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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 OSTI2012

Crystal structure analysis of tungsten bronzes {beta}-SrTa{sub 2}O{sub 6} and {beta} Prime -SrTa{sub 2}O{sub 6} by synchrotron X-ray and neutron powder diffraction

Strontium ditantalum oxide SrTa{sub 2}O{sub 6} exists in {alpha}-, {beta}-, and {beta} Prime -polymorphs. Herein the crystal structures of the latter two were studied using synchrotron X-ray and constant-wavelength neutron powder diffraction. While {beta} Prime -SrTa{sub 2}O{sub 6} [space group P4/mbm, a=12.47099(1) A, c=3.898210(5) A, V=606.271(2) Angstrom-Sign {sup 3}, Z=5] belongs to the regular tetragonal tungsten bronze (TTB) family, it contains locally disordered strontium atoms within the pentagonal channel. {beta}-SrTa{sub 2}O{sub 6} [space group Pnam, a=12.36603(2) Angstrom-Sign , b=12.43467(2) A, c=7.72403(1) A, V=1187.705(4) Angstrom-Sign {sup 3}, Z=10] can be described as an orthorhombic modification of the TTB, where the octahedral tilting distortion effectively alleviates the bonding strains around TaO{sub 6} and SrO{sub 13} polyhedra. For comparison, rynersonite type {alpha}-SrTa{sub 2}O{sub 6} [space group Pnma, a=11.00610(6) Angstrom-Sign , b=7.63397(3) Angstrom-Sign , c=5.62634(3) Angstrom-Sign , V=472.727(5) Angstrom-Sign {sup 3}, and Z=4] is built from edge-shared dimer units of TaO{sub 6} octahedra. As measured by diffuse-reflection absorption spectroscopy, {alpha}-, {beta}-, and {beta} Prime -SrTa{sub 2}O{sub 6} have indirect band gap energies of 4.4, 4.0, and 3.8 eV, respectively. - Graphical Abstract: Difference Fourier map for {beta} Prime -SrTa{sub 2}O{sub 6} at z=0. Highlights: Black-Right-Pointing-Pointer Structure refinements of {beta}-SrTa{sub 2}O{sub 6} and {beta} Prime -SrTa{sub 2}O{sub 6}. Black-Right-Pointing-Pointer Strontium disorder in tetragonal tungsten bronze {beta} Prime -SrTa{sub 2}O{sub 6}. Black-Right-Pointing-Pointer Orthorhombic distortion and cell doubling in {beta}-SrTa{sub 2}O{sub 6}.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2011

Relation between the 2{nu}{beta}{beta} and 0{nu}{beta}{beta} nuclear matrix elements

A formal relation between the GT part of the nuclear matrix elements M{sub GT}{sup 0{nu}} of 0{nu}{beta}{beta} decay and the closure matrix elements M{sub cl}{sup 2{nu}} of 2{nu}{beta}{beta} decay is established. This relation is based on the integral representation of these quantities in terms of their dependence on the distance r between the two nucleons undergoing transformation. We also discuss the difficulties in determining the correct values of the closure 2{nu}{beta}{beta} decay matrix elements.

73 NUCLEAR PHYSICS AND RADIATION PHYSICS↗
DOE OSTI2017

Polypeptides having beta-glucosidase activity, beta-xylosidase activity, or beta-glucosidase and beta-xylosidase activity and polynucleotides encoding same

The present invention relates to isolated polypeptides having beta-glucosidase activity, beta-xylosidase activity, or beta-glucosidase and beta-xylosidase activity and isolated polynucleotides encoding the polypeptides. The invention also relates to nucleic acid constructs, vectors, and host cells comprising the polynucleotides as well as methods of producing and using the polypeptides.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2019

Polypeptides having beta-glucosidase activity, beta-xylosidase activity, or beta-glucosidase and beta-xylosidase activity and polynucleotides encoding same

The present invention relates to isolated polypeptides having beta-glucosidase activity, beta-xylosidase activity, or beta-glucosidase and beta-xylosidase activity and isolated polynucleotides encoding the polypeptides. The invention also relates to nucleic acid constructs, vectors, and host cells comprising the polynucleotides as well as methods of producing and using the polypeptides.

Morant, Marc↗
DOE OSTI2014

The MAJORANA DEMONSTRATOR Neutrinoless Double-Beta Decay Experiment

The MAJORANA DEMONSTRATOR will search for the neutrinoless double-beta (ββ(0ν)) decay of the isotope 76 Ge with a mixed array of enriched and natural germanium detectors. The observation of this rare decay would indicate that the neutrino is its own antiparticle, demonstrate that lepton number is not conserved, and provide information on the absolute mass scale of the neutrino. The DEMONSTRATOR is being assembled at the 4850-foot level of the Sanford Underground Research Facility in Lead, South Dakota. The array will be situated in a low-background environment and surrounded by passive and active shielding. Here we describe the science goals of the DEMONSTRATOR and the details of its design.

Abgrall, N.↗
NASA NTRS2002

Ca2+-dependent dephosphorylation of kinesin heavy chain on beta-granules in pancreatic beta-cells. Implications for regulated beta-granule transport and insulin exocytosis

The specific biochemical steps required for glucose-regulated insulin exocytosis from beta-cells are not well defined. Elevation of glucose leads to increases in cytosolic [Ca2+]i and biphasic release of insulin from both a readily releasable and a storage pool of beta-granules. The effect of elevated [Ca2+]i on phosphorylation of isolated beta-granule membrane proteins was evaluated, and the phosphorylation of four proteins was found to be altered by [Ca2+]i. One (a 18/20-kDa doublet) was a Ca2+-dependent increase in phosphorylation, and, surprisingly, three others (138, 42, and 36 kDa) were Ca2+-dependent dephosphorylations. The 138-kDa beta-granule phosphoprotein was found to be kinesin heavy chain (KHC). At low levels of [Ca2+]i KHC was phosphorylated by casein kinase 2, but KHC was rapidly dephosphorylated by protein phosphatase 2B beta (PP2Bbeta) as [Ca2+]i increased. Inhibitors of PP2B specifically reduced the second, microtubule-dependent, phase of insulin secretion, suggesting that dephosphorylation of KHC was required for transport of beta-granules from the storage pool to replenish the readily releasable pool of beta-granules. This is distinct from synaptic vesicle exocytosis, because neurotransmitter release from synaptosomes did not require a Ca2+-dependent KHC dephosphorylation. These results suggest a novel mechanism for regulating KHC function and beta-granule transport in beta-cells that is mediated by casein kinase 2 and PP2B. They also implicate a novel regulatory role for PP2B/calcineurin in the control of insulin secretion downstream of a rise in [Ca2+]i.

NASA Discipline Neuroscience↗
DOE OSTI2011

Integrin {alpha}{beta}1, {alpha}{sub v}{beta}, {alpha}{sub 6}{beta} effectors p130Cas, Src and talin regulate carcinoma invasion and chemoresistance

Research highlights: {yields} Proteomics of clustered integrin {alpha}{beta}1, {alpha}{sub v}{beta}, {alpha}{sub 6}{beta} receptors in oral carcinoma. {yields} p130Cas, Dek, Src and talin regulate oral carcinoma invasion. {yields} p130Cas, talin, Src and zyxin regulate oral carcinoma resistance to cisplatin. -- Abstract: Ligand engagement by integrins induces receptor clustering and formation of complexes at the integrin cytoplasmic face that controls cell signaling and cytoskeletal dynamics critical for adhesion-dependent processes. This study searches for a subset of integrin effectors that coordinates both tumor cell invasion and resistance to the chemotherapeutic drug cisplatin in oral carcinomas. Candidate integrin effectors were identified in a proteomics screen of proteins recruited to clustered integrin {alpha}{beta}1, {alpha}{sub v}{beta} or {alpha}{sub 6}{beta} receptors in oral carcinomas. Proteins with diverse functions including microtubule and actin binding proteins, and factors involved in trafficking, transcription and translation were identified in oral carcinoma integrin complexes. Knockdown of effectors in the oral carcinoma HN12 cells revealed that p130Cas, Dek, Src and talin were required for invasion through Matrigel. Disruption of talin or p130Cas by RNA interference increased resistance to cisplatin, whereas targeting Dek, Src or zyxin reduced HN12 resistance to cisplatin. Analysis of the spreading of HN12 cells on collagen I and laminin I revealed that a decrease in p130Cas or talin expression inhibited spreading on both matrices. Interestingly, a reduction in zyxin expression enhanced spreading on laminin I and inhibited spreading on collagen I. Reduction of Dek, Src, talin or zyxin expression reduced HN12 proliferation by 30%. Proliferation was not affected by a reduction in p130Cas expression. We conclude that p130Cas, Src and talin function in both oral carcinoma invasion and resistance to cisplatin.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2011

New Limit on Time-Reversal Violation in Beta Decay

We report the results of an improved determination of the triple correlation DP{center_dot}(p{sub e}xp{sub v}) that can be used to limit possible time-reversal invariance in the beta decay of polarized neutrons and constrain extensions to the standard model. Our result is D=[-0.96{+-}1.89(stat){+-}1.01(sys)]x10{sup -4}. The corresponding phase between g{sub A} and g{sub V} is {phi}{sub AV}=180.013 deg. {+-}0.028 deg. (68% confidence level). This result represents the most sensitive measurement of D in nuclear {beta} decay.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2014

The Majorana Demonstrator: Progress towards showing the feasibility of a tonne–scale 76 Ge neutrinoless double–beta decay experiment

The Majorana Demonstrator will search for the neutrinoless double–beta decay (0vββ) of the 76 Ge isotope with a mixed array of enriched and natural germanium detectors. The observation of this rare decay would indicate the neutrino is its own anti–particle, demonstrate that lepton number is not conserved, and provide information on the absolute mass–scale of the neutrino. The Demonstrator is being assembled at the 4850 foot level of the Sanford Underground Research Facility in Lead, South Dakota. The array will be contained in a low–background environment and surrounded by passive and active shielding. The goals for the Demonstrator are: demonstrating a background rate less than 3 t -1 y -1 in the 4 keV region of interest (ROI) surrounding the 2039 keV 76 Ge endpoint energy; establishing the technology required to build a tonne–scale germanium based double–beta decay experiment; testing the recent claim of observation of 0vββ [1]; and performing a direct search for light WIMPs (3-10 GeV/c 2 ).

Finnerty, P.↗
DOE OSTI2011

TGF-{beta}-stimulated aberrant expression of class III {beta}-tubulin via the ERK signaling pathway in cultured retinal pigment epithelial cells

Highlights: Black-Right-Pointing-Pointer TGF-{beta} induces aberrant expression of {beta}III in RPE cells via the ERK pathway. Black-Right-Pointing-Pointer TGF-{beta} increases O-GlcNAc modification of {beta}III in RPE cells. Black-Right-Pointing-Pointer Mature RPE cells have the capacity to express a neuron-associated gene by TGF-{beta}. -- Abstract: The class III {beta}-tubulin isotype ({beta}{sub III}) is expressed exclusively by neurons within the normal human retina and is not present in normal retinal pigment epithelial (RPE) cells in situ or in the early phase of primary cultures. However, aberrant expression of class III {beta}-tubulin has been observed in passaged RPE cells and RPE cells with dedifferentiated morphology in pathologic epiretinal membranes from idiopathic macular pucker, proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR). Transforming growth factor-{beta} (TGF-{beta}) has been implicated in dedifferentiation of RPE cells and has a critical role in the development of proliferative vitreoretinal diseases. Here, we investigated the potential effects of TGF-{beta} on the aberrant expression of class III {beta}-tubulin and the intracellular signaling pathway mediating these changes. TGF-{beta}-induced aberrant expression and O-linked-{beta}-N-acetylglucosamine (O-GlcNac) modification of class III {beta}-tubulin in cultured RPE cells as determined using Western blotting, RT-PCR and immunocytochemistry. TGF-{beta} also stimulated phosphorylation of ERK. TGF-{beta}-induced aberrant expression of class III {beta}-tubulin was significantly reduced by pretreatment with U0126, an inhibitor of ERK phosphorylation. Our findings indicate that TGF-{beta} stimulated aberrant expression of class III {beta}-tubulin via activation of the ERK signaling pathway. These data demonstrate that mature RPE cells have the capacity to express a neuron-associated gene in response to TGF-{beta} stimulation and provide useful information towards understanding the pathogenesis of proliferative vitreoretinal diseases.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2011

The {sup 150}Nd({sup 3}He,t) and {sup 150}Sm(t,{sup 3}He) reactions with applications to {beta}{beta} decay of {sup 150}Nd

The {sup 150}Nd({sup 3}He,t) reaction at 140 MeV/u and {sup 150}Sm(t,{sup 3}He) reaction at 115 MeV/u were measured, populating excited states in {sup 150}Pm. The transitions studied populate intermediate states of importance for the (neutrinoless) {beta}{beta} decay of {sup 150}Nd to {sup 150}Sm. Monopole and dipole contributions to the measured excitation-energy spectra were extracted by using multipole decomposition analyses. The experimental results were compared with theoretical calculations obtained within the framework of the quasiparticle random-phase approximation, which is one of the main methods employed for estimating the half-life of the neutrinoless {beta}{beta} decay (0{nu}{beta}{beta}) of {sup 150}Nd. The present results thus provide useful information on the neutrino responses for evaluating the 0{nu}{beta}{beta} and 2{nu}{beta}{beta} matrix elements. The 2{nu}{beta}{beta} matrix element calculated from the Gamow-Teller transitions through the lowest 1{sup +} state in the intermediate nucleus is maximally about half that deduced from the half-life measured in 2{nu}{beta}{beta} direct counting experiments, and at least several transitions through 1{sup +} intermediate states in {sup 150}Pm are required to explain the 2{nu}{beta}{beta} half-life. Because Gamow-Teller transitions in the {sup 150}Sm(t,{sup 3}He) experiment are strongly Pauli blocked, the extraction of Gamow-Teller strengths was complicated by the excitation of the 2({h_bar}/2{pi}){omega}, {Delta}L=0, {Delta}S=1 isovector spin-flip giant monopole resonance (IVSGMR). However, the near absence of Gamow-Teller transition strength made it possible to cleanly identify this resonance, and the strength observed is consistent with the full exhaustion of the non-energy-weighted sum rule for the IVSGMR.

73 NUCLEAR PHYSICS AND RADIATION PHYSICS↗
DOE OSTI2024

Searching for beyond the Standard Model physics using the improved description of 100 Mo $2\nu \beta \beta$ decay spectral shape with CUPID-Mo

The current experiments searching for neutrinoless double-β ($0\nu \beta \beta$) decay also collect large statistics of Standard Model allowed two-neutrino double-β ($2\nu \beta \beta$ ) decay events. These can be used to search for Beyond Standard Model (BSM) physics via $2\nu \beta \beta$ decay spectral distortions. 100 Mo has a natural advantage due to its relatively short half-life, allowing higher $2\nu \beta \beta$ decay statistics at equal exposures compared to the other isotopes. We demonstrate the potential of the dual read-out bolometric technique exploiting a 100 Mo exposure of 1.47 kg years, acquired in the CUPID-Mo experiment at the Modane underground laboratory (France). We set limits on $0\nu \beta \beta$ decays with the emission of one or more Majorons, on $2\nu \beta \beta$ decay with Lorentz violation, and $2\nu \beta \beta$ decay with a sterile neutrino emission. In this analysis, we investigate the systematic uncertainty induced by modeling the $2\nu \beta \beta$ decay spectral shape parameterized through an improved model, an effect never considered before. This work motivates searches for BSM processes in the upcoming CUPID experiment, which will collect the largest amount of $2\nu \beta \beta$ decay events among the next-generation experiments.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2010

Extracellular heat shock protein HSP90{beta} secreted by MG63 osteosarcoma cells inhibits activation of latent TGF-{beta}1

Transforming growth factor-beta 1 (TGF-{beta}1) is secreted as a latent complex, which consists of latency-associated peptide (LAP) and the mature ligand. The release of the mature ligand from LAP usually occurs through conformational change of the latent complex and is therefore considered to be the first step in the activation of the TGF-{beta} signaling pathway. So far, factors such as heat, pH changes, and proteolytic cleavage are reportedly involved in this activation process, but the precise molecular mechanism is still far from clear. Identification and characterization of the cell surface proteins that bind to LAP are important to our understanding of the latent TGF-{beta} activation process. In this study, we have identified heat shock protein 90 {beta} (HSP90{beta}) from the cell surface of the MG63 osteosarcoma cell line as a LAP binding protein. We have also found that MG63 cells secrete HSP90{beta} into extracellular space which inhibits the activation of latent TGF-{beta}1, and that there is a subsequent decrease in cell proliferation. TGF-{beta}1-mediated stimulation of MG63 cells resulted in the increased cell surface expression of HSP90{beta}. Thus, extracellular HSP90{beta} is a negative regulator for the activation of latent TGF-{beta}1 modulating TGF-{beta} signaling in the extracellular domain. -- Research highlights: {yields} Transforming growth factor-beta 1 (TGF-{beta}1) is secreted as a latent complex. {yields} This complex consists of latency-associated peptide (LAP) and the mature ligand. {yields} The release of the mature ligand from LAP is the first step in TGF-{beta} activation. {yields} We identified for the first time a novel mechanism for this activation process. {yields} Heat shock protein 90 {beta} is discovered as a negative regulator for this process.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2012

Solid-state NMR analysis of the {beta}-strand orientation of the protofibrils of amyloid {beta}-protein

Highlights: Black-Right-Pointing-Pointer The supramolecular structure of A{beta}42 protofibrils was analyzed by solid-state NMR. Black-Right-Pointing-Pointer The Ala-21 residue in the A{beta}42 protofibrils is included in a slightly disordered {beta}-strand. Black-Right-Pointing-Pointer The A{beta}42 protofibrils do not form intermolecular in-register parallel {beta}-sheets. -- Abstract: Alzheimer's disease (AD) is caused by abnormal deposition (fibrillation) of a 42-residue amyloid {beta}-protein (A{beta}42) in the brain. During the process of fibrillation, the A{beta}42 takes the form of protofibrils with strong neurotoxicity, and is thus believed to play a crucial role in the pathogenesis of AD. To elucidate the supramolecular structure of the A{beta}42 protofibrils, the intermolecular proximity of the Ala-21 residues in the A{beta}42 protofibrils was analyzed by {sup 13}C-{sup 13}C rotational resonance experiments in the solid state. Unlike the A{beta}42 fibrils, an intermolecular {sup 13}C-{sup 13}C correlation was not found in the A{beta}42 protofibrils. This result suggests that the {beta}-strands of the A{beta}42 protofibrils are not in an in-register parallel orientation. A{beta}42 monomers would assemble to form protofibrils with the {beta}-strand conformation, then transform into fibrils by forming intermolecular parallel {beta}-sheets.

60 APPLIED LIFE SCIENCES↗