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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 937 records · Page 52
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Enhanced Charge Transport and Stability Conferred by Iron(III)‐Coordination in a Conjugated Polymer Thin‐Film Transistors

Abstract A high performance diketopyrrolopyrrole (DPP)–based semiconducting polymer is modified with ligands to enable metal coordination, and its subsequent effect as field‐effect transistors is investigated. In specific, pyridine‐2,6‐dicarboxamide (PDCA) units are incorporated in a DPP–based polymer backbone with a content from 0 to 30 mol%, and the resulting polymers are then mixed with Fe(II) ions. The coordination and spontaneous oxidation converts Fe(II) to Fe(III) ions to result in Fe(III)‐containing metallopolymers. The resulting metallopolymers are observed to show good solubility in organic solvents and can be easily processed as thin films. The charge transport characteristics are subsequently investigated through the fabrication of field–effect transistor devices, in which an enhanced charge carrier mobility with the Fe(III)‐containing metallopolymers is observed. In specific, an almost twofold improvement in the charge carrier mobility is obtained for the 20% PDCA‐containing polymer after Fe coordination (from 0.96 to 1.84 cm 2 V −1 s −1 ). Furthermore, the operation stability of the metallopolymer‐based devices is found to be significantly improved with low bias stress. Its superior electrical characteristics are attributed to the doping effect of the Fe ions. This study indicates that incorporation of appropriate metallic ions to polymer presents a viable approach to enhance the performance of polymer–based transistor devices.

Wu, Hung‐Chin↗
DOE OSTI2018

The Phase-1 Upgrade of the ATLAS Level-1 Endcap Muon Trigger. In: Proceedings of International Conference on Technology and Instrumentation in Particle Physics 2017

The Level-1 muon trigger for the ATLAS experiment identifies muons with high transverse momentum. Under the high luminosity condition in LHC Run 3, more powerful trigger system is needed to reject the backgrounds. New trigger processor board for Run 3 has been produced to achieve the required performance, by combining information from five different detectors. The performance of the new board and the readout system has been confirmed by a beam test. The new algorithms to make use of the new detectors have been developed, and are tested by MC simulation. With the new algorithms, the trigger rate is estimated to become lower than the required rate in Run 3.

Akatsuka, Shunichi↗
DOE OSTI2018

Simulation of the ATLAS New Small Wheel (NSW) System. In: Proceedings of International Conference on Technology and Instrumentation in Particle Physics 2017

New Small Wheel (NSW) is a major detector upgrade project of the ATLAS muon spectrometer for the LHC luminosity upgrade. NSW comprises sTGC and Micromegas as muon tracking detectors of high rate capability, and front- and back-end electronics for upgrading the muon level-1 trigger. Detailed simulation of the detectors and the electronics has been developed and used for the study of expected performance. An overview of the NSW system and some results of the trigger performance with the Micromegas are presented.

ATLAS↗
DOE OSTI2018

Tracking and Vertexing with the ATLAS Inner Detector in the LHC Run-2. In: Proceedings of International Conference on Technology and Instrumentation in Particle Physics 2017

Run-2 of the Large Hadron Collider (LHC) has provided new challenges to track and vertex reconstruction with higher centre-of-mass energies and luminosity leading to increasingly high-multiplicity environments, and boosted, highly-collimated physics objects. We present an overview of the ATLAS Inner Detector tracker in Run-2 including the track reconstruction algorithm, time-dependent alignment, tracking and vertexing performance.

ATLAS Inner Detector↗
DOE OSTI2018

CMOS Pixel Development for the ATLAS Experiment at HL-LHC. In: Proceedings of International Conference on Technology and Instrumentation in Particle Physics 2017

The high luminosity upgrade of the LHC necessitates a complete exchange of the current ATLAS Inner Tracker for a purely silicon one. Large areas therefore have to be covered by radiation tolerant, low cost and low material budget silicon detectors. New approaches are being explored using CMOS pixel sensors, providing charge collection in a depleted layer. They are based on technologies that allow to use high depletion voltages and high resistivity wafers for large depletion depths with multiple nested wells, enabling for CMOS electronics to be embedded safely into the sensor substrate. We are investigating depleted CMOS pixel detectors with monolithic or hybrid designs in view of their suitability for high trigger rates, fast timing and the high radiation environment at HL-LHC. This paper will discuss recent results of the main candidate technologies and the current developments towards a monolithic solution.

ATLAS ITk↗
DOE OSTI2015

Crystal Structure and Biochemical Characterization of Chlamydomonas FDX2 Reveal Two Residues that, When Mutated, Partially Confer FDX2 the Redox Potential and Catalytic Properties of FDX1

The green alga Chlamydomonas reinhardtii contains six plastidic [2Fe2S]-cluster ferredoxins (FDXs), with FDX1 as the predominant isoform under photoautotrophic growth. FDX2 is highly similar to FDX1 and has been shown to interact with specific enzymes (such as nitrite reductase), as well as to share interactors with FDX1, such as the hydrogenases (HYDA), ferredoxin:NAD(P) reductase I (FNR1), and pyruvate:ferredoxin oxidoreductase (PFR1), albeit performing at low catalytic rates. Here we report the FDX2 crystal structure solved at 1.18 Å resolution. Based on differences between the Chlorella fusca FDX1 and C. reinhardtii FDX2 structures, we generated and purified point-mutated versions of the FDX2 protein and assayed them in vitro for their ability to catalyze hydrogen and NADPH photo-production. The data show that structural differences at two amino acid positions contribute to functional differences between FDX1 and FDX2, suggesting that FDX2 might have evolved from FDX1 toward a different physiological role in the cell. Moreover, we demonstrate that the mutations affect both the midpoint potentials of the FDX and kinetics of the FNR reaction, possibly due to altered binding between FDX and FNR. An effect on H 2 photo-production rates was also observed, although the kinetics of the reaction were not further characterized.

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

Overexpression of Arabidopsis NADPH-dependent thioredoxin reductase C (AtNTRC) confers freezing and cold shock tolerance to plants

Overexpression of AtNTRC (AtNTRC{sup OE}) in Arabidopsis thaliana led to a freezing and cold stress tolerance, whereas a knockout mutant (atntrc) showed a stress-sensitive phenotype. Biochemical analyses showed that the recombinant AtNTRC proteins exhibited a cryoprotective activity for malate dehydrogenase and lactic dehydrogenase. Furthermore, conclusive evidence of its interaction with nucleic acids in vitro is provided here on the basis of gel shift and electron microscopy analysis. Recombinant AtNTRC efficiently protected RNA and DNA from RNase A and metal catalyzed oxidation damage, respectively. The C-terminal thioredoxin domain is required for the nucleic acid–protein complex formation. From these results, it can be hypothesized that AtNTRC, which is known to be an electron donor of peroxiredoxin, contributes the stability of macromolecules under cold stress. - Highlights: • AtNTRC has a cryoprotective activity in vitro. • Overexpression of AtNTRC increases tolerance to freezing and cold shock stresses. • Thioredoxin domain of AtNTRC protects nucleic acids in vitro. • AtNTRC inhibits protein aggregation under freezing stress in vitro.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

LDH-A promotes malignant progression via activation of epithelial-to-mesenchymal transition and conferring stemness in muscle-invasive bladder cancer

Lactate dehydrogenase-A(LDH-A) is an important rate-limiting enzyme in the Warburg effect. Survival analysis indicated poor clinical outcomes in MIBC with high LDH-A expression. The results of in vitro experiment indicated that LDH-A promotes MIBC cells proliferation, invasion and migration. The positive relationship between LDH-A expression and CSC/EMT markers was confirmed both in invasive bladder cell line and in 136 MIBC specimens. Thus, we conclude that LDH-A may be a promising target for MIBC. - Highlights: • Survival analysis indicated poor clinical outcomes in MIBC with high LDH-A expression. • IHC analysis of 136 MIBC specimens revealed increased LDH-A is correlated with positive Oct4 and negative E-cadherin. • In vitro experiments demonstrated LDH-A promotes MIBC progression by positive regulation of EMT/CSC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Cereblon deficiency confers resistance against polymicrobial sepsis by the activation of AMP activated protein kinase and heme-oxygenase-1

Cereblon (CRBN) has a pleiotropic role in important cellular processes and is a potential therapeutic target in several diseases, including mental retardation, cancer, and metabolic disorders. The role of CRBN in polymicrobial sepsis induced by cecal ligation and puncture (CLP) was investigated using CRBN-deficient (KO) mice. Survival following CLP was significantly higher in KO mice compared to wild-type (WT) controls (50% vs 0% at day 6 after CLP). The improved survival of KO mice was accompanied by reduced peripheral blood bacterial load and lung injury. Serum tumor necrosis factor (TNF)-α and high mobility group box 1 (HMGB1) concentrations were significantly lower in KO mice than in WT mice. Peritoneal macrophages from KO mice with CLP-induced septic mouse had higher levels of activation of AMPK and heme oxygenase-1 (HO-1). Forced expression of CRBN in macrophage of KO mice suppressed activation of 5′ adenosine monophosphate-activated protein kinase (AMPK) and HO-1 and augmented expression of TNF-α and HMGB1 as inhibition of AMPK by compound C. These studies demonstrate the contribution of CRBN expression to the pathogenesis of CLP-induced sepsis and peritoneal macrophage responses and suggest a novel therapeutic modality for polymicrobial sepsis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Induction of MEK/ERK activity by AZD8055 confers acquired resistance in neuroblastoma

Highlights: • Prolonged mTOR inhibitor, AZD8055 exposure induced resistance in NB cells. • Resistance against AZD8055 correlated with over-activation of MEK/ERK signaling. • Combination of AZD8055 and U0126 overcome resistance in vitro and in vivo. Mammalian target of rapamycin (mTOR) complex (mTORC) is frequently activated in diverse cancers. Although dual mTORC1/2 inhibitors are currently under development to treat various malignancies, the emergence of drug resistance has proven to be a major complication. AZD8055 is a novel, potent ATP-competitive and specific inhibitor of mTOR kinase activity, which blocks both mTORC1 and mTORC2 activation. In this study, we acquired AZD8055-resistant neuroblastoma (NB) cell sublines by using prolonged stepwise escalation of AZD8055 exposure (4–12 weeks). Here we demonstrate that the AZD8055-resistant sublines (TGW-R and SMS-KAN-R) exhibited marked resistance to AZD8055 compared to the parent cells (TGW and SMS-KAN). The cell cycle G1/S transition was advanced in resistant cells. In addition, the resistance against AZD8055 correlated with over-activation of MEK/ERK signaling pathway. Furthermore, combination of AZD8055 and MEK inhibitor U0126 enhanced the growth inhibition of resistant cells significantly in vitro and in vivo. In conclusion, these data show that targeting mTOR kinase and MEK/ERK signaling simultaneously might help to overcome AZD8055 resistance in NB.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Glycine confers neuroprotection through PTEN/AKT signal pathway in experimental intracerebral hemorrhage

Highlights: • Glycine attenuated brain injuries after rats ICH. • Glycine down-regulated PTEN in rats ICH. • The neuroprotective effect of glycine was mediated through PTEN/Akt signal pathway in experimental rat ICH. Glycine has been shown to protect against ischemic stroke through various mechanisms. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) which antagonize Akt-dependent cell survival has been linked to neuronal damage. However, whether glycine has a neuroprotective property in intracerebral hemorrhage (ICH) was unknown. This study aimed to determine the protective effect of glycine in rats ICH. Adult male Sprague-Dawley (SD) rats were subjected to left striatum infusion of autologous blood. ICH animals received glycine (0.2–3 mg/kg, icv) at 1 h after ICH with or without pre-injection of Akt Inhibitor IV (100 μM, 2 μl, icv) 0.5 h prior to glycine treatment. Our results showed that in the perihematomal area PTEN was up-regulated in the early stage after ICH. However, glycine treatment decreased PTEN protein level and increased the phosphorylation level of AKT (p-AKT) in the perihematomal area. With the administration of glycine, neuronal death was significantly reduced and Evans blue leakage was alleviated as well as the brain edema after ICH. Moreover, hematoma volume was decreased and neurobehavioral outcome was improved. Nevertheless, Akt Inhibitor IV abolished the neuroprotective effects of glycine after ICH. Together, our findings demonstrate, for the first time, the protective role of glycine on ICH rats, and suggest that the neuroprotective effect of glycine was mediated through PTEN/Akt signal pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

UCA1 confers paclitaxel resistance to ovarian cancer through miR-129/ABCB1 axis

Highlights: • UCA1 was up-regulated in paclitaxel-resistant ovarian cancer cells. • Knockdown of UCA1 sensitized paclitaxel-resistant ovarian cancer cells to paclitaxel. • Our study first demonstrated a ceRNA regulatory mechanism among UCA1, miR-129 and ABCB1 existed in ovarian cancer. • UCA1/miR-129/ABCB1 axis contributed to paclitaxel resistance in ovarian cancer. • Our study first elucidated the role and molecular mechanisms of UCA1 in ovarian cancer paclitaxel resistance. Increasing evidence has demonstrated the involvement of dysregulated long non-coding RNAs (lncRNAs) in chemoresistance acting as potential oncogenes or tumor suppressors in various cancers. Nevertheless, the profound molecular mechanisms of lncRNAs in ovarian cancer (OC) chemoresistance is not well elucidated. The objective of this work was to investigate the role and molecular mechanisms of urothelial carcinoma associated 1 (UCA1) in paclitaxel (PTX) resistance in OC. Our results indicated that UCA1 was significantly up-regulated in PTX-resistant OC cells (SKOV3/PTX and HeyA-8/PTX) compared with their parental cells (SKOV3 and HeyA-8). Functionally, UCA1 knockdown sensitized SKOV3/PTX and HeyA-8/PTX cells to PTX through enhancing PTX-induced apoptosis. Mechanistically, UCA1 silencing induced PTX sensitivity of SKOV3/PTX and HeyA-8/PTX cells by de-repressing ABCB1 through sponging miR-129. Collectively, our study elaborated a novel UCA1/miR-129/ABCB1 regulatory axis underlying PTX resistance of OC cells, providing a potential therapeutic target for OC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

HDAC9 overexpression confers invasive and angiogenic potential to triple negative breast cancer cells via modulating microRNA-206

Highlights: • HDAC9 is upregulated in TNBC compared to non-TNBC cell lines and tissues. • Increased levels of HDAC9 are inversely consistent with expression levels of miR-206. • HDAC9 inhibition upregulates miR-206 expression in TNBC cells. • Selective HDAC9 inhibition represses TNBC breast cell invasion and angiogenesis. • HDAC9 inhibition decreased expression of VEGF and MAPK3 via modulating miR-206. Triple negative breast cancer (TNBC) is among the most aggressive breast cancer subtypes with poor prognosis. The purpose of this study is to better understand the molecular basis of TNBC as well as develop new therapeutic strategies. Our results demonstrate that HDAC9 is overexpressed in TNBC compared to non-TNBC cell lines and tissues and is inversely proportional with miR-206 expression levels. We show that HDAC9 selective inhibition blocked the invasion of TNBC cells in vitro and repressed the angiogenesis shown via in vivo Matrigel plug assays. Subsequent HDAC9 siRNA knockdown was then shown to restore miR-206 while also decreasing VEGF and MAPK3 levels. Furthermore, the inhibition of miR-206 neutralized the action of HDAC9 siRNA on decreasing VEGF and MAPK3 levels. This study highlights HDAC9 as a mediator of cell invasion and angiogenesis in TNBC cells through VEGF and MAPK3 by modulating miR-206 expression and suggests that selective inhibition of HDAC9 may be an efficient route for TNBC therapy.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MUC1/KL-6 expression confers an aggressive phenotype upon myeloma cells

Highlights: • EMM cell line was established from a patient with serum KL-6 elevation. • EMM1 is the first myeloma cell line that expresses high levels of MUC1. • Knockdown of MUC1 induces S phase cell cycle arrest and apoptosis in EMM1 cells. • Xenograft mice with EMM1 cells reproduce the MM patient with serum KL-6 elevation. • Knockdown of MUC1 inhibits EMM1 tumor growth in a mouse xenograft model. The sialic glycoprotein, MUC1, is known to be involved in the pathogenesis of various types of cancers. KL-6 is one of the surface antigens of MUC1 and also a marker of interstitial pneumonitis. A fraction of patients with myeloma (3.9%) have elevated serum KL-6 levels without any evidence of interstitial pneumonitis and their myeloma cells have high MUC1 expression. We established a myeloma cell line designated EMM1 from a patient with multiple myeloma accompanied with elevated serum KL-6. EMM1 cells expressed high levels of MUC1 compared with other myeloma cell lines. Knockdown of MUC1 in EMM1 cells induced cell cycle arrest during S phase and apoptosis, suggesting that the MUC1 expression is involved in accelerated growth of EMM1 cells. RNA-seq analysis suggests that MUC1 expression activates k-ras and TNFα-induced NFκB pathways in EMM1 cells. We injected EMM1 cells subcutaneously into Rag2{sup −/−}Jak3{sup −/−} Balb/c mice to establish a mouse xenograft model. These mice had aggressive tumor growth that was accompanied by high serum KL-6 levels. In addition, MUC1 knockdown in EMM1 cells led to inhibited tumor growth. These findings demonstrate that MUC1 serves as a potential target for developing drugs for treatment of patients with KL-6{sup +} myeloma, and EMM1 cells and EMM1-engrafted mice are useful tools for the development of such novel agents.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2020

Salmonella Typhoid Toxin PltB Subunit and Its Non-typhoidal Salmonella Ortholog Confer Differential Host Adaptation and Virulence

Typhoidal and non-typhoidal Salmonelleae (NTS) cause typhoid fever and gastroenteritis, respectively, in humans. Salmonella typhoid toxin contributes to typhoid disease progression and chronic infection, but little is known about the role of its NTS ortholog. We found that typhoid toxin and its NTS ortholog induce different clinical presentations. The PltB subunit of each toxin exhibits different glycan-binding preferences that correlate with glycan expression profiles of host cells targeted by each bacterium at the primary infection or intoxication sites. Through co-crystal structures of PltB subunits bound to specific glycan receptor moieties, we show that they induce markedly different glycan-binding preferences and virulence outcomes. Furthermore, immunization with the NTS S. Javiana or its toxin offers cross-reactive protection against lethal-dose typhoid toxin challenge. Cumulatively, these results offer insights into the evolution of host adaptations in Salmonella AB toxins, their cell and tissue tropisms, and the design for improved typhoid vaccines and therapeutics.

59 BASIC BIOLOGICAL SCIENCES↗