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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 1,117 records · Page 62
All sourcesNASA NTRSDOE OSTI
DOE OSTI2012

The role of amino acid electron-donor/acceptor atoms in host-cell binding peptides is associated with their 3D structure and HLA-binding capacity in sterile malarial immunity induction

Highlights: Black-Right-Pointing-Pointer Fundamental residues located in some HABPs are associated with their 3D structure. Black-Right-Pointing-Pointer Electron-donor atoms present in {beta}-turn, random, distorted {alpha}-helix structures. Black-Right-Pointing-Pointer Electron-donor atoms bound to HLA-DR53. Black-Right-Pointing-Pointer Electron-acceptor atoms present in regular {alpha}-helix structure bound to HLA-DR52. -- Abstract: Plasmodium falciparum malaria continues being one of the parasitic diseases causing the highest worldwide mortality due to the parasite's multiple evasion mechanisms, such as immunological silence. Membrane and organelle proteins are used during invasion for interactions mediated by high binding ability peptides (HABPs); these have amino acids which establish hydrogen bonds between them in some of their critical binding residues. Immunisation assays in the Aotus model using HABPs whose critical residues had been modified have revealed a conformational change thereby enabling a protection-inducing response. This has improved fitting within HLA-DR{beta}1{sup Asterisk-Operator} molecules where amino acid electron-donor atoms present in {beta}-turn, random or distorted {alpha}-helix structures preferentially bound to HLA-DR53 molecules, whilst HABPs having amino acid electron-acceptor atoms present in regular {alpha}-helix structure bound to HLA-DR52. This data has great implications for vaccine development.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Phase II enzyme induction by a carotenoid, lutein, in a PC12D neuronal cell line

Highlights: • Lutein reduced ROS levels in a PC12D neuronal cell line. • Lutein induced mRNAs of phase II antioxidative enzymes in PC12D neuronal cells. • Lutein increased protein levels of HO-1, SOD2, and NQO-1 in PC12D neuronal cells. • Lutein had no effect on intranuclear Nrf2 levels in PC12D neuronal cells. • Lutein did not activate potential upstream Nrf2 nuclear translocation pathways. - Abstract: The mechanism by which lutein, a carotenoid, acts as an antioxidant in retinal cells is still not fully understood. Here, lutein treatment of a neuronal cell line (PC12D) immediately resulted in reduced intracellular ROS levels, implying that it has a direct role in ROS scavenging. Significantly, lutein treatment also induced phase II antioxidative enzyme expression, probably via a nuclear factor-like 2 (Nrf2) independent pathway. This latter mechanism could explain why lutein acts diversely to protect against oxidative/cytotoxic stress, and why it is physiologically involved in the human neural tissue, such as the retina.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Retinal hypoxia induces vascular endothelial growth factor through induction of estrogen-related receptor γ

Ischemic retinopathies causing overexpression of pro-angiogenic factors, including vascular endothelial growth factor (VEGF), are the most common cause of blindness. Thus, understanding the pathophysiology of targetable pathways that regulate retinal VEGF is of great interest. A conserved binding site for estrogen-related receptor γ (ERRγ) has been identified in the promoter of the Vegfa gene. ERRγ is a constitutively active orphan nuclear receptor and its expression is increased by hypoxic stimuli in metabolically active tissues. This study evaluated the role of ERRγ in the ischemic retina and the anti-VEGF potential of GSK5182, a selective inverse agonist of ERRγ. In an oxygen-induced retinopathy (OIR) mouse model, immunohistochemistry showed significantly increased ERRγ expression in the ganglion cell layer at postnatal day (P) 17. In a ganglion cell line (RGC-5), mRNA and protein levels of ERRγ were increased by desferrioxamine treatment and hypoxic conditions (1% O{sub 2}). Transient transfection of RGC-5 cells revealed that ERRγ regulated Vegfa expression and this was inhibited by GSK5182. Intravitreal injection of GSK5182 into the OIR model at P14 inhibited retinal Vegfa mRNA expression at P17. GSK5182 suppresses hypoxia-induced VEGF expression via ERRγ; therefore, ERRγ could be a treatment target for ischemic retinopathies. - Highlights: • OIR mice exhibited increased ERRγ expression in the ganglion cell layer. • Hypoxia-induced ERRγ expression was observed in retinal ganglion cells. • ERRγ overexpression increased VEGFA expression in retinal ganglion cells. • An ERRγ inverse agonist suppressed VEGFA expression in retinal ganglion cells. • Intravitreal injection of an ERRγ inverse agonist suppressed VEGFA in OIR mice.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

A method for direct, semi-quantitative analysis of gas phase samples using gas chromatography-inductively coupled plasma-mass spectrometry

A new and complete GC–ICP-MS method is described for direct analysis of trace metals in a gas phase process stream. The proposed method is derived from standard analytical procedures developed for ICP-MS, which are regularly exercised in standard ICP-MS laboratories. In order to implement the method, a series of empirical factors were generated to calibrate detector response with respect to a known concentration of an internal standard analyte. Calibrated responses are ultimately used to determine the concentration of metal analytes in a gas stream using a semi-quantitative algorithm. The method was verified using a traditional gas injection from a GC sampling valve and a standard gas mixture containing either a 1 ppm Xe + Kr mix with helium balance or 100 ppm Xe with helium balance. Data collected for Xe and Kr gas analytes revealed that agreement of 6–20% with the actual concentration can be expected for various experimental conditions. To demonstrate the method using a relevant “unknown” gas mixture, experiments were performed for continuous 4 and 7 hour periods using a Hg-containing sample gas that was co-introduced into the GC sample loop with the xenon gas standard. System performance and detector response to the dilute concentration of the internal standard were pre-determined, which allowed semi-quantitative evaluation of the analyte. The calculated analyte concentrations varied during the course of the 4 hour experiment, particularly during the first hour of the analysis where the actual Hg concentration was under predicted by up to 72%. Calculated concentration improved to within 30–60% for data collected after the first hour of the experiment. Similar results were seen during the 7 hour test with the deviation from the actual concentration being 11–81% during the first hour and then decreasing for the remaining period. The method detection limit (MDL) was determined for the mercury by injecting the sample gas into the system following a period of equilibration. The MDL for Hg was calculated as 6.8 μg · m -3 . This work describes the first complete GC–ICP-MS method to directly analyze gas phase samples, and detailed sample calculations and comparisons to conventional ICP-MS methods are provided.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2021

Effect of hydrogen isotope on plasma impedance and thermal pinching induced by single aerosol droplets injected into an inductively coupled plasma

The mass of the hydrogen isotope in micrometer-sized aqueous droplets introduced into an ICP has been found to affect the degree of resulting plasma perturbation. Studied plasma perturbations include local plasma cooling, plasma shrinkage due to thermal pinching, and changes in plasma impedance. The local cooling effect caused by a vaporizing aerosol droplet was found to be similar between H 2 O and D 2 O. This finding is likely a result of the similar heat capacities and vaporization rates of H 2 O and D 2 O droplets and of the comparable thermal conductivities and dissociation kinetics of H 2 O and D 2 O vapor. In contrast, a clear isotope effect was observed for plasma shrinkage and impedance change, with H 2 O causing a considerably stronger effect. Plasma shrinkage, gauged by the reduction in Ar emission at the edge of the plasma, was detected at all observation heights within the load-coil region, with D 2 O droplets causing as much as 30% less of an effect than H 2 O. Likewise, D 2 O droplets induce significantly less change in plasma impedance than H 2 O droplets. Depending on experimental conditions and the probing method, changes in plasma impedance caused by monodisperse D 2 O droplets were only 52%–80% that of H 2 O. The lower influence on plasma shrinkage and impedance change for D 2 O droplets is believed to be related to the much lower thermal conductivity of atomic deuterium, around 70% that of atomic hydrogen (protium). The time required for the plasma impedance to return to its original steady-state value was comparatively long (~10 ms) and similar for H 2 O and D 2 O droplets.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗
DOE OSTI2015

HIF-2alpha-dependent PAI-1 induction contributes to angiogenesis in hepatocellular carcinoma

Hypoxia promotes progression of hepatocellular carcinoma (HCC), not only affecting tumor cell proliferation and invasion, but also angiogenesis and thus, increasing the risk of metastasis. Hypoxia inducible factors (HIF)-1α and -2α cause adaptation of tumors to hypoxia, still with uncertainties towards the angiogenic switch. We created a stable knockdown of HIF-1α and HIF-2α in HepG2 cells and generated cocultures of HepG2 spheroids with embryonic bodies as an in vitro tumor model mimicking the cancer microenvironment. The naturally occuring oxygen and nutrient gradients within the cocultures allow us to question the role of distinct HIF isoforms in regulating HCC angiogenesis. In cocultures with a HIF-2α knockdown, angiogenesis was attenuated, while the knockdown of HIF-1α was without effect. Microarray analysis identified plasminogen activator inhibitor 1 (PAI-1) as a HIF-2α target gene in HepG2 cells. The knockdown of PAI-1 in HepG2 cells also lowered angiogenesis. Blocking plasmin, the downstream target of PAI-1, with aprotinin in HIF-2α knockdown (k/d) cells proved a cause–effect relation and restored angiogenesis, with no effect on control cocultures. Suggestively, HIF-2α increases PAI-1 to lower concentrations of active plasmin, thereby supporting angiogenesis. We conclude that the HIF-2α target gene PAI-1 favors the angiogenic switch in HCC. - Highlights: • HepG2 were cocultured with stem cells to mimic a cancer microenvironment in vitro. • A knockdown of HIF-2α reduces angiogenesis. • PAI-1 was identified as a HIF-2α target gene in HCC by microarray analysis. • HIF-2α induces the angiogenic switch via inhibition of plasmin.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Targeting glucosylceramide synthase induction of cell surface globotriaosylceramide (Gb3) in acquired cisplatin-resistance of lung cancer and malignant pleural mesothelioma cells

Background: Acquired resistance to cisplatin treatment is a caveat when treating patients with non-small cell lung cancer (NSCLC) and malignant pleural mesothelioma (MPM). Ceramide increases in response to chemotherapy, leading to proliferation arrest and apoptosis. However, a tumour stress activation of glucosylceramide synthase (GCS) follows to eliminate ceramide by formation of glycosphingolipids (GSLs) such as globotriaosylceramide (Gb3), the functional receptor of verotoxin-1. Ceramide elimination enhances cell proliferation and apoptosis blockade, thus stimulating tumor progression. GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux. We investigated the expression of Gb3, MDR1 and MRP1 in NSCLC and MPM cells with acquired cisplatin resistance, and if GCS activity or MDR1 pump inhibitors would reduce their expression and reverse cisplatin-resistance. Methods: Cell surface expression of Gb3, MDR1 and MRP1 and intracellular expression of MDR1 and MRP1 was analyzed by flow cytometry and confocal microscopy on P31 MPM and H1299 NSCLC cells and subline cells with acquired cisplatin resistance. The effect of GCS inhibitor PPMP and MDR1 pump inhibitor cyclosporin A for 72 h on expression and cisplatin cytotoxicity was tested. Results: The cisplatin-resistant cells expressed increased cell surface Gb3. Cell surface Gb3 expression of resistant cells was annihilated by PPMP whereas cyclosporin A decreased Gb3 and MDR1 expression in H1299 cells. No decrease of MDR1 by PPMP was noted in using flow cytometry, whereas a decrease of MDR1 in H1299 and H1299res was indicated with confocal microscopy. No certain co-localization of Gb3 and MDR1 was noted. PPMP, but not cyclosporin A, potentiated cisplatin cytotoxicity in all cells. Conclusions: Cell surface Gb3 expression is a likely tumour biomarker for acquired cisplatin resistance of NSCLC and MPM cells. Tumour cell resistance to MDR1 inhibitors of cell surface MDR1 and Gb3 could explain the aggressiveness of NSCLC and MPM. Therapy with GCS activity inhibitors or toxin targeting of the Gb3 receptor may substantially reduce acquired cisplatin drug resistance of NSCLC and MPM cells. - Highlights: • The cisplatin-resistant cells had increased cell surface Gb3 and MDR1. • PPMP decreased extracellular Gb3 in the resistant cell lines. • Cyclosporin A decreased extracellular Gb3 and MDR1 in H1299 cells. • PPMP, but not cyclosporin A, potentiated cisplatin cytotoxicity in all cells. • Resistance to inhibitors of MDR1 and Gb3 could explain aggressiveness of NSCLC and MPM.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Induction of oxidative and nitrosative stresses in human retinal pigment epithelial cells by all-trans-retinal

Delayed clearance of free form all-trans-retinal (atRAL) is estimated be the key cause of retinal pigment epithelium (RPE) cells injury during the pathogenesis of retinopathies such as age-related macular degeneration (AMD), however, the underlying molecular mechanisms are far from clear. In this study, we investigated the cytotoxicity effect and underlying molecular mechanism of atRAL on human retinal pigment epithelium ARPE-19 cells. The results indicated that atRAL could cause cell dysfunction by inducing oxidative and nitrosative stresses in ARPE-19 cells. The oxidative stress induced by atRAL was mediated through up-regulation of reactive oxygen species (ROS) generation, activating mitochondrial-dependent and MAPKs signaling pathways, and finally resulting in apoptosis of ARPE-19 cells. The NADPH oxidase inhibitor apocynin could partly attenuated ROS generation, indicating that NADPH oxidase activity was involved in atRAL-induced oxidative stress in ARPE-19 cells. The nitrosative stress induced by atRAL was mainly reflected in increasing nitric oxide (NO) production, enhancing iNOS, ICAM-1 and VCAM-1 expressions, and promoting monocyte adhesion. Furthermore, above effects could be dramatically blocked by using a nuclear factor kappa B (NF-κB) inhibitor SN50, indicated that atRAL-induced oxidative and nitrosative stresses were mediated by NF-κB. The results provide better understanding of atRAL-induced toxicity in human RPE cells. - Highlights: • atRAL induces oxidative stress-mediated apoptosis in ARPE-19 cells. • atRAL induces oxidative stress-mediated inflammation in ARPE-19 cells. • NF-κB is involved in atRAL-induced oxidative and nitrosative stresses.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2012

Selective killing of ovarian cancer cells through induction of apoptosis by nonequilibrium atmospheric pressure plasma

Two independent ovarian cancer cell lines and fibroblast controls were treated with nonequilibrium atmospheric pressure plasma (NEAPP). Most ovarian cancer cells were detached from the culture dish by continuous plasma treatment to a single spot on the dish. Next, the plasma source was applied over the whole dish using a robot arm. In vitro cell proliferation assays showed that plasma treatments significantly decreased proliferation rates of ovarian cancer cells compared to fibroblast cells. Flow cytometry and western blot analysis showed that plasma treatment of ovarian cancer cells induced apoptosis. NEAPP could be a promising tool for therapy for ovarian cancers.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

Induction of electron injection and betatron oscillation in a plasma-waveguide-based laser wakefield accelerator by modification of waveguide structure

By adding a transverse heater pulse into the axicon ignitor-heater scheme for producing a plasma waveguide, a variable three-dimensionally structured plasma waveguide can be fabricated. With this technique, electron injection in a plasma-waveguide-based laser wakefield accelerator was achieved and resulted in production of a quasi-monoenergetic electron beam. The injection was correlated with a section of expanding cross-section in the plasma waveguide. Moreover, the intensity of the X-ray beam produced by the electron bunch in betatron oscillation was greatly enhanced with a transversely shifted section in the plasma waveguide. The technique opens a route to a compact hard-X-ray pulse source.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗
DOE OSTI2021

Observation of second harmonic electron cyclotron resonance heating and current-drive transition during non-inductive plasma start-up experiment in QUEST

Here, noninductive plasma current start-up using 2nd harmonic electron cyclotron resonance heating (ECRH) with oblique radio frequency (RF) injection is demonstrated in a Q-shu University experiment with steady-state spherical tokamak. A strong transition was observed in the heating and plasma current ramp-up. The initial bulk electron heating regime exhibits T ebulk ~ 140 eV and no hard x-ray (HXR) emission with a low I p of ~15 kA; it abruptly transitions to a regime that exhibits a low T ebulk of ~10 eV and a strong HXR emission with a high I p of ~50 kA. This behavior is distinctly different from that observed in previous fundamental ECRH experiments. The mechanism of the heating and current drive transition are investigated considering wave power absorption and plasma power balance. The results indicate that the transition is caused by the favorable heating of tail electrons where the RF power absorption at the 2nd harmonic increases nearly linearly with T etail , while the power transfer from the tail electrons to the bulk electrons decreases with 1/T etail 0.5 . This causes a rapid transition to a state with high T etail while reducing T ebulk towards colder ion temperature. The understanding of the transition mechanism helps to consider plasma current start-up using 2nd harmonic ECRH for tokamak reactors such as JT-60 SA and ITER.

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