sup 2}H/H and {sup 18}O/{sup 16}O isotope ratios of H{sub 2}O of the IS showed an intensive accumulation of ions and discrimination of the light isotopes vs. the GW. These isotope signals of the IS clearly revealed evaporation at distinct relative humidities. From ion accumulation and isotope fractionation individual total and current evaporation degrees were estimated. Our combined elemental and isotopic approach verified wetting–drying cycles within a highly dynamic concrete-solution-atmosphere system. Based on these boundary conditions, key factors controlling thaumasite formation are discussed regarding the development of more sulfate-resistant concrete and concrete structures.

36 MATERIALS SCIENCE↗
DOE OSTI2015

A speciation solver for cement paste modeling and the semismooth Newton method

The mineral assemblage of a cement paste may vary considerably with its environment. In addition, the water content of a cement paste is relatively low and the ionic strength of the interstitial solution is often high. These conditions are extreme conditions with respect to the common assumptions made in speciation problem. Furthermore the common trial and error algorithm to find the phase assemblage does not provide any guarantee of convergence. We propose a speciation solver based on a semismooth Newton method adapted to the thermodynamic modeling of cement paste. The strong theoretical properties associated with these methods offer practical advantages. Results of numerical experiments indicate that the algorithm is reliable, robust, and efficient.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗
DOE OSTI2021

Evaluation of microstructural changes in fresh cement paste using AC impedance spectroscopy vs. oscillation rheology and 1H NMR relaxometry

AC impedance spectroscopy (ACIS) is a promising technique for monitoring the microstructure evolution of fresh cement paste in real-time. This paper compared the change of bulk electric resistivity (ρ{sub bulk}) obtained from ACIS with the developments of storage modulus (G′) and the mean transverse relaxation times (T{sub 2}) of fresh Portland cement pastes within 5 h. It was found that the three different phases (Phase I, II, and III) on the microstructural build-up process of fresh paste can be accurately distinguished by analyzing ρ{sub bulk}, as well as G′ and T{sub 2}. The use of ρ{sub bulk} fails to characterize the microstructural changes in Phase I due to the great sensitivity on the electrical conductivity of the interstitial solution. However, it can successfully reflect the developing features of microstructure in Phases II and III, and reliably evaluate the impacts of water to cement ratio, superplasticizer, and supplementary cementitious materials on the microstructural development.

36 MATERIALS SCIENCE↗