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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 163 records · Page 9
All sourcesNASA NTRSDOE OSTI
DOE OSTI2024

2024 Sustainable Aviation Energy Conference: 5 Key Messages From the Airport Enabling Efforts Workshop

At the 2024 Sustainable Aviation Energy Conference, more than 100 aviation leaders gathered in Dallas, Texas, to discuss collaboration and research needed to clear the path to widespread adoption of sustainable aviation technologies. During open workshops, participants from state and federal agencies; airports; aircraft and engine manufacturers; liquid fuel producers; and other stakeholder groups brainstormed the biggest barriers and opportunities for realizing a sustainable aviation ecosystem. This fact sheets presents five key messages and discussion points that emerged during a workshop on airport enabling efforts.

advanced air mobility↗
DOE OSTI2025

RE+Microgrid Conference Presentation

Conference presentation about Idaho National Laboratory tools for damage prediction and resilience, along with an overview of microgrid capabilities.

Grid↗
DOE OSTI2020

The C‐Terminal Domain of α‐Synuclein Confers Steric Stabilization on Synaptic Vesicle‐Like Surfaces

Abstract While α‐synuclein, an intrinsically disordered protein linked to Parkinson's disease, has been shown to associate with membrane organelles, its overall cellular function remains nebulous. α‐Synuclein binds to membranes through its amino‐terminal domain (first ≈100 residues), but there is no consensus on the biophysical function of the carboxyl‐terminal domain (last ≈40 residues) due, in part, to its lack of strong interaction partners and persisting intrinsic disorder even when membrane bound. Here, by directly applying force on α‐synuclein bound to spherical nanoparticle‐supported lipid bilayers (SSLBs) and tracking higher‐order structural changes through small‐angle X‐ray scattering, strong evidence is presented that α‐synuclein sterically stabilizes membrane surfaces through its carboxyl‐terminal domain. Full‐length α‐synuclein dramatically increases the critical osmotic pressure at which SSLBs cluster ( P C ≈ 1.3 × 10 5 Pa) compared to α‐synuclein without the carboxyl‐terminal domain ( P C ≈ 1.9 × 10 4 Pa) at physiological salt and temperature conditions. This clustering of α‐synuclein‐bound SSLBs is shown to be reversible and sensitive to monovalent/divalent salt, both features of grafted polyelectrolyte‐mediated steric stabilization. In elucidating the biophysical function of α‐synuclein in the framework of polymer science, it is demonstrated that the carboxyl‐terminal domain can potentially utilize its persisting intrinsic disorder to functionalize membrane surfaces.

Chung, Peter J.↗
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↗
DOE OSTI2021

IRS4 promotes the progression of non-small cell lung cancer and confers resistance to EGFR-TKI through the activation of PI3K/Akt and Ras-MAPK pathways

IRS4 is a member of the insulin receptor substrate (IRS) protein family. It acts as a cytoplasmic adaptor protein, integrating and transmitting signals from receptor protein tyrosine kinases to the intracellular environment. IRS4 can induce mammary tumorigenesis and is usually overexpressed in non-small cell lung cancer (NSCLC). However, little is known about the role of IRS4 in the development and progression of lung cancer. In this study, we show that IRS4 knockout suppresses the proliferation, colony formation, migration, and invasion of A549 lung cancer cells, as well as tumor growth in a nude mouse xenograft model. In contrast, stable expression of IRS4 showed the opposite effects. As expected, IRS4 was found to activate the PI3K/Akt and Ras-MAPK pathways, and we also showed that IRS4 depletion significantly enhanced the sensitivity of EGFR tyrosine kinase inhibitor (EGFR-TKI)-resistant cells to gefitinib. Taken together, these results show that IRS4 promotes NSCLC progression and may represent a potential therapeutic target for EGFR-TKI-resistant NSCLC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Sorafenib derivatives-functionalized gold nanoparticles confer protection against tumor angiogenesis and proliferation via suppression of EGFR and VEGFR-2

Sorafenib is a multi-kinase inhibitor that has been highlighted as a tumor suppressor due to its anti-proliferative and anti-angiogenic properties, whereas the clinical application of Sorafenib is restricted by the side effects it may cause. The past decade has witnessed the development of a series of sorafenib derivatives to improve the clinical performance of sorafenib. Gold nanoparticles (AuNPs) have been widely utilized in drug delivery systems due to their unique properties, including biocompatible nature, simple preparation, and easy surface modification. Herein, this study is aimed to investigate the anti-tumor effects of new sorafenib derivatives-capped gold nanoparticles (AuNPs-New Sor) in tumor formation and metastasis as well as the underlying mechanisms. Initially, new sorafenib derivatives were constructed and combined with AuNPs to form AuNPs-New Sor, and the properties of synthesized AuNPs-New Sor were identified in a mouse model of tumorigenesis. The effect of AuNPs-New Sor on tumor vascular normalization was investigated by assessing vascular permeability and perfusion rate. Next, we evaluated the effect of AuNPs-New Sor on migration and viability of tumor cells and human umbilical vein endothelial cells (HUVECs) as well as on HUVEC angiogenesis in vitro. A melanoma mouse model was further established for in vivo substantiation of the anti-tumor effect of AuNPs-New Sor. According to the results, AuNPs could deliver new sorafenib derivatives into tumor tissues and downregulate the expression of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor-2 (VEGFR-2), thereby suppressing tumor migration, EMT, and angiogenesis in vitro. In addition, AuNPs-New Sor displayed competitive anti-tumor activities in vivo. Taken together, AuNPs-New Sor may attenuate tumor development and angiogenesis through downregulation of EGFR and VEGFR-2.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2020

Two-State Reactivity in Iron-Catalyzed Alkene Isomerization Confers σ-Base Resistance

A low-coordinate, high spin (S = 3/2) organometallic iron(I) complex is a catalyst for the isomerization of alkenes. A combination of experimental and computational mechanistic studies supports a mechanism in which alkene isomerization occurs by the allyl mechanism. Importantly, while substrate binding occurs on the S = 3/2 surface, oxidative addition to an η 1 -allyl intermediate only occurs on the S = 1/2 surface. In conclusion, since this spin state change is only possible when the alkene substrate is bound, the catalyst has high immunity to typical σ-base poisons due to the antibonding interactions of the high spin state.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2025

A miniature CRISPR–Cas10 enzyme confers immunity by inhibitory signalling

Microbial and viral co-evolution has created immunity mechanisms involving oligonucleotide signalling that share mechanistic features with human antiviral systems1. In these pathways, including cyclic oligonucleotide-based antiphage signalling systems (CBASSs) and type III CRISPR systems in bacteria and cyclic GMP–AMP synthase–stimulator of interferon genes (cGAS–STING) in humans, oligonucleotide synthesis occurs upon detection of virus or foreign genetic material in the cell, triggering the antiviral response2, 3–4. Here, in an unexpected inversion of this process, we show that the CRISPR-related enzyme mCpol synthesizes cyclic oligonucleotides constitutively as part of an active mechanism that represses a toxic effector. Cell-based experiments demonstrated that the absence or loss of mCpol-produced cyclic oligonucleotides triggers cell death, preventing the spread of viruses that attempt immune evasion by depleting host cyclic nucleotides. Structural and mechanistic investigation revealed mCpol to be a di-adenylate cyclase whose product, c-di-AMP, prevents toxic oligomerization of the effector protein 2TMβ. Analysis of cells by fluorescence microscopy showed that lack of mCpol allows 2TMβ-mediated cell death due to inner membrane collapse. These findings unveil a powerful defence strategy against virus-mediated immune suppression, expanding our understanding of the role of oligonucleotides in immunity.

Doherty, Erin E↗
DOE OSTI2022

Knockout of ABC transporter gene ABCA2 confers resistance to Bt toxin Cry2Ab in Helicoverpa zea

Evolution of pest resistance reduces the benefits of widely cultivated genetically engineered crops that produce insecticidal proteins derived from Bacillus thuringiensis (Bt). Better understanding of the genetic basis of pest resistance to Bt crops is needed to monitor, manage, and counter resistance. Previous work shows that in several lepidopterans, resistance to Bt toxin Cry2Ab is associated with mutations in the gene encoding the ATP-binding cassette protein ABCA2. The results here show that mutations introduced by CRISPR/Cas9 gene editing in the Helicoverpa zea (corn earworm or bollworm) gene encoding ABCA2 (HzABCA2) can cause resistance to Cry2Ab. Disruptive mutations in HzABCA2 facilitated the creation of two Cry2Ab-resistant strains. A multiple concentration bioassay with one of these strains revealed it had > 200-fold resistance to Cry2Ab relative to its parental susceptible strain. All Cry2Ab-resistant individuals tested had disruptive mutations in HzABCA2. We identified five disruptive mutations in HzABCA2 gDNA. The most common mutation was a 4-bp deletion in the expected Cas9 guide RNA target site. The results here indicate that HzABCA2 is a leading candidate for monitoring Cry2Ab resistance in field populations of H. zea.

60 APPLIED LIFE SCIENCES↗