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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 55 records · Page 3
All sourcesNASA NTRSDOE OSTI
DOE OSTI2021

Protective effects of intravitreal administration of mesenchymal stem cell-derived exosomes in an experimental model of optic nerve injury

Traumatic optic neuropathy results in the loss of retinal ganglion cells (RGCs), leading to unavoidable visual impairment. However, there is no effective therapy by far. Accumulated studies support the perception that mesenchymal stem cells (MSCs) secrete exosomes that serve as a protective paracrine factor. The study aimed to explore and evaluate the potential therapeutic effects of intravitreal transplantation of MSC-derived exosomes (MSC-exos) in an experimental model of optic nerve crush (ONC). Exosomes were isolated from rat MSCs and characterized by transmission electron microscope and western blotting. At the onset of ONC, a single intravitreal injection of exosomes or PBS was administered to the rats. At day 30, hematoxylin and eosin staining, immunohistochemistry, and βIII-tubulin staining were performed to evaluate the survival of RGCs. Moreover, TUNEL assay was used to examine the apoptosis of RGCs. Inflammation-relevant factors were identified via quantitative polymerase chain reaction. The expression levels of cell apoptosis-related molecules and key members of the PI3K/AKT signaling pathway were determined via western blot analysis. We found that MSC-exos exhibited typical characteristic morphologies (cup-shaped) and sizes (peak size of 93 nm). Furthermore, they exhibited substantial expression of the exosome markers CD63 and TSG101, but lacked the expression of the cellular marker GM130. Treatment with intravitreal MSC-exos notably promoted the survival of RGCs in ONC rats. The level of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6, IL-8, and MCP-1, were reduced, whereas those of the anti-inflammatory factor IL-10 were increased. Moreover, the apoptosis induced by ONC was decreased by the administration of MSC-exos via upregulation of the Bcl-2/Bax ratio and downregulation of caspase-3 activity. Furthermore, MSC-exos significantly stimulated AKT phosphorylation, whereas LY294002 restored the apoptosis-preventing effects of MSC-exos. The results of our results demonstrated that intravitreal administration of MSC-exos ameliorates ONC-induced injury in a rat model. These findings might aid in the development of effective exosome-based therapeutic strategies for the treatment of optic nerve degeneration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

CLEC12B suppresses lung cancer progression by inducing SHP-1 expression and inactivating the PI3K/AKT signaling pathway

Lung cancer is the leading cause of cancer mortality worldwide. CLEC12B, a C-type lectin-like receptor, is low-expressed in lung cancer tissues. However, the function of CLEC12B in lung cancer and its underlying mechanism remain unclear. Here, an obvious down-regulation of CLEC12B was observed in lung cancer cells compared with the normal lung epithelial cells. CLEC12B over-expression suppressed cell viability and cell cycle entry in lung cancer, along with the reduction of PCNA and cyclin D1 expressions, while silencing CLEC12B possessed the opposite effects. Over-expression of CLEC12B promoted lung cancer cell apoptosis, accompanied by decreased Bcl-2 and increased Bax, cleaved caspase-3 and cleaved caspase-9. Moreover, CLEC12B decreased phosphorylation of PI3K-p85 and AKT proteins. By contrast, CLEC12B knockdown activated the PI3K/AKT pathway. In vivo, CLEC12B inhibited tumor growth in lung cancer, which can be reversed by CLEC12B inhibition. Co-IP and immunofluorescence assays confirmed the interaction between CLEC12B and SHP-1, and CLEC12B over-expression increased SHP-1 level. Furthermore, knocking down SHP-1 abrogated the above biological phenotypes caused by CLEC12B elevation. Taken together, our findings demonstrate that CLEC12B serves as a tumor-suppressing gene in lung cancer through positively regulating SHP-1 expression, which may be mediated by the PI3K/AKT signaling pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2025

Discovery of Macrocyclic Myeloid Cell Leukemia 1 (Mcl-1)Inhibitors that Demonstrate Potent Cellular Efficacy and In Vivo Activity in a Mouse Solid Tumor Xenograft Model

Abstract The B cell lymphoma 2 (Bcl-2) family of proteins are key regulators of intrinsic apoptosis. The antiapoptotic protein myeloid cell leukemia 1 (Mcl-1), which is associated with high tumor grade, poor survival, and resistance to treatment, has emerged as a promising candidate for treating hematological and solid cancers. Herein, we report the structure-guided design of small molecule macrocyclic Mcl-1 inhibitors based on the (R)-methyl-dihydropyrazinoindolone scaffold our group has previously disclosed. The macrocyclic inhibitors bind Mcl-1 with subnanomolar affinity and offer improved potency in cell culture growth inhibition assays. Inhibitor 13 achieved tumor regression in a lung cancer-derived tumor xenograft model in mice as a monotherapy. The improved potency of the macrocyclic series allowed replacement of heretofore conserved indole carboxylic acid moiety, resulting in neutral inhibitors. Amide inhibitor 25 displayed a >10-fold increase in oral bioavailability as compared to acid-containing macrocyclic or acyclic inhibitors.

Pharmacology & Pharmacy↗
DOE OSTI2024

Dual blockade of IL-10 and PD-1 leads to control of SIV viral rebound following analytical treatment interruption

Human immunodeficiency virus (HIV) persistence during antiretroviral therapy (ART) is associated with heightened plasma interleukin-10 (IL-10) levels and PD-1 expression. We hypothesized that IL-10 and PD-1 blockade would lead to control of viral rebound following analytical treatment interruption (ATI). Twenty-eight ART-treated, simian immunodeficiency virus (SIV)mac 239 -infected rhesus macaques (RMs) were treated with anti-IL-10, anti-IL-10 plus anti-PD-1 (combo) or vehicle. ART was interrupted 12 weeks after introduction of immunotherapy. Durable control of viral rebound was observed in nine out of ten combo-treated RMs for >24 weeks post-ATI. Induction of inflammatory cytokines, proliferation of effector CD8 + T cells in lymph nodes and reduced expression of BCL-2 in CD4 + T cells pre-ATI predicted control of viral rebound. Twenty-four weeks post-ATI, lower viral load was associated with higher frequencies of memory T cells expressing TCF-1 and of SIV-specific CD4 + and CD8 + T cells in blood and lymph nodes of combo-treated RMs. These results map a path to achieve long-lasting control of HIV and/or SIV following discontinuation of ART.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2022

β -Ga 2 O 3 Schottky barrier diodes with 4.1 MV/cm field strength by deep plasma etching field-termination Available

In this work, we demonstrate a deep mesa etch design for efficient edge field termination in β-Ga 2 O 3 Schottky barrier diodes (SBDs). The proposed design enabled parallel plate fields higher than 4.1 MV/cm with negligible change to the device ON characteristics. The effect of BCl 3 /Cl 2 -based dry etch on (100) and (010) etched vertical sidewalls is also analyzed. A remarkable anisotropy in depletion was observed for etch along (100) and (010) sidewalls. In conclusion, this work provides insight into the impact of etching on n-type Ga 2 O 3 and shows a promising method to realize efficient field termination for high breakdown field strength SBDs.

42 ENGINEERING↗
DOE OSTI2024

Altered post-fracture systemic bone loss in a mouse model of osteocyte dysfunction

Femur fracture leads to loss of bone at uninjured skeletal sites, which may increase risk of subsequent fracture. Osteocytes, the most abundant bone cells, can directly resorb bone matrix and regulate osteoclast and osteoblast activity, but their role in systemic bone loss after fracture remains poorly understood. In this study we used a transgenic (TG+) mouse model that overexpresses human B-cell lymphoma 2 (BCL-2) in osteoblasts and osteocytes. This causes enhanced osteoblast proliferation, followed by disruption in lacunar-canalicular connectivity and massive osteocyte death by 10 wk of age. We hypothesized that reduced viable osteocyte density would decrease the magnitude of systemic bone loss after femur fracture, reduce perilacunar remodeling, and alter callus formation. Bone remodeling was assessed using serum biomarkers of bone formation and resorption at 5 d post-fracture. We used micro-computed tomography, high resolution x-ray microscopy, mechanical testing, and Raman spectroscopy to quantify the magnitude of systemic bone loss, as well as changes in osteocyte lacunar volume, bone strength, and bone composition 2 wk post-fracture. Fracture was associated with a reduction in circulating markers of bone resorption in non-transgenic (TG-) animals. TG+ mice exhibited high bone mass in the limbs, greater cortical elastic modulus and reduced post-yield displacement. After fracture, TG+ mice lost less trabecular bone than TG- mice, but conversely TG+ mice exhibited trends toward a lower yield point and reduced femoral cortical thickness after fracture, though these were not statistically significant. Lacunar density was greater in TG+ mice, but fracture did not alter lacunar volume in TG+ or TG- mice. These findings suggest that osteocytes potentially play a significant role in the post-traumatic systemic response to fracture, though the effects differ between trabecular and cortical bone.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2020

Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity

The accumulation of senescent cells (SnCs) is a causal factor of various age-related diseases as well as some of the side effects of chemotherapy. Pharmacological elimination of SnCs (senolysis) has the potential to be developed into novel therapeutic strategies to treat these diseases and pathological conditions. Here we show that ubiquitin-specific peptidase 7 (USP7) is a novel target for senolysis because inhibition of USP7 with an inhibitor or genetic depletion of USP7 by RNA interference induces apoptosis selectively in SnCs. The senolytic activity of USP7 inhibitors is likely attributable in part to the promotion of the human homolog of mouse double minute 2 (MDM2) ubiquitination and degradation by the ubiquitin–proteasome system. This degradation increases the levels of p53, which in turn induces the pro-apoptotic proteins PUMA, NOXA, and FAS and inhibits the interaction of BCL-XL and BAK to selectively induce apoptosis in SnCs. Further, we show that treatment with a USP7 inhibitor can effectively eliminate SnCs and suppress the senescence-associated secretory phenotype (SASP) induced by doxorubicin in mice. These findings suggest that small molecule USP7 inhibitors are novel senolytics that can be exploited to reduce chemotherapy-induced toxicities and treat age-related diseases.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2022

Hole in one: Pathways to deterministic single-acceptor incorporation in Si(100)-2 x 1

We report that stochastic incorporation kinetics can be a limiting factor in the scalability of semiconductor fabrication technologies using atomic-precision techniques. While these technologies have recently been extended from donors to acceptors, the extent to which kinetics will impact single-acceptor incorporation has yet to be assessed. To identify the precursor molecule and dosing conditions that are promising for deterministic incorporation, we develop and apply an atomistic model for the single-acceptor incorporation rates of several recently demonstrated molecules: diborane (B 2 H 6 ), boron trichloride (BCl 3 ), and aluminum trichloride in both monomer (AlCl 3 ) and dimer forms (Al 2 Cl 6 ). While all three precursors can realize single-acceptor incorporation, we predict that diborane is unlikely to realize deterministic incorporation, boron trichloride can realize deterministic incorporation with modest heating (50 °C), and aluminum trichloride can realize deterministic incorporation at room temperature. We conclude that both boron and aluminum trichloride are promising precursors for atomic-precision single-acceptor applications, with the potential to enable the reliable production of large arrays of single-atom quantum devices.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗
DOE OSTI2022

Protective Effect of Phloretin against Hydrogen Peroxide-Induced Oxidative Damage by Enhancing Autophagic Flux in DF-1 Cells

Phloretin (PHL) is a dihydrochalcone flavonoid isolated from the peel and root bark of apples, strawberries, and other plants with antioxidative characteristic. In this study, we aimed to investigate the protective effect and the potential mechanism of PHL on hydrogen peroxide (H2O2)-induced oxidative damage in DF-1 cells. The results showed that PHL exhibited no cytotoxic effect on DF-1 cells at concentration below 20 μM. PHL markedly increased H2O2-reduced cell viability, decreased H2O2-induced apoptosis, as evidenced by reduced apoptosis rate, the upregulation of gene and protein level of Bcl-2, and the downregulation of gene and protein level of Bax and Cleaved caspase3. In addition, PHL reduced H2O2-induced reactive oxygen species (ROS) production and restored antioxidant enzymes activities as well as mitochondrial membrane potential in a dose-dependent manner. Moreover, PHL prior to H2O2 further increased LC3-II level, promoted p62 turnover and improved lysosomal function. Importantly, autophagy inhibitor chloroquine (CQ) reversed the protective effect of PHL, and increased H2O2-induced apoptosis. Furthermore, PHL inhibited the phosphorylation levels of ERK, p38, and JNK. Collectively, these results indicate that PHL could attenuate H2O2-induced oxidative injury and apoptosis by maintaining lysosomal function and promoting autophagic flux, and MAPKs pathway may be involved in this process. Our study provides evidence that PHL could as a new strategy to against oxidative damage in poultry industry.

Song, Dan↗
DOE OSTI2020

Materials Data on LiB6S4(Cl3O4)2 by Materials Project

Li(SO2)4(BCl)6 crystallizes in the triclinic P-1 space group. The structure is zero-dimensional and consists of twelve chloroborane molecules and one Li(SO2)4 cluster. In the Li(SO2)4 cluster, Li1+ is bonded in a trigonal bipyramidal geometry to five O2- atoms. There are a spread of Li–O bond distances ranging from 2.03–2.28 Å. There are four inequivalent S+0.75+ sites. In the first S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. In the second S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. There is one shorter (1.45 Å) and one longer (1.46 Å) S–O bond length. In the third S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. In the fourth S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. There are eight inequivalent O2- sites. In the first O2- site, O2- is bonded in a linear geometry to one Li1+ and one S+0.75+ atom. In the second O2- site, O2- is bonded in a bent 150 degrees geometry to one Li1+ and one S+0.75+ atom. In the third O2- site, O2- is bonded in a bent 150 degrees geometry to one Li1+ and one S+0.75+ atom. In the fourth O2- site, O2- is bonded in a single-bond geometry to one S+0.75+ atom. In the fifth O2- site, O2- is bonded in a bent 150 degrees geometry to one Li1+ and one S+0.75+ atom. In the sixth O2- site, O2- is bonded in a single-bond geometry to one S+0.75+ atom. In the seventh O2- site, O2- is bonded in a bent 150 degrees geometry to one Li1+ and one S+0.75+ atom. In the eighth O2- site, O2- is bonded in a single-bond geometry to one S+0.75+ atom.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Materials Data on AlB6H6(CCl3)2 by Materials Project

AlB2H6(CCl)2(BCl)4 crystallizes in the monoclinic P2_1/c space group. The structure is zero-dimensional and consists of sixteen chloroborane molecules and four AlB2H6(CCl)2 clusters. In each AlB2H6(CCl)2 cluster, Al3+ is bonded in a distorted trigonal pyramidal geometry to two C+3.50- and two Cl1- atoms. Both Al–C bond lengths are 1.95 Å. There are one shorter (2.47 Å) and one longer (2.52 Å) Al–Cl bond lengths. There are two inequivalent B1+ sites. In the first B1+ site, B1+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.83 Å. In the second B1+ site, B1+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.83 Å. There are two inequivalent C+3.50- sites. In the first C+3.50- site, C+3.50- is bonded to one Al3+ and three H+0.67+ atoms to form corner-sharing CAlH3 tetrahedra. There is one shorter (1.09 Å) and two longer (1.10 Å) C–H bond length. In the second C+3.50- site, C+3.50- is bonded to one Al3+ and three H+0.67+ atoms to form corner-sharing CAlH3 tetrahedra. There is one shorter (1.09 Å) and two longer (1.10 Å) C–H bond length. There are six inequivalent H+0.67+ sites. In the first H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. In the second H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. In the third H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. In the fourth H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. In the fifth H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. In the sixth H+0.67+ site, H+0.67+ is bonded in a single-bond geometry to one C+3.50- atom. There are two inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a water-like geometry to one Al3+ and one B1+ atom. In the second Cl1- site, Cl1- is bonded in a water-like geometry to one Al3+ and one B1+ atom.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Materials Data on B11H2CCl11 by Materials Project

B5CHCl5(BCl)4B2HCl2 crystallizes in the triclinic P-1 space group. The structure is zero-dimensional and consists of sixteen chloroborane molecules, four B2HCl2 clusters, and four B5CHCl5 clusters. In two of the B2HCl2 clusters, there are two inequivalent B+1.36+ sites. In the first B+1.36+ site, B+1.36+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.85 Å. In the second B+1.36+ site, B+1.36+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.84 Å. H is bonded in a linear geometry to two Cl1- atoms. There is one shorter (1.53 Å) and one longer (1.65 Å) H–Cl bond length. There are two inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a water-like geometry to one B+1.36+ and one H atom. In the second Cl1- site, Cl1- is bonded in a water-like geometry to one B+1.36+ and one H atom. In two of the B2HCl2 clusters, there are two inequivalent B+1.36+ sites. In the first B+1.36+ site, B+1.36+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.85 Å. In the second B+1.36+ site, B+1.36+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.84 Å. H is bonded in a linear geometry to two Cl1- atoms. There is one shorter (1.59 Å) and one longer (1.60 Å) H–Cl bond length. There are two inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a water-like geometry to one B+1.36+ and one H atom. In the second Cl1- site, Cl1- is bonded in a water-like geometry to one B+1.36+ and one H atom. In two of the B5CHCl5 clusters, there are five inequivalent B+1.36+ sites. In the first B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.71 Å. The B–Cl bond length is 1.76 Å. In the second B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.72 Å. The B–Cl bond length is 1.77 Å. In the third B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.72 Å. The B–Cl bond length is 1.76 Å. In the fourth B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.71 Å. The B–Cl bond length is 1.76 Å. In the fifth B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.73 Å. The B–Cl bond length is 1.76 Å. C4- is bonded in a 1-coordinate geometry to five B+1.36+ and one H atom. The C–H bond length is 1.09 Å. H is bonded in a single-bond geometry to one C4- atom. There are five inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the second Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the third Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the fourth Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the fifth Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In two of the B5CHCl5 clusters, there are five inequivalent B+1.36+ sites. In the first B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.73 Å. The B–Cl bond length is 1.76 Å. In the second B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.71 Å. The B–Cl bond length is 1.76 Å. In the third B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.72 Å. The B–Cl bond length is 1.77 Å. In the fourth B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.72 Å. The B–Cl bond length is 1.76 Å. In the fifth B+1.36+ site, B+1.36+ is bonded in a bent 120 degrees geometry to one C4- and one Cl1- atom. The B–C bond length is 1.71 Å. The B–Cl bond length is 1.76 Å. C4- is bonded in a 1-coordinate geometry to five B+1.36+ and one H atom. The C–H bond length is 1.09 Å. H is bonded in a single-bond geometry to one C4- atom. There are five inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the second Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the third Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the fourth Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom. In the fifth Cl1- site, Cl1- is bonded in a single-bond geometry to one B+1.36+ atom.

36 MATERIALS SCIENCE↗
DOE OSTI2020

Materials Data on KB6S4(Cl3O4)2 by Materials Project

KB3S4O8Cl3(BCl)3 crystallizes in the monoclinic P2_1/c space group. The structure is one-dimensional and consists of twelve chloroborane molecules and two KB3S4O8Cl3 ribbons oriented in the (0, 0, 1) direction. In each KB3S4O8Cl3 ribbon, K1+ is bonded in a 6-coordinate geometry to six O2- and three Cl1- atoms. There are a spread of K–O bond distances ranging from 2.82–2.99 Å. There are a spread of K–Cl bond distances ranging from 3.43–3.57 Å. There are three inequivalent B3+ sites. In the first B3+ site, B3+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.81 Å. In the second B3+ site, B3+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.80 Å. In the third B3+ site, B3+ is bonded in a single-bond geometry to one Cl1- atom. The B–Cl bond length is 1.80 Å. There are four inequivalent S+0.75+ sites. In the first S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. In the second S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. In the third S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. In the fourth S+0.75+ site, S+0.75+ is bonded in a bent 120 degrees geometry to two O2- atoms. Both S–O bond lengths are 1.45 Å. There are eight inequivalent O2- sites. In the first O2- site, O2- is bonded in a single-bond geometry to one S+0.75+ atom. In the second O2- site, O2- is bonded in a 2-coordinate geometry to one K1+ and one S+0.75+ atom. In the third O2- site, O2- is bonded in a distorted single-bond geometry to one K1+ and one S+0.75+ atom. In the fourth O2- site, O2- is bonded in a distorted bent 150 degrees geometry to one K1+ and one S+0.75+ atom. In the fifth O2- site, O2- is bonded in a distorted single-bond geometry to one K1+ and one S+0.75+ atom. In the sixth O2- site, O2- is bonded in a distorted single-bond geometry to one K1+ and one S+0.75+ atom. In the seventh O2- site, O2- is bonded in a distorted single-bond geometry to one K1+ and one S+0.75+ atom. In the eighth O2- site, O2- is bonded in a single-bond geometry to one S+0.75+ atom. There are three inequivalent Cl1- sites. In the first Cl1- site, Cl1- is bonded in a single-bond geometry to one K1+ and one B3+ atom. In the second Cl1- site, Cl1- is bonded in a single-bond geometry to one K1+ and one B3+ atom. In the third Cl1- site, Cl1- is bonded in a single-bond geometry to one K1+ and one B3+ atom.

36 MATERIALS SCIENCE↗
DOE OSTI2022

Variations to the z-Expansion of the Form Factor Describing the Decay of B Mesons

We examine the decay rate of the particle decay B 0 → D -ℓ +νℓ using data collected from the Belle Collaboration. We studied three parameterizations of the form factor which describe the differential decay rate, the Caprini, Lellouch, and Neubert (CLN) parametrization, the Boyd, Grinstein, and Lebed (BGL) parametrization, and the Bourrely, Caprini, and Lellouch (BCL) parameterization. The form factor is a function of the hadronic recoil variable w, and each parameterization contains unique free parameters which are the focus of this work. We test the extrapolations of the form factor by fitting many different subsets of the low w data and then compare the prediction of the fit to the high w data using a χ 2 -metric. By only fitting the low w data we are able to examine the stability of extrapolations which will be informative for lattice simulations.

Simons, Daniel↗
NASA NTRS1973

Development of high temperature strain gages

High temperature electric resistance wire strain gages were developed and evaluated for use at temperatures exceeding 922 K (1200 F). A special high temperature strain gage alloy (Fe-25Cr-7.5A1), designated BCL-3, was used to fabricate the gages. Pertinent gage characteristics were determined at temperatures up to 1255 K (1800 F). The results of the evaluation were reported in graphical and tabular form. It was concluded that the gages will perform satisfactorily at temperatures to at least 1089 K (1500 F) for at least one hour.

Lemcoe, M. M.↗
NASA NTRS1979

Process Feasibility Study in Support of Silicon Material, Task 1

During this reporting period, major activies were devoted to process system properties, chemical engineering and economic analyses. Analyses of process system properties was continued for materials involved in the alternate processes under consideration for solar cell grade silicon. The following property data are reported for silicon tetrafluoride: critical constants, vapor pressure, heat of varporization, heat capacity, density, surface tension, viscosity, thermal conductivity, heat of formation and Gibb's free energy of formation. Chemical engineering analysis of the BCL process was continued with primary efforts being devoted to the preliminary process design. Status and progress are reported for base case conditions; process flow diagram; reaction chemistry; material and energy balances; and major process equipment design.

Li, K. Y.↗
NASA NTRS1992

Strain sensing technology for high temperature applications

This review paper discusses the status of strain sensing technology for high temperature applications. Technologies covered are those supported by NASA such as required for applications in hypersonic vehicles and engines, advanced subsonic engines, as well as material and structure development. The applications may be at temperatures of 540 C (1000 F) to temperatures in excess of 1400 C (2500 F). The most promising technologies at present are the resistance strain gage and remote sensing schemes. Resistance strain gages discussed include the BCL gage, the LaRC compensated gage, and the PdCr gage. Remote sensing schemes such as laser based speckle strain measurement, phase-shifting interferometry and X-ray extensometry will be discussed. Present status and limitations of these technologies are presented.

Williams, W. D.↗
NASA NTRS1993

Strain sensing technology for high temperature applications

This review discusses the status of strain sensing technology for high temperature applications. Technologies covered are those supported by NASA such as required for applications in hypersonic vehicles and engines, advanced subsonic engines, as well as material and structure development. The applications may be at temperatures of 540 C (1000 F) to temperatures in excess of 1400 C (2500 F). The most promising technologies at present are the resistance strain gage and remote sensing schemes. Resistance strain gages discussed include the BCL gage, the LaRC compensated gage, and the PdCr gage. Remote sensing schemes such as laser based speckle strain measurement, phase-shifling interferometry, and x-ray extensometry are discussed. Present status and limitations of these technologies are presented.

Williams, W. Dan↗