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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 1,081 records · Page 60
All sourcesNASA NTRSDOE OSTI
DOE OSTI2021

Establishing a unified framework for ion solvation and transport in liquid and solid electrolytes

Electrolytes used in rechargeable batteries must enable rapid translation of the working ion between macroscopically separated electrodes. These electrolytes are, however, usually designed and synthesized using atomic-level insights. Whether the ideal electrolyte for a particular battery is a solid or a liquid remains an important unresolved question, especially as solids with conductivities comparable with liquids are discovered. Here, to help resolve such questions, we present the first steps toward a unified framework for relating atomic and continuum scale phenomena. Solvation shells in liquids are entities that translate with the working ion for a short while before they break up due to Brownian motion. By contrast, solvation cages in classical solids and polymers cannot not translate with the working ion. Mobility of the entities that make up the cages and shells, which is quantified by an order parameter, is shown to influence translation of the working ion on continuum length scales.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2024

Innovative biphasic solvent systems for lignocellulosic biorefinery

Bioconversion of lignocellulosics to ethanol is significantly hindered by biomass recalcitrance and, therefore, often requires a biomass pretreatment step. Furan-based compounds such as furfural (FF) and 5-hydroxymethylfurfural (HMF) are versatile building blocks for fuels and chemicals. However, their production during pretreatment often suffers from low yield and low separation efficiency. Biphasic solvent systems are capable of reducing biomass recalcitrance and extracting furans into the organic phase, thus preventing their degradation, increasing their yield, and allowing much easier separation. The development of a sustainable biphasic solvent system is essential to the furan-driven biorefinery and has drawn significant attention. Finally, this review systematically summarizes recent advances in the development of biphasic solvent systems in lignocellulosic biorefinery for improving the production of liquid fuels and furan-based compounds.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2023

Mn(III)-mediated bisphenol a degradation: Mechanisms and products

Bisphenol A (BPA) is a high production volume chemical with potential estrogenic effects susceptible to abiotic degradation by MnO 2 . BPA transformation products and reaction mechanisms with MnO 2 have been investigated, but detailed process understanding of Mn(III)-mediated degradation has not been attained. Rapid consumption of BPA occurred in batch reaction vessels with 1 mM Mn(III) and 63.9 ± 0.7% of 1.76 ± 0.02 μmol BPA was degraded in 1 hour at circumneutral pH. BPA was consumed at 1.86 ± 0.09-fold higher rates in vessels with synthetic MnO 2 comprising approximately 13 mol% surface-associated Mn(III) versus surface-Mn(III)-free MnO 2 , and 10–35% of BPA transformation could be attributed to Mn(III) during the initial 10-min reaction phase. High-resolution tandem mass spectrometry (HRMS/MS) analysis detected eight transformation intermediates in reactions with Mn(III), and quantum calculations proposed 14 BPA degradation products, nine of which had not been observed during MnO 2 -mediated BPA degradation, suggesting mechanistic differences between Mn(III)- versus MnO 2 -mediated BPA degradation. Finally, the findings demonstrate that both Mn(III) and Mn(IV) can effectively degrade BPA and indicate that surface-associated Mn(III) increases the reactivity of synthetic MnO 2 , offering opportunities for engineering more reactive oxidized Mn species for BPA removal.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2020

Fiber-Shaped Fluidic Nanogenerator with High Power Density for Self-Powered Integrated Electronics

Flow-based hydrovoltaic nanogenerators have attracted particular attention as efficient and facile miniature energy-harvesting devices. However, they deliver relatively low output power density and limited power conversion efficiency owing to inefficient charge separation and poor charge accumulation. Here, we report the fabrication of high-performance, fiber-shaped fluidic nanogenerators (FFNGs) that use MoS 2 -encapsulated C fibers. The FFNGs deliver stable output voltages of 540 mV and an ultrahigh power density of 10.8 W m -2 . With experiments and density functional theory calculations, improvements in output performance can be attributed to smaller energy requirements for Na + cation adsorption, increased charge separation, and diffusion layer formations on the near surface. Moreover, self-powered, integrated devices achieve a maximum total power conversion-storage efficiency of ~11% and stable output voltage up to 3.1 V, which is applicable for use in consumer electronics devices.

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

High safety and cycling stability of ultrahigh energy lithium ion batteries

High-nickel layered oxide Li-ion batteries (LIBs) dominate the electric vehicle market, but their potentially poor safety and thermal stability remain a public concern. Here, we show that an ultrahigh-energy LIB (292 Wh kg –1 ) becomes intrinsically safer when a small amount of triallyl phosphate (TAP) is added to standard electrolytes. TAP passivates the electrode-electrolyte interfaces and limits the maximum cell temperature during nail penetration to 55°C versus complete cell destruction (>950°C) without TAP. The downside of this reliable safety solution is higher interfacial impedance and hence lower battery power; however, thermal modulation for battery operation around 60°C can restore power completely. When cycled at 60°C, the cell stabilized with TAP achieved 2,413 cycles at 76% capacity retention. Such an unconventional combination of interface-passivating electrolyte additive with cell thermal modulation renders the most energy-dense LIBs even safer than LiFePO 4 chemistry, while enjoying high power and cycling stability concurrently.

25 ENERGY STORAGE↗
DOE OSTI2021

Mitoferrin 2 deficiency prevents mitochondrial iron overload-induced endothelial injury and alleviates atherosclerosis

Endothelial dysfunction is an early step in the development of atherosclerotic cardiovascular disease. Iron overload can lead to excessive mitochondrial reactive oxygen species (mtROS) production, resulting in mitochondrial dysfunction and vascular endothelial cell (EC) damage. Mitoferrin 2 (Mfrn2) is an iron transporter in the inner mitochondrial membrane. This study aimed to assess whether Mfrn2 and mitochondrial iron overload were involved in atherosclerosis progression and to explore the potential mechanism. We observed significant upregulation of Mfrn2 in the arteries of high-fat diet (HFD)-fed Apolipoprotein E{sup −/-} (ApoE{sup −/-}) mice and in TNF-α-induced mouse aortic endothelial cells (MAECs). Mfrn2 gene silencing inhibited mitochondrial iron overload, stabilized mitochondrial membrane potential and improved mitochondrial function in TNF-α-induced MAECs. Vascular EC-specific knockdown of Mfrn2 in ApoE{sup −/-} mice markedly decreased atherosclerotic lesion formation and the levels of ICAM-1 in aortas and reduced monocyte infiltration into the vascular wall. Furthermore, TNF-α increased the binding of 14-3-3 epsilon (ε) and Mfrn2, preventing Mfrn2 degradation and leading to mitochondrial iron overload in ECs, while 14-3-3ε overexpression increased Mfrn2 stability by inhibiting its ubiquitination. Together, our results reveal that Mfrn2 deficiency attenuates endothelial dysfunction by decreasing iron levels within the mitochondria and mitochondrial dysfunction. These findings may provide new insights into preventive and therapeutic strategies against vascular endothelial dysfunction in atherosclerotic disease.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Histone transcription regulator Slm9 is required for cytoophidium biogenesis

The cytoophidium, a subcellular structure composed of CTP synthase, can be observed during the division of Schizosaccharomyces pombe. Cytoophidium formation changes periodically with the cell cycle of yeast cells. Here, we find that histone chaperone Slm9 is required for the integrity of cytoophidia in fission yeast. When the slm9 gene is knocked out, we observe that morphological characteristics, the abundance of cytoophidia and the division of the yeast cells are significantly affected. Fragmented cytoophidia occur in slm9 mutant cells, a phenomenon rarely observed in wild-type cells. Our study reveals a potential link between a chromosomal regulatory factor and cytoophidium biogenesis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

YAP/STAT3 promotes the immune escape of larynx carcinoma by activating VEGFR1-TGFβ signaling to facilitate PD-L1 expression in M2-like TAMs

Larynx carcinoma (LC) is the most prevalent head and neck cancer among adults. LC xenograft mouse model was generated to verify the effect of VEGF on macrophage polarization and tumor growth in vivo. EdU assay was performed to measure the cell proliferation. Transwell assay was applied to assess cell migration. The expression of YAP and STAT3 was also significantly increased in LC tumor tissues. Moreover, both YAP and STAT3 overexpression in LC cells promoted the proliferation, migration, as well as the secretion of PD-L1 in M2-like TAMs. Mechanistically, the interaction between YAP and STAT3 facilitated the transcription of VEGF. Moreover, with a co-culture system, VEGF secretion in LC cells enhanced PD-L1 expression in M2-like TAMs via activating VEGFR1-TGFβ signaling pathway. Furthermore, VEGF secreted from LC cells also promoted the tumor growth of LC in vivo. We revealed that dysregulated YAP/STAT3 activity in LC cells could enhance the secretion of VEGF, which then functioned on M2-like TAMs via activating VEGFR1-TGFββ pathway to promote the expression of PD-L1 and immunosuppressive function of M2-like TAMs. Therefore, VEGF and PD-L1 might have a pivotal crosstalk between M2-like TAMs and LC cells, which provided a novel therapeutic target in regulating the metastasis of LC in future.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

HA15 alleviates bone loss in ovariectomy-induced osteoporosis by targeting HSPA5

The imbalance between osteogenesis and adipogenesis in the bone marrow is the main characteristic of osteoporosis (OP). Thus, exploring regulation of the differentiation of bone marrow stromal cells (BMSCs) into osteoblasts and adipocytes is important to identify novel targets for the treatment of OP. In the present study, the master regulator of endoplasmic reticulum (ER) stress, heat shock protein family A (Hsp70) member 5 (HSPA5) was shown to significantly accumulate in osteoblasts and adipocytes, but not in osteoclasts in bone sections from aged and postmenopausal OP mice. In vitro study revealed that HSPA5 negatively modulated osteogenic differentiation and positively promoted adipogenic differentiation, and that targeting HSPA5 with its inhibitor HA15 enhanced osteogenic differentiation and inhibited adipogenic differentiation. Also, HA15 treatment induces ER stress and autophagy, and decreases apoptosis in cells. We constructed a postmenopausal OP model in mice with ovariectomy surgery, and treated the mice with HA15. The results showed that HA15 treatment induced appropriate ER stress, activated autophagy and decreased apoptosis in osteoblasts, thereby alleviating bone loss in vivo. Our results indicated that HSPA5 participated in OP pathogenesis by regulating the differentiation of BMSCs. HSPA5 may serve as a new target for the treatment of OP, and targeting HSPA5 with HA15 prevents the progression of OP and provides a candidate therapeutic molecule for postmenopausal OP.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

USP18 promotes tumor metastasis in esophageal squamous cell carcinomas via deubiquitinating ZEB1

Highlights: • High USP18 expression is positively correlated with the malignant phenotype and poor survival in ESCC patients. • Knockdown of USP18 suppressed the metastasis ability of ESCC cells in vitro and in vivo. • USP18 contributes to ESCC cell metastasis by inducing ZEB1 mediated EMT process. • USP18 acts as a deubiquitinase, and stabilises ZEB1 by reducing its poly-ubiquitination. The dysregulation of deubiquitinating enzymes (DUBs), which regulate the stability of most cellular proteins, have been implicated in many human diseases, including cancers. Ubiquitin-specific protease 18 (USP18), a member of the DUBs family, functions as a potential tumour promoter in various cancers. However, the biological function and clinical significance of USP18 in esophageal squamous cell carcinomas (ESCC) are still unclear. Here, we found that ESCC tumors had higher USP18 expression compared with that of normal esophageal epithelial tissues, and high USP18 level was significantly correlated with malignant phenotype and shorter survival in patients with ESCC. In functional experiments, USP18 knockdown significantly inhibited ESCC invasion and metastasis in vitro. Consistently, a xenograft assay showed that knockdown of USP18 in ESCC cell suppressed their dissemination to lung tissue in vivo. Furthermore, we showed that USP18 promoted ESCC cell metastasis by inducing ZEB1 mediated epithelial-mesenchymal transition (EMT). Importantly, our results demonstrated that the oncogenic effect of USP18 in ESCC is partially dependent on ZEB1 enhancement. Mechanistic investigations revealed that USP18 directly bound ZEB1 and decreased its ubiquitination to enhance the protein stability of ZEB1 in ESCC cells. Overall, our data highlighted an essential role of USP18 in ESCC metastasis, suggesting that it could be a potential diagnostic and therapeutic target for ESCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

MicroRNA-22 inhibition promotes the development of atherosclerosis via targeting interferon regulator factor 5

Atherosclerosis is generally accepted as a chronic inflammatory disease and is the most important pathological process underlying the cardiovascular diseases. MiR-22 exerts an important role in tumorgenesis, obesity and NAFLD development, as well as cardiovascular diseases. However, a certain role of miR-22 in the pathogenesis of atherosclerosis remains undetermined. Here, we showed that miR-22 exhibited a negative association with the deteriorated atherosclerotic plaque and showed significant downregulated expression in macrophages. Next, treatment of ApoE deficiency (ApoE{sup −/-}) mice with miR-22 inhibitors which were then subjected to high fat diet (HFD) for 12 weeks were performed to investigate the function of miR-22 on atherogenesis. The results exhibited that miR-22 inhibition dramatically promoted atherosclerotic plaques but attenuated plaque stabilization which were accompanied by decreased smooth muscle cell and collagen content, but increased macrophage infiltration and lipid accumulation. More importantly, the in vivo and in vitro experiments suggested that miR-22 inhibition accelerated inflammatory response and foam cell formation. Mechanistically, we demonstrated interferon regulator factor 5 (IRF5) was an important target of miR-22 and it was required for the regulation of inflammation mediated by miR-22 inhibition. Collectively, these evidences revealed that miR-22 inhibition promoted the atherosclerosis progression through activation of IRF5.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Ad-apoptin inhibits glycolysis, migration and invasion in lung cancer cells targeting AMPK/mTOR signaling pathway

Ad-apoptin is a recombinant oncolytic adenovirus constructed by our laboratory that can express apoptin. It can selectively kill tumor cells without damaging normal cells. This study investigated the effects of Ad-apoptin on glycolysis, migration and invasion of non-small cell lung cancer. Cell viability and apoptosis were detected by CCK-8 and flow cytometry, respectively. Glycolysis was investigated by glucose consumption, lactic acid production and glycolytic key enzyme protein levels. Migration and invasion were evaluated via wound healing, transwell assays and epithelial-mesenchymal transition (EMT) protein levels. The interaction between apoptin and AMPK was detected by Co-IP. A nude mice tumor model was established to investigate the anti-cancer role of Ad-apoptin in vivo. The results showed that Ad-apoptin inhibits cell viability and induces apoptosis of A549 and NCI–H23 cells. Ad-apoptin can reduce the glucose uptake and lactic production in lung cancer cells, and reduce the expression of related glycolysis-limiting enzymes. At the same time, Ad-apoptin inhibited the migration and invasion of lung cancer. Immunoprecipitation showed that apoptin and AMPK could interact directly. Moreover, knockdown of AMPK significantly attenuated the inhibitory effect of Ad-apoptin on glycolysis, migration and invasion of A549 and NCI–H23 cells. Ad-apoptin can inhibit the growth of tumors in nude mice. Compared with the control group, Ad-apoptin had a significant inhibitory effect on AMPK knockdown tumors. The immunohistochemical results of tumor tissues were consistent with those in vitro. Collectively, Ad-apoptin targets AMPK and inhibits glycolysis, migration and invasion of lung cancer cells through the AMPK/mTOR signaling pathway. This suggests that Ad-apoptin may have therapeutic potential for lung cancer by targeting AMPK activation.

60 APPLIED LIFE SCIENCES↗