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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 19 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

Electrochemical and microstructural characterization of magnetron-sputtered ATO thin films as Li–ion storage materials

Highlights: • Nano-structured ATO thin films prepared by RF magnetron sputtering at 25 °C, 100 °C and 200 °C, respectively. • ATO thin films show a high reversible capacity and high rate performance. • Electrochemical reaction mechanism of the ATO thin film was revealed by transmission electron microscopy. - Abstract: Sb-doped SnO{sub 2} (ATO) nanostructured thin films were prepared by using radio frequency magnetron sputtering at the substrate temperatures of 25 °C, 100 °C and 200 °C, respectively. All the ATO thin films have the similar redox characteristics in the cyclic voltammetry measurements. The ATO thin film sputtered at 200 °C shows the lowest charge transfer resistance and best electrochemical performance, and has a high reversible capacity of 679 mA h g{sup −1} at 100 mA g{sup −1} after 200 charge–discharge cycles and high rate performance of 483 mA h g{sup −1} at 800 mA g{sup −1}. The electrochemical mechanisms were investigated by analyzing the phase evolution of the ATO electrodes that had been electrochemically induced at various stages. The results reveal that the ATO underwent reversible lithiation/delithiation processes during the electrochemical cycles, i.e., the SnO{sub 2} reacted with Li{sup +} to produce metallic Sn and followed by the formation of the Li{sub x}Sn alloys during discharge process, and then Li{sub x}Sn alloys de-alloyed, Sn reacted with Li{sub 2}O, and even partially formed SnO{sub 2} during charge process.

36 MATERIALS SCIENCE↗
DOE OSTI2019

Wear and Corrosive Behaviors of Electroless Ni-LaCl{sub 3} Composites on Nanoporous ATO Surface of Ti Substrate

Ti and its alloys, because of its poor wear and oxidation resistance, have seriously restricted its industrial applications in the dry friction conditions. Herein we reported an easy-handling and effective approach for electroless Ni-LaCl{sub 3} nanocomposite films on nanoporous ATO surface of Ti substrate to modify its surface properties. Anodized titanium oxide, shorted as ATO, was designed as a template to deposit Ni-LaCl{sub 3} films on Ti surface with superior bonding interface. By adjusting the anodizing voltage from DC 60 to 240 V, the surface of ATO templates was manipulated to achieve a suitable diameter of nanopores using high voltage with low-current density state. The as-received Ni-LaCl{sub 3} film with a leaflike surface was successfully formed on to ATO surface. With an increase in LaCl{sub 3} addition from 0 to 4.0 g L{sup −1} in bath, results indicated that the diversified orientations of Ni crystals along Ni (111), (200), (220) and (311) were detected for Ni-LaCl{sub 3} films, rather than preferred directions of Ni (111) and (200) for pure Ni sample. As expected, the specific wear rate was ~ 10{sup −5} mm{sup 3} (N m){sup −1} for Ni-4.0 g L{sup −1} LaCl{sub 3} films, which was two times lower than that of the un-coated Ti substrate. Besides a lower microhardness of ~ 629 HV{sub 0.2} was detected for pure Ni, which was much lower that of ~ 752 HV{sub 0.2} for Ni-LaCl{sub 3} films, but higher than that of ~ 336 HV{sub 0.2} for Ti substrate. In addition, a superior corrosion resistance was obtained for Ni-LaCl{sub 3} composites relative to pure Ni, which was ascribed to the coexistence of La{sup 3+} ions and its La-rich insoluble products on its corroded surfaces for completing the pitting holes. In view of these, the as-deposited Ni-LaCl{sub 3} films on the surface of Ti substrate could guide an available proposal for surface modifying of Ti alloys against the wear corrosive failures, further intensifying their servicing life as subjected to harsh conditions.

36 MATERIALS SCIENCE↗
DOE OSTI2015

Effective bond orders from two-step spin–orbit coupling approaches: The I{sub 2}, At{sub 2}, IO{sup +}, and AtO{sup +} case studies

The nature of chemical bonds in heavy main-group diatomics is discussed from the viewpoint of effective bond orders, which are computed from spin–orbit wave functions resulting from spin–orbit configuration interaction calculations. The reliability of the relativistic correlated wave functions obtained in such two-step spin–orbit coupling frameworks is assessed by benchmark studies of the spectroscopic constants with respect to either experimental data, or state-of-the-art fully relativistic correlated calculations. The I{sub 2}, At{sub 2}, IO{sup +}, and AtO{sup +} species are considered, and differences and similarities between the astatine and iodine elements are highlighted. In particular, we demonstrate that spin–orbit coupling weakens the covalent character of the bond in At{sub 2} even more than electron correlation, making the consideration of spin–orbit coupling compulsory for discussing chemical bonding in heavy (6p) main group element systems.

74 ATOMIC AND MOLECULAR PHYSICS↗
DOE OSTI2016

Photocurrent Generation by Photosynthetic Purple Bacterial Reaction Centers Interfaced with a Porous Antimony-Doped Tin Oxide (ATO) Electrode

The ability to exchange energy and information between biological and electronic materials is critical in the development of hybrid electronic systems in biomedicine, environmental sensing, and energy applications. While sensor technology has been extensively developed to collect detailed molecular information, less work has been done on systems that can specifically modulate the chemistry of the environment with temporal and spatial control. The bacterial photosynthetic reaction center represents an ideal photonic component of such a system in that it is capable of modifying local chemistry via light-driven redox reactions with quantitative control over reaction rates and has inherent spectroscopic probes for monitoring function. Here we present a well-characterized model system, consisting of a transparent, porous electrode (antimony-doped tin oxide) which is electrochemically coupled to the reaction center via a cytochrome c molecule. Upon illumination, the reaction center performs the 2-step, 2-electron reduction of a ubiquinone derivative which exchanges with oxidized quinone in solution. Electrons from the electrode then move through the cytochrome to reoxidize the reaction center electron donor. The result is a facile platform for performing redox chemistry that can be optically and electronically controlled in time and space.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Astatine partitioning between nitric acid and conventional solvents: indication of covalency in ketone complexation of AtO +

Astatine-211 has been produced at Texas A&M University on the K150 cyclotron, with a yield of 890 ± 80 MBq through the 209 Bi(α,2n) 211 At reaction via an 8 h bombardment with a beam current of 4–8 μA and an α-particle beam energy of 28.8 MeV. The target was then dissolved in HNO 3 and the extraction of 211 At was investigated into a variety of organic solvents in 1–3 M HNO 3 . Extraction of 211 At with distribution ratios as high as 11.3 ± 0.6, 12.3 ± 0.8, 42.2 ± 2.2, 69 ± 4, and 95 ± 6 were observed for diisopropyl ether, 1-decanol, 1-octanol, 3-octanone, and methyl isobutyl ketone, respectively, while the distribution ratios for 207 Bi were ≤0.05 in all cases. The extraction of 211 At into both methyl isobutyl ketone and 3-octanone showed a strong, linear dependence on the HNO 3 initial aqueous concentration and better extraction than other solvents. DFT calculations show stronger binding between the carbonyl oxygen of the ketone and the At metal center.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2015

TG-interacting factor transcriptionally induced by AKT/FOXO3A is a negative regulator that antagonizes arsenic trioxide-induced cancer cell apoptosis

Arsenic trioxide (ATO) is a multi-target drug approved by the Food and Drug Administration as the first-line chemotherapeutic agent for the treatment of acute promyelocytic leukemia. In addition, several clinical trials are being conducted with arsenic-based drugs for the treatment of other hematological malignancies and solid tumors. However, ATO's modest clinical efficacy on some cancers, and potential toxic effects on humans have been reported. Determining how best to reduce these adverse effects while increasing its therapeutic efficacy is obviously a critical issue. Previously, we demonstrated that the JNK-induced complex formation of phosphorylated c-Jun and TG-interacting factor (TGIF) antagonizes ERK-induced cyclin-dependent kinase inhibitor CDKN1A (p21{sup WAF1/CIP1}) expression and resultant apoptosis in response to ATO in A431 cells. Surprisingly, at low-concentrations (0.1–0.2 μM), ATO increased cellular proliferation, migration and invasion, involving TGIF expression, however, at high-concentrations (5–20 μM), ATO induced cell apoptosis. Using a promoter analysis, TGIF was transcriptionally regulated by ATO at the FOXO3A binding site (− 1486 to − 1479 bp) via the c-Src/EGFR/AKT pathway. Stable overexpression of TGIF promoted advancing the cell cycle into the S phase, and attenuated 20 μM ATO-induced apoptosis. Furthermore, blockage of the AKT pathway enhanced ATO-induced CDKN1A expression and resultant apoptosis in cancer cells, but overexpression of AKT1 inhibited CDKN1A expression. Therefore, we suggest that TGIF is transcriptionally regulated by the c-Src/EGFR/AKT pathway, which plays a role as a negative regulator in antagonizing ATO-induced CDKN1A expression and resultant apoptosis. Suppression of these antagonistic effects might be a promising therapeutic strategy toward improving clinical efficacy of ATO. - Highlights: • ATO-induced biphasic survival responses of cancer cells depend on low- or high-concentrations. • TGIF mediates low-concentration ATO-induced cancer cell proliferation, migration, and invasion. • ATO transcriptionally regulates TGIF expression via c-Src/EGFR/AKT/FOXO3A signalings. • Increased TGIF or AKT activation attenuates high-concentration ATO-induced CDKN1A expression and cellular apoptosis. • Suppression of these negative regulators might be a promising therapeutic strategy to improve therapeutic efficacy of ATO.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2011

Enhanced suppression of tumor growth by concomitant treatment of human lung cancer cells with suberoylanilide hydroxamic acid and arsenic trioxide

The efficacy of arsenic trioxide (ATO) against acute promyelocytic leukemia (APL) and relapsed APL has been well documented. ATO may cause DNA damage by generating reactive oxygen intermediates. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, modulates gene and protein expression via histone-dependent or -independent pathways that may result in chromatin decondensation, cell cycle arrest, differentiation, and apoptosis. We investigated whether ATO and SAHA act synergistically to enhance the death of cancer cells. Our current findings showed that combined treatment with ATO and SAHA resulted in enhanced suppression of non-small-cell lung carcinoma in vitro in H1299 cells and in vivo in a xenograft mouse model. Flow cytometric analysis of annexin V+ cells showed that apoptotic cell death was significantly enhanced after combined treatment with ATO and SAHA. At the doses used, ATO did not interfere with cell cycle progression, but SAHA induced p21 expression and led to G1 arrest. A Comet assay demonstrated that ATO, but not SAHA, induced DNA strand breaks in H1299 cells; however, co-treatment with SAHA significantly increased ATO-induced DNA damage. Moreover, SAHA enhanced acetylation of histone H3 and sensitized genomic DNA to DNase I digestion. Our results suggest that SAHA may cause chromatin relaxation and increase cellular susceptibility to ATO-induced DNA damage. Combined administration of SAHA and ATO may be an effective approach to the treatment of lung cancer. -- Highlights: Black-Right-Pointing-Pointer ATO and SAHA are therapeutic agents with different action modes. Black-Right-Pointing-Pointer Combination of ATO and SAHA synergistically inhibits tumor cell growth. Black-Right-Pointing-Pointer SAHA loosens chromatin structure resulting in increased sensitivity to DNase I. Black-Right-Pointing-Pointer ATO-induced DNA damage and apoptosis are enhanced by co-treatment with SAHA.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Activating transcription factor 4 underlies the pathogenesis of arsenic trioxide-mediated impairment of macrophage innate immune functions

Chronic arsenic exposure to humans is considered immunosuppressive with augmented susceptibility to several infectious diseases. The exact molecular mechanisms, however, remain unknown. Earlier, we showed the involvement of unfolded protein response (UPR) signaling in arsenic-mediated impairment of macrophage functions. Here, we show that activating transcription factor 4 (ATF4), a UPR transcription factor, regulates arsenic trioxide (ATO)-mediated dysregulation of macrophage functions. In ATO-treated ATF4{sup +/+} wild-type mice, a significant down-regulation of CD11b expression was associated with the reduced phagocytic functions of peritoneal and lung macrophages. This severe immuno-toxicity phenotype was not observed in ATO-treated ATF4{sup +/−} heterozygous mice. To confirm these observations, we demonstrated in Raw 264.7 cells that ATF4 knock-down rescues ATO-mediated impairment of macrophage functions including cytokine production, bacterial engulfment and clearance of engulfed bacteria. Sustained activation of ATF4 by ATO in macrophages induces apoptosis, while diminution of ATF4 expression protects against ATO-induced apoptotic cell death. Raw 264.7 cells treated with ATO also manifest dysregulated Ca{sup ++} homeostasis. ATO induces Ca{sup ++}-dependent calpain-1 and caspase-12 expression which together regulated macrophage apoptosis. Additionally, apoptosis was also induced by mitochondria-regulated pathway. Restoring ATO-impaired Ca{sup ++} homeostasis in ER/mitochondria by treatments with the inhibitors of inositol 1,4,5-trisphosphate receptor (IP3R) and voltage-dependent anion channel (VDAC) attenuate innate immune functions of macrophages. These studies identify a novel role for ATF4 in underlying pathogenesis of macrophage dysregulation and immuno-toxicity of arsenic. - Highlights: • ATF4 regulates arsenic-mediated impairment in macrophage functions. • Arsenic-mediated alterations in pulmonary macrophage are diminished in ATF4{sup +/−} mice. • Changes in macrophage functions can be attenuated by Ca{sup ++} homeostasis regulators.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

Unfolded protein response (UPR) signaling regulates arsenic trioxide-mediated macrophage innate immune function disruption

Arsenic exposure is known to disrupt innate immune functions in humans and in experimental animals. In this study, we provide a mechanism by which arsenic trioxide (ATO) disrupts macrophage functions. ATO treatment of murine macrophage cells diminished internalization of FITC-labeled latex beads, impaired clearance of phagocytosed fluorescent bacteria and reduced secretion of pro-inflammatory cytokines. These impairments in macrophage functions are associated with ATO-induced unfolded protein response (UPR) signaling pathway characterized by the enhancement in proteins such as GRP78, p-PERK, p-eIF2α, ATF4 and CHOP. The expression of these proteins is altered both at transcriptional and translational levels. Pretreatment with chemical chaperon, 4-phenylbutyric acid (PBA) attenuated the ATO-induced activation in UPR signaling and afforded protection against ATO-induced disruption of macrophage functions. This treatment also reduced ATO-mediated reactive oxygen species (ROS) generation. Interestingly, treatment with antioxidant N-acetylcysteine (NAC) prior to ATO exposure, not only reduced ROS production and UPR signaling but also improved macrophage functions. These data demonstrate that UPR signaling and ROS generation are interdependent and are involved in the arsenic-induced pathobiology of macrophage. These data also provide a novel strategy to block the ATO-dependent impairment in innate immune responses. - Highlights: • Inorganic arsenic to humans and experimental animals disrupt innate immune responses. • The mechanism underlying arsenic impaired macrophage functions involves UPR signaling. • Chemical chaperon attenuates arsenic-mediated macrophage function impairment. • Antioxidant, NAC blocks impairment in arsenic-treated macrophage functions.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Inhibition of nicotinamide phosphoribosyltransferase and depletion of nicotinamide adenine dinucleotide contribute to arsenic trioxide suppression of oral squamous cell carcinoma

Emerging evidence suggests that increased nicotinamide phosphoribosyltransferase (NAMPT) expression is associated with the development and prognosis of many cancers, but it remains unknown regarding its role in oral squamous cell carcinoma (OSCC). In the present study, the results from tissue microarray showed that NAMPT was overexpressed in OSCC patients and its expression level was directly correlated with differential grades of cancer. Interestingly, treatment of OSCC cells with chemotherapy agent arsenic trioxide (ATO) decreased the levels of NAMPT protein and increased cellular death in an ATO dose- and time-dependent manner. Most importantly, combination of low concentration ATO with FK866 (a NAMPT inhibitor) exerted enhanced inhibitive effect on NAMPT protein and mRNA expressions, leading to synergistic cytotoxicity on cancer cells through increasing cell apoptosis and depleting intracellular nicotinamide adenine dinucleotide levels. These findings demonstrate the crucial role of NAMPT in the prognosis of OSCC and reveal inhibition of NAMPT as a novel mechanism of ATO in suppressing cancer cell growth. Our results suggest that ATO can significantly enhance therapeutic efficacy of NAMPT inhibitor, and combined treatment may be a novel and effective therapeutic strategy for OSCC patients. - Highlights: • Level of overexpressed NAMPT is associated with differential grade of OSCC patients. • Arsenic trioxide (ATO) exerts anti-cancer effects through NAMPT inhibition. • ATO enhances tumor cell killing efficacy of NAMPT inhibitor through depleting NAD. • Combined ATO/NAMPT inhibitor may be a novel therapy for advanced OSCC patients.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Lithium intercalation in sputter deposited antimony-doped tin oxide thin films: Evidence from electrochemical and optical measurements

Transparent conducting oxides are used as transparent electrical contacts in a variety of applications, including in electrochromic smart windows. In the present work, we performed a study of transparent conducting antimony-doped tin oxide (ATO) thin films by chronopotentiometry in a Li{sup +}-containing electrolyte. The open circuit potential vs. Li was used to investigate ATO band lineups, such as those of the Fermi level and the ionization potential, as well as the dependence of these lineups on the preparation conditions for ATO. Evidence was found for Li{sup +} intercalation when a current pulse was set in a way so as to drive ions from the electrolyte into the ATO lattice. Galvanostatic intermittent titration was then applied to determine the lithium diffusion coefficient within the ATO lattice. The electrochemical density of states of the conducting oxide was studied by means of the transient voltage recorded during the chronopotentiometry experiments. These measurements were possible because, as Li{sup +} intercalation took place, charge compensating electrons filled the lowest part of the conduction band in ATO. Furthermore, the charge insertion modified the optical properties of ATO according to the Drude model.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗
DOE OSTI2014

Knockdown of TWIST1 enhances arsenic trioxide- and ionizing radiation-induced cell death in lung cancer cells by promoting mitochondrial dysfunction

Highlights: • Knockdown of TWIST1 enhanced ATO- and IR-induced cell death in NSCLCs. • Intracellular ROS levels were increased in cells treated with TWIST1 siRNA. • TWIST1 siRNA induced MMP loss and mitochondrial fragmentation. • TWIST1 siRNA upregulated the fission-related proteins FIS1 and DRP1. - Abstract: TWIST1 is implicated in the process of epithelial mesenchymal transition, metastasis, stemness, and drug resistance in cancer cells, and therefore is a potential target for cancer therapy. In the present study, we found that knockdown of TWIST1 by small interfering RNA (siRNA) enhanced arsenic trioxide (ATO)- and ionizing radiation (IR)-induced cell death in non-small-cell lung cancer cells. Interestingly, intracellular reactive oxygen species levels were increased in cells treated with TWIST1 siRNA and further increased by co-treatment with ATO or IR. Pretreatment of lung cancer cells with the antioxidant N-acetyl-cysteine markedly suppressed the cell death induced by combined treatment with TWIST1 siRNA and ATO or IR. Moreover, treatment of cells with TWIST1 siRNA induced mitochondrial membrane depolarization and significantly increased mitochondrial fragmentation (fission) and upregulated the fission-related proteins FIS1 and DRP1. Collectively, our results demonstrate that siRNA-mediated TWIST1 knockdown induces mitochondrial dysfunction and enhances IR- and ATO-induced cell death in lung cancer cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2011

Cytotoxicity of arsenic trioxide is enhanced by (-)-epigallocatechin-3-gallate via suppression of ferritin in cancer cells

Arsenic trioxide (ATO) treatment is a useful therapy against human acute promyelocytic leukemia (APL), however, it concomitantly brings potential adverse consequences including serious side effect, human carcinogenicity and possible development of resistance. This investigation revealed that those problems might be relaxed by simultaneous application with (-)-epigallocatechin-3-gallate (EGCG), one of the major components from green tea. EGCG significantly lowered down the ATO concentration required for an effective control of APL cells, HL-60. The simultaneous treatment of ATO with EGCG induced a mitochondria-dependent apoptosis in HL-60 cells significantly, which accounted for more than 70% of the cell death in the treatment. The mechanism of apoptosis induction was elucidated. EGCG in HL-60 cells acted as a pro-oxidant enhancing intracellular hydrogen peroxide significantly. ATO, on the other hand, induced heme oxygenase-1 (HO-1) to catalyze heme degradation, thereby provided ferrous iron for EGCG-induced hydrogen peroxide to precede Fenton reaction, which in turn generated deleterious reactive oxygen species to damage cell. In addition, EGCG inhibited expression of ferritin, which supposedly to sequester harmful ferrous iron, thereby augmented the occurrence of Fenton reaction. This investigation also provided evidence that ATO, since mainly acted to induce HO-1 in simultaneous treatment with EGCG, could be replaced by other HO-1 inducer with much less human toxicity. Furthermore, several of our preliminary investigations revealed that the enhanced cytotoxicity induced by combining heme degradation and Fenton reaction is selectively toxic to malignant but not non-malignant cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Self-Anchored Platinum-Decorated Antimony-Doped-Tin Oxide as a Durable Oxygen Reduction Electrocatalyst

The lifetime of commercial Proton Exchange Membrane Fuel Cells (PEMFCs) is circumscribed by the insufficient durability of commercial catalysts. The use of metal oxide supports in place of carbon significantly increases electrocatalyst durability. Herein, following density functional theory (DFT) predictions of improved Platinum (Pt) stability on antimony doped tin oxide (ATO) supports, we synthesized ATO whose morphology and crystal structure was engineered using a Pt anchoring technique. X-ray photoelectron spectroscopy (XPS) indicated that the Pt anchor sites aided in the reduction of Pt precursors to Pt on the ATO surface. X-ray absorption near-edge spectroscopy (XANES) revealed the existence of strong-metal-support interactions (SMSI) between Pt and ATO. The combination of SMSI and high control over Pt dispersion enabled the Pt/Pt-aerogel-ATO (Pt supported on aerogel ATO with Pt anchor sites) electrocatalyst to achieve 2x the area specific activity of Pt/C in ex-situ testing. In a H 2 /air PEMFC Pt/Pt-aerogel-ATO cathodes enabled 20% higher peak power density and <1/6 the loss of active surface area as compared to Pt/C. Notably, in a PEMFC under rigorous potential cycling, the Pt/Pt-aerogel-ATO retained its initial peak power density as opposed to a 58% loss for Pt/C. Further, cost models indicate that Pt/Pt-aerogel-ATO is 26% less expensive than Pt/C over its useful lifetime.

25 ENERGY STORAGE↗
DOE OSTI2019

Room–Temperature Insulating Ferromagnetic (Ni,Co) 1+2 x Ti 1– x O 3 Thin Films

Insulating uniaxial room–temperature ferromagnets are a prerequisite for commonplace spin wave–based devices, the obstacle in contemporary ferromagnets being the coupling of ferromagnetism with large conductivity. It is shown that the uniaxial A 1 + 2x Ti 4+ 1 – x O 3 (ATO), A = Ni 2+ ,Co 2+ , and 0.6 < x ≤ 1, thin films are electrically insulating ferromagnets already at room temperature. Here, the octahedra network of the ATO and the corundum and ilmenite structures are the same yet different octahedra–filling proved to be a route to switch from the antiferromagnetic to ferromagnetic regime. Octahedra can continuously be filled up to x = 1, or vacated (–0.24 < x < 0) in the ATO structure. TiO–layers, which separate the ferromagnetic (Ni,Co)O–layers and intermediate the antiferromagnetic coupling between the ferromagnetic layers in the NiTiO 3 and CoTiO 3 ilmenites, can continuously be replaced by (Ni,Co)O–layers to convert the ATO–films to ferromagnetic insulator with abundant direct cation interactions.

36 MATERIALS SCIENCE↗