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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 289 records · Page 16
All sourcesNASA NTRSDOE OSTI
DOE OSTI2014

Carcinoembryonic antigen promotes colorectal cancer progression by targeting adherens junction complexes

Oncomarkers play important roles in the detection and management of human malignancies. Carcinoembryonic antigen (CEA, CEACAM5) and epithelial cadherin (E-cadherin) are considered as independent tumor markers in monitoring metastatic colorectal cancer. They are both expressed by cancer cells and can be detected in the blood serum. We investigated the effect of CEA production by MIP101 colorectal carcinoma cell lines on E-cadherin adherens junction (AJ) protein complexes. No direct interaction between E-cadherin and CEA was detected; however, the functional relationships between E-cadherin and its AJ partners: α-, β- and p120 catenins were impaired. We discovered a novel interaction between CEA and beta-catenin protein in the CEA producing cells. It is shown in the current study that CEA overexpression alters the splicing of p120 catenin and triggers the release of soluble E-cadherin. The influence of CEA production by colorectal cancer cells on the function of E-cadherin junction complexes may explain the link between the elevated levels of CEA and the increase in soluble E-cadherin during the progression of colorectal cancer. - Highlights: • Elevated level of CEA increases the release of soluble E-cadherin during the progression of colorectal cancer. • CEA over-expression alters the binding preferences between E-cadherin and its partners: α-, β- and p120 catenins in adherens junction complexes. • CEA produced by colorectal cancer cells interacts with beta-catenin protein. • CEA over-expression triggers the increase in nuclear beta-catenin. • CEA over-expression alters the splicing of p120 catenin protein.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Expansion of CD26 positive fibroblast population promotes keloid progression

Background: Keloid is a skin fibrosis disease that characterised by invasive growth of fibroblasts and aberrant deposition of extracellular matrix. Studies indicated that keloid fibroblasts (KFs) is a class of ‘activated’ fibroblasts, which show accelerated proliferation and excessive extracellular matrix formation as compared with normal fibroblasts (NFs). However, the mechanism underlying keloid fibroblasts dysfunction is still unknown. Objective: To verify CD26 expression difference between KFs and NFs, and investigate the function of CD26 positive fibroblasts in keloid progression. Methods: KFs and NFs were isolated from Keloid tissues and normal skin tissues respectively. Flow cytometry was performed to isolate CD26+/CD26- fibroblasts from KFs and NFs. Proliferation of different fibroblasts were analyzed by CCK8 assay and Ki 67 straining. Profibrotic phenotype difference was detected by qRT-PCR, western blot, ELISA and immunofluorescence. Scratching experiment and transwell assay were used to assess invasion ability of CD26+/CD26- fibroblasts. Diprotin A was used as a CD26 inhibitor to further investigated the function of CD26 fibroblasts in keloid disease. Result: CD26 expression was increased in KFs, and the proportion of CD26+ fibroblasts was significantly increased in KFs. Cell viability analysis showed that CD26+ fibroblasts was more active in proliferation. Furthermore, the expression of profibrotic genes were increased in CD26+ fibroblasts, including TGF-β1, IGF-1, IL6, collagen 1, collagen 3 and fibronectin. And meanwhile, CD26+ fibroblasts showed stronger invasion ability as compared to CD26- fibroblasts. Moreover, Diprotin A significantly suppressed proliferation and extracellular matrix secretion of CD26+ fibroblasts isolated from keloid tissues. Conclusion: Our findings suggest that CD26+ fibroblasts possess proliferation advantage in compare to CD26- fibroblasts, and the advantage caused expansion of CD26 positive fibroblast population promotes keloid progression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Gastric cancer tissue-derived mesenchymal stem cells impact peripheral blood mononuclear cells via disruption of Treg/Th17 balance to promote gastric cancer progression

Highlights: • GC-MSCs educate PBMCs to promote gastric cancer progression. • GC-MSCs disrupt the Treg/Th17 balance in PBMCs. • GC-MSCs induce Treg cell differentiation and suppress Th17 cell proliferation. Gastric cancer tissue-derived mesenchymal stem cells (GC-MSCs) are important resident stromal cells in the tumor microenvironment (TME) and have been shown to play a key role in gastric cancer progression. Whether GC-MSCs exert a tumor-promoting function by affecting anti-tumor immunity is still unclear. In this study, we used GC-MSC conditioned medium (GC-MSC-CM) to pretreat peripheral blood mononuclear cells (PBMCs) from healthy donors. We found that GC-MSC-CM pretreatment markedly reversed the inhibitory effect of PBMCs on gastric cancer growth in vivo, but did not affect functions of PBMCs on gastric cancer cell proliferation, cell cycle and apoptosis in vitro. PBMCs pretreated with GC-MSC-CM significantly promoted gastric cancer migration and epithelial-mesenchymal transition in vitro and liver metastases in vivo. Flow cytometry analysis showed that GC-MSC-CM pretreatment increased the proportion of Treg cells and reduced that of Th17 cells in PBMCs. CFSE labeling and naïve CD4{sup +} T cells differentiation analysis revealed that GC-MSC-CM disrupted the Treg/Th17 balance in PBMCs by suppressing Th17 cell proliferation and inducing differentiation of Treg cells. Overall, our collective results indicate that GC-MSCs impair the anti-tumor immune response of PBMCs through disruption of Treg/Th17 balance, thus providing new evidence that gastric cancer tissue-derived MSCs contribute to the immunosuppressive TME.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Diacylglycerol lipase alpha promotes tumorigenesis in oral cancer by cell-cycle progression

Highlights: • DAGLA was up-regulated in human oral squamous cell carcinoma (OSCC) cells compared with human normal oral keratinocytes (HNOKs). • Overexpression of DAGLA in OSCCs controlled cell proliferation through cell-cycle progression. • The tumoral volume of the orlistat-treated group was clearly smaller than that of the control group in vivo. • DAGLA expression level might be a useful diagnostic indicator and a new therapeutic target for OSCCs. Diacylglycerol lipase alpha (DAGLA), which catalyzes the hydrolysis of diacylglycerol to 2-arachidonoylglycerol and free fatty acid, is required for axonal growth during the brain development and for retrograde synaptic signaling at mature synapses. So far, no information was found regarding the possible role of DAGLA in human tumorigenesis. Thus, the current study sought to clarify the contribution of DAGLA in oral squamous cell carcinomas (OSCCs) and assess the clinical possibilities for OSCC treatment. Using real-time quantitative reverse transcription-polymerase chain reaction, immunoblotting, and immunohistochemistry, we found a significant up-regulation of DAGLA in OSCCs compared with normal cells and tissues both at mRNA and protein expression levels. Knockdown models in OSCC-derived cell lines for DAGLA (siDAGLA) and treatment with a lipase inhibitor (orlistat) showed several depressed cellular functions, including cellular proliferation and migratory activities through cell-cycle arrest at G1 phase. Furthermore, we found that DAGLA-positive OSCC samples were correlated highly with the primary tumoral size. We concluded that DAGLA may be a key determinant in tumoral progression and might be a therapeutic target for OSCCs.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

TRIM24 promotes hepatocellular carcinoma progression via AMPK signaling

Highlights: • TRIM24 expression is up-regulated in HCC, increased along with the progression of HCC. • TRIM24 promotes cell proliferation and migration of HCC cell line. • TRIM24 promotes HCC progression through AMPK signaling. • TRIM24 negatively regulated AMPK expression in vitro and in vivo. • TRIM24 expression levels negatively correlated with AMPK in HCC clinical samples. Hepatocellular carcinoma (HCC) is one of the most common cancers diagnosed worldwide. However, the mechanism underlying HCC pathogenesis remains unknown. In the present study, TRIM24 was found increased in human HCC clinical samples and positively correlated with HCC tumor grade. Furthermore, TRIM24 knockdown inhibits proliferation and migration in a human HCC cell line in vitro while also inhibiting tumor growth in vivo. Mechanistically, TRIM24 appears to promote liver tumor development via AMPK signaling as AMPK knockdown alleviated the in vitro and in vivo effects of TRIM24 knockdown in a human HCC cell line. Taken together, these data enhance our understanding of HCC development in addition to highlighting TRIM24-regulated AMPK signaling as a potential therapeutic target for HCC treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms

Highlights: • Tumor suppressor p21protein is reactivated via withaferin A (WA) and sulforaphane (SFN). • Combinatorial nutritive compounds have the ability to impede cell cycle progression. • Mutant p53 is down-regulated via the studied compounds where wild type p53 is not. • Epigenetic mechanisms are regulated by WA and SFN. • The H3K4Me3 marker is increased at the p21 promoter after WA and SFN treatment. Little is known about the effects of combinatorial dietary compounds on the regulation of epigenetic mechanisms involved in breast cancer prevention. The human diet consists of a multitude of components, and there is a need to elucidate how certain compounds interact in collaboration. Withaferin A (WA), found in the Indian winter cherry and documented as a DNA methyltransferase (DNMT) inhibitor, and sulforaphane (SFN), a well-known histone deacetylase (HDAC) inhibitor found in cruciferous vegetables, are two epigenetic modifying compounds that have only recently been studied in conjunction. The use of DNMT and HDAC inhibitors to reverse the malignant expression of certain genes in breast cancer has shown considerable promise. Previously, we found that SFN + WA synergistically promote breast cancer cell death. Herein, we determined that these compounds inhibit cell cycle progression from S to G2 phase in MDA-MB-231 and MCF-7 breast cancer. Furthermore, we demonstrate that this unique combination of epigenetic modifying compounds down-regulates the levels of Cyclin D1 and CDK4, and pRB; conversely, the levels of E2F mRNA and tumor suppressor p21 are increased independently of p53. We find these events coincide with an increase in unrestricted histone methylation. We propose SFN + WA-induced breast cancer cell death is attributed, in part, to epigenetic modifications that result in the modulated expression of key genes responsible for the regulation of cancer cell senescence.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

TPC2 mediates autophagy progression and extracellular vesicle secretion in cancer cells

Autophagy is an evolutionarily conserved lysosomal degradation process, and is involved in various cellular processes. Here we studied the role of two pore channel 2 (TPC2), a lysosomal non-selective Na{sup +}/Ca{sup 2+} channel, in autophagy progression. We found that TPC overexpression in 4T1 mouse breast cancer cell line or in HeLa human cervical cancer cell line inhibited the fusion between autophagosome and lysosome, resulting in the accumulation of autophagosomes accompanied with increased lysosomal pH and TFEB nuclear localization. Interestingly, we also found that extracellular vesicle (EV) secretion was markedly decreased in TPC2 overexpressing cells but was induced in TPC2 knockdown cells. In addition, migration of TPC2 knockdown cells, not TPC2 overexpressing cells, was inhibited. Taken together, these results support a role of TPC2 in autophagy progression and EV trafficking in cancer cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Surgical trauma contributes to progression of colon cancer by downregulating CXCL4 and recruiting MDSCs

Highlights: • Laparotomy promotes tumor growth and angiogenesis in vivo. • Laparotomy results in a decrease of CXCL4 expression. • CXCL4 inhibits tumor growth and angiogenesis. • CXCL4 inhibits the recruitment of myeloid-derived suppressor cells. • The expression of CXCL4 and MDSC percentage are correlated with clinical overall survival rates. Surgical stress has been shown to facilitate the tumor growth and metastasis of colon cancer. To unravel the mechanisms underlying surgery induced-colon cancer progression, a syngeneic transplantation tumor model was established with murine colon cancer CT26 cells and the effect of laparotomy on tumor progression was investigated. Especially the expression of several CXC chemokines was assayed, and its roles in regulating myeloid-derived suppressor cells (MDSCs) recruitment were analyzed. We found that laparotomy promoted in vivo tumor growth and angiogenesis. CXCL4 expression was significantly downregulated by laparotomy in the tumor tissue and the peritoneal cavity. Functionally, CXCL4 overexpression significantly reduces tumor volume compared to control. Through analysis of CD11b{sup +}/Gr1{sup +} MDSCs cell, we found an upregulated proportion of MDSCs in the tumor tissues and peritoneal cavity following laparotomy, and this enhancement was blocked after CXCL4 overexpression. Further, a negative correlation was found between CXCL4 expression and MDSC amounts in clinical samples. Higher CXCL4 expression and lower MDSCs proportion is positively related to overall survival.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

AFF4 facilitates melanoma cell progression by regulating c-Jun activity

Melanoma is characterized by high mortality and poor prognosis due to metastasis. AFF4 (AF4/FMR2 family member 4), as a scaffold protein, is a component of the super elongation complex (SEC), and is involved in the progression of tumors, e.g., leukemia, head and neck squamous cell carcinoma (HNSCC). However, few studies on AFF4 have focused on melanoma. Here, AFF4 expression levels and clinicopathological features were evaluated in melanoma tissue samples. Then, we performed cell proliferation, migration and invasion assays in A375 and A2058 cells lines in vitro to evaluate the role of AFF4 in melanoma. The effects of AFF4 knockdown in vivo were characterized via a xenograft mouse model. Finally, the correlation between c-Jun and AFF4 protein levels in melanoma was analyzed by rescue assay and immunohistochemistry (IHC). We found that AFF4 expression was upregulated in melanoma tumor tissues and that AFF4 protein expression was also closely related to the prognosis of patients with cutaneous melanoma. Moreover, AFF4 could promote the invasion and migration of melanoma cells by mediating epithelial to mesenchymal transition (EMT). AFF4 might regulate c-Jun activity to promote the invasion and migration of melanoma cells. Importantly, c-Jun was regulated by the AFF4 promoted melanoma tumorigenesis in vivo. Taken together, AFF4 may be a novel oncogene that promotes melanoma progression through regulation of c-Jun activity.

60 APPLIED LIFE 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

Deubiquitinating enzyme USP46 suppresses the progression of hepatocellular carcinoma by stabilizing MST1

Highlights: • Low USP46 level is correlated with poor prognosis in HCC. • USP46 suppresses the proliferation and metastasis of HCC. • USP46 suppress the progression of HCC by inhibiting the expression of YAP1. • MST1 mediates the regulation of USP46 on YAP1. • USP46 stabilized MST1 protein through inhibiting its ubiquitination and degradation. The deubiquitinating enzyme USP46 (ubiquitin-specific protease 46) is implicated in various cancers. However, its role and regulatory mechanism in HCC (hepatocellular carcinoma) are still unknown. In this study, we showed that USP46 is downregulated in HCC tissues and that low USP46 levels are associated with poor prognosis in HCC patients. In functional experiments, overexpression of USP46 impaired proliferation and metastasis of HCC cells, whereas knockdown of USP46 enhanced cell proliferation and invasiveness in vitro and in vivo. Furthermore, we found that USP46 suppresses HCC cell proliferation and metastasis by inhibiting YAP1. Ectopic expression of YAP1 rescued the inhibition of cell proliferation and metastasis caused by USP46 overexpression. Mechanistically, USP46 promotes the degradation of YAP1 by increasing expression of MST1, and the increase in MST1 protein antagonizes YAP1 to suppress HCC progression. Finally, we demonstrated that USP46 stabilizes the MST1 protein by directly binding to it and decreasing its ubiquitination. Taken together, our results demonstrated that USP46 may be a novel tumor suppressor in HCC. Moreover, USP46 acts as a deubiquitinating enzyme of MST1 to potentiate MST1 kinase activity to suppress tumor growth and metastasis, indicating that USP46 activation may represent a potential treatment strategy for HCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Aberrant FBXW7-mediated ubiquitination and degradation of ZMYND8 enhances tumor progression and stemness in bladder cancer

ZMYND8, an epigenetic regulator, was identified as a common oncogene across various tumors. However, little was reported about the association between ZMYND8 and bladder cancer. Besides, aberrant mechanisms that contribute to abnormal ZMYND8 expressions still remain unclear. In the current study, we first found that ZMYND8 protein levels were significantly elevated in Bca samples versus normal tissues, but not the mRNA levels. We then utilized the Cell Counting Kit-8 (CCK-8) assay, clone formation assay and transwell analysis to confirm that ZMYND8 could remarkably promote the tumor progression in vitro, including growth capacity and migration. Bioinformatic predictive analysis revealed that E3 ubiquitin ligase FBXW7 interacts directly with ZMYND8 and degrades ZMYND8 in a polyubiquitination manner. Low FBXW7 was a hazard factor for promoting and depending on accumulated ZMYND8 proteins to promote Bca progression. Gene set enrichment analysis (GSEA) further indicated that ZMYND8 was notably associated with stemness process, which was well functionally validated. Lastly, ZMYND8 deficiency was observed to inhibit tumor growth of Bca in vivo, revealing a promising translational significance in Bca treatment. In conclusion, our study for the first time provided evidence for a novel mechanism of FBXW7/ZMYND8 axis in Bca, providing therapeutic vulnerability for individualized cancer treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2022

Pre-planetary nebulae: a context for principles, progress, and questions on how binaries and magnetic fields produce jets

Astrophysical outflows treated initially as spherically symmetric often show evidence for asymmetry once seen at higher resolution. The preponderance of aspherical and multipolar planetary nebulae (PN) and pre-planetary nebulae (PPN) was evident after many observations from the Hubble Space Telescope. Binary interactions have long been thought to be essential for shaping asymmetric PN/PPN, but how? PPN are the more kinematically demanding of the two, and warrant particular focus. I address how progress from observation and theory suggests two broad classes of accretion driven PPN jets: one for wider binaries (PPN-W) where the companion is outside the outer radius of the giant and accretes via Roche lobe overflow, and the other which occurs in the later stages of CE for close binaries (PPN-C). Furthermore, the physics within these scenarios connects to progress and open questions about the role and origin of magnetic fields in the engines and in astrophysical jets more generally.

(ISM:) planetary nebulae: general↗
DOE OSTI2025

Electrochemical Random-Access Memory: Progress, Perspectives, and Opportunities

Non-von Neumann computing using neuromorphic systems based on analogue synaptic and neuronal elements has emerged as a potential solution to tackle the growing need for more efficient data processing, but progress toward practical systems has been stymied due to a lack of materials and devices with the appropriate attributes. Recently, solid state electrochemical ion-insertion, also known as electrochemical random access memory (ECRAM) has emerged as a promising approach to realize the needed device characteristics. ECRAM is a three terminal device that operates by tuning electronic conductance in functional materials through solid-state electrochemical redox reactions. This mechanism can be considered as a gate-controlled bulk modulation of dopants and/or phases in the channel. Early work demonstrating that ECRAM can achieve nearly ideal analogue synaptic characteristics has sparked tremendous interest in this approach. More recently, the realization that electrochemical ion insertion can be used to tune the electronic properties of many types of materials including transition metal oxides, layered two-dimensional materials, organic and coordination polymers, and that the changes in conductance can span orders of magnitude has further attracted interest in ECRAM as the basis for analogue synaptic elements for inference accelerators as well as for dynamical devices that can emulate a wide range of neuronal characteristics for implementation in analogue spiking neural networks. At its core, ECRAM shares many fundamental aspects with rechargeable batteries, where ion insertion materials are used extensively for their ability to reversibly store charge and energy. Computing applications, however, present drastically different requirements: systems will require many millions of devices, scaled down to tens of nanometers, all while achieving reliable electronic-state tuning at scaled-up rates and endurances, and with minimal energy dissipation and noise. Further, in this review, we discuss the history, basic concepts, recent progress, as well as the challenges and opportunities for different types of ECRAM, broadly grouped by their primary mobile ionic charge carrier, including Li, protons, and oxygen vacancies.

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

Critical adjustment of land mitigation pathways for assessing countries' climate progress

Collective progress towards the Paris Agreement’s temperature targets will be assessed by the Agreement’s Global Stocktake process. Global emission pathways by Integrated Assessment Models (IAMs) are a likely benchmark against which aggregated countries’ greenhouse gas mitigation pledges will be assessed. However, this approach requires comparability, which is currently hampered by a 5 GtCO2yr-1 mismatch between the estimated global land anthropogenic flux of IAMs and countries’ GHG inventories (GHGIs) for 2005-2015. We show that this gap is mostly the result of differences in how the anthropogenic forest sink is defined. Countries define managed forest more broadly than IAMs, and on this larger area typically consider anthropogenic also fluxes due to human-induced environmental change, which IAMs do not include their pathways. Using five IAMs and a dynamic global vegetation model (DGVM), we present and apply a novel method that adjusts IAM results to the countries’ definition, closing the gap with GHGIs at global and regional scale. When expressed in a way compatible with GHGIs, adjusted 1.5°C and well-below 2°C pathways have a cumulative CO2 balance until carbon neutrality that is 110–176 GtCO2 lower than the original IAMs pathways. The use of these country-compatible emission pathways under the Global Stocktake would therefore be essential for an accurate assessment of the collective progress towards the Paris Agreement’s climate goals.

Grassi, Giacomo↗
DOE OSTI2021

Dynamic spatial progression of isolated lithium during battery operations

The increasing demand for next-generation energy storage systems necessitates the development of high-performance lithium batteries. Unfortunately, current Li anodes exhibit rapid capacity decay and a short cycle life, owing to the continuous generation of solid electrolyte interface and isolated Li (i-Li). The formation of i-Li during the nonuniform dissolution of Li dendrites leads to a substantial capacity loss in lithium batteries under most testing conditions. Because i-Li loses electrical connection with the current collector, it has been considered electrochemically inactive or ‘dead’ in batteries. In this work, contradicting this commonly accepted presumption, we show that i-Li is highly responsive to battery operations, owing to its dynamic polarization to the electric field in the electrolyte. Simultaneous Li deposition and dissolution occurs on two ends of the i-Li, leading to its spatial progression toward the cathode (anode) during charge (discharge). Revealed by our simulation results, the progression rate of i-Li is mainly affected by its length, orientation and the applied current density. Moreover, we successfully demonstrate the recovery of i-Li in Cu–Li cells with >100% Coulombic efficiency and realize LiNi 0.5 Mn 0.3 Co 0.2 O 2 (NMC)–Li full cells with extended cycle life.

25 ENERGY STORAGE↗
DOE OSTI2018

Progress on ternary oxide-based photoanodes for use in photoelectrochemical cells for solar water splitting

Solar water splitting using photoelectrochemical cells (PECs) has emerged as one of the most promising routes to produce hydrogen as a clean and renewable fuel source. Among various semiconductors that have been considered as photoelectrodes for use in PECs, oxide-based photoanodes are particularly attractive because of their stability in aqueous media in addition to inexpensive and facile processing compared to other types of semiconductors. However, they typically suffer from poor charge carrier separation and transport. In the past few years, there has been tremendous progress in developing ternary oxide-based photoelectrodes, specifically, photoanodes. The use of ternary oxides provides more opportunities to tune the composition and electronic structure of the photoelectrode compared to binary oxides, thus providing more freedom to tune the photoelectrochemical properties. In this article, we outline the important characteristics to analyze when evaluating photoanodes and review the major recent progress made on the development of ternary oxide-based photoanodes. For each system, we highlight the favorable and unfavorable features and summarize the strategies utilized to address the challenges associated with each material. Finally, by combining our analyses of all the photoanodes surveyed in this review, we provide possible future research directions for each compound and an outlook for constructing more efficient oxide-based PECs. Overall, this review will provide a critical overview of current ternary oxide-based photoanodes and will serve as a platform for the design of future oxide-based PECs.

25 ENERGY STORAGE↗
DOE OSTI2026

Full-wave modeling of RF waves in fusion plasmas with finite element method: Progress in past decades and its future role

This paper reviews the progress in computing radio frequency (RF) wave fields in fusion plasmas, specifically focusing on simulations utilizing the finite element method (FEM) over the past few decades. Computing RF wave fields in fusion plasmas presents unique challenges due to large simulation domains, complex antenna structures, non-local dielectric properties, and wide ranges of spatial scales. It highlights key developments and outlines future directions, primarily addressing waves in the ion cyclotron (IC) to lower hybrid (LH) frequency range. We begin with briefly revisiting earlier developments before the widespread availability of modern computer-aided engineering (CAE) software based on FEM. This historical perspective illuminates early progress and the physics difficulties that motivated ongoing work within the community. Modern wave simulations for RF antennas based on FEM are characterized by the use of detailed 3D antenna model geometry generated from engineering CAD software and localized wave dielectric model. Significant advancements have also been made in improving physics models to include phenomena such as RF sheath rectification and wave scattering. FEM-based RF simulations have also been applied to compute wave propagation in the core region, where the inclusion of non-local dielectric response is crucial. This is a challenging goal, and several promising approaches have been proposed in this area. Additionally, RF simulation development initiatives based on open-source libraries have gained popularity, demonstrating scalability and flexibility in extending physics models. This paper will discuss the advantages and disadvantages of using such a publicly available FEM library.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗