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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

A mixed formulation of the plane-stress problem to facilitate reuse of constitutive models in finite-element programs

Here, the plane-stress assumption can be challenging to support in a finite element program because it traditionally requires separate implementations of constitutive models than those intended for three-dimensional or two-dimensional plane-strain simulations. As a solution to this issue, this paper presents a method to solve the plane-stress problem using a mixed formulation. In this formulation, the out-of-plane strain is treated as a field variable that is solved for in addition to the standard in-plane displacement variables, in a manner that weakly enforces the condition that the out-of-plane stress is zero. The proposed formulation is non-intrusive, requiring no modifications to the constitutive models in contrast to the conventional plane-stress formulation. The proposed mixed formulation has been benchmarked against analytical solutions and numerical solutions, with good performance and accuracy.

97 MATHEMATICS AND COMPUTING↗
DOE OSTI2022

Assessing high fidelity multi-component models to facilitate safeguards at Gas Centrifuge Enrichment Plants

We report that the International Atomic Energy Agency (IAEA) inspectors routinely carry out environmental sampling (ES) as a verification method. Collection of environmental swipe samples at various locations in Gas Centrifuge Enrichment Facilities (GCEPs) is an important process in detecting misuse of a declared facility and possibly the existence of undeclared nuclear material. These samples are measured for isotopic composition in uranium containing particles by Thermal Ionization Mass Spectrometry (TIMS) or Inductively Coupled Plasma Mass Spectrometry (ICP-MS). Even though ES is highly effective in detecting the absolute value of enrichments and their deviations from the declared values, it cannot explain the cause of those changes. Several potential explanations can serve as possibilities for particles detected above or other than the declared enrichment. These include normal and non-malicious events such as the design of the enrichment cascades, unintentional failures of the machines, or overshoot during startup of a cascade. It can also be the result of deliberate misuse by the facility operators. The primary objective of this work is to understand how these factors affect the enrichments produced by a cascade and quantify anticipated multi-isotopic concentrations for each case. The following methodology is employed to determine signatures at a particular facility. 1) Utilize a new two-dimensional multi-component diffusion code to obtain centrifuge performance data and use that information to design and perform cascade analysis. Compare and contrast the results with previous 1-D radially averaged solutions from the Pancake code. 2) Design a GCEP cascade with the production goal of 19.75% 235 U for each set of machine data above. Investigate two cascade scenarios that include enrichment of natural uranium (NU) feed to 19.75% 235U in a single cascade compared to a two-step process of NU to 5% and then 5% to 19.75%. 3) Simulate the intentional vs. unintentional off-normal scenarios in the cascades to assess the differences in isotopic concentrations. A non-ideal squared-off cascade model developed at the University of Virginia is used to calculate flow rates and isotopic concentrations of the process gas. The analysis is performed using the Rome machine model operated at 600 m/s rotor speed. The upper and lower bounds of normal and abnormal enrichments in a typical facility are used in conjunction with ES results to understand the root causes of such observations.

98 NUCLEAR DISARMAMENT, SAFEGUARDS, AND PHYSICAL P↗
DOE OSTI2020

Do Cell Wall Esters Facilitate Forest Response to Climate?

Terrestrial ecosystem dynamics are strongly modified by stresses associated with climate change, impacting plant growth and development, mortality, and ecological succession. Finally, we highlight the potential role of plant cell wall esters to link changes in cell wall structure and function with biosphere-atmosphere fluxes of methanol, acetic acid, carbon dioxide (CO 2 ), and water (H 2 O).

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2021

Pristane promotes anaerobic glycolysis to facilitate proinflammatory activation of macrophages and development of arthritis

Highlights: • Pristane-induced arthritis is dependent on macrophages with M1 phenotype. • Pristane causes mitochondrial dysfunction and metabolic abnormalities in macrophages. • Macrophages treated by pristane show increased glycolysis flux and enzyme activity. • Metabolic reprogramming of macrophages controls M1 polarization and arthritis. Pristane-induced arthritis (PIA) could be adoptively transferred by splenic T cells in rats, and innate immunity should play critical roles in T cell activation. However, in pre-clinical stage, the activation mechanism of innate cells like macrophages remains unclear. Here we found that PIA was dependent on macrophages since cell depletion alleviated disease severity. Splenic macrophages of PIA rats showed M1 phenotypic shifting. The quantitative proteomics analysis suggested that macrophages initiated metabolic reprogramming with the conversion of aerobic oxidation to glycolysis in response to pristane in vivo. Notably, macrophages treated with pristane showed mitochondrial dysregulation and increased glycolysis flux and enzyme activity. Additionally, TNFα production, strongly associating with the glycolysis enzyme Ldha/Ldhb, could be reduced as glycolysis was inhibited or be enhanced as citrate cycle was blocked. This work provides detailed insights into the molecular mechanisms of pristane-mediated metabolic reprogramming in macrophages and suggests a new therapeutic strategy for arthritic disorders.

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

TRIM46 contributes to high glucose-induced ferroptosis and cell growth inhibition in human retinal capillary endothelial cells by facilitating GPX4 ubiquitination

Increased permeability of retinal capillary endothelial cells is a key feature in the progression of diabetic retinopathy (DR). Precisely why and how diabetes causes dysfunction in retinal capillary endothelial cells is not well understood, making it challenging to explore more advanced therapeutics.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

NFATc1 promotes epithelial-mesenchymal transition and facilitates colorectal cancer metastasis by targeting SNAI1

Highlights: • Metastasis remains a major cause of colorectal cancer (CRC) mortality. • In this study, we examined the role of nuclear factor of activated T cells 1 (NFATc1), which showed increased expression in metastatic CRC tissues and positively correlated with CRC clinical stages. • Mechanistically, SNAI1 was transcriptionally activated by NFATc1 and interacted with SLUG to promote EMT and CRC metastasis. • Calcineurin-NFAT inhibitor FK506 could reverse these effects, offering novel therapeutic strategies for metastatic CRC. Metastatic recurrence remains a major cause of colorectal cancer (CRC) mortality. In this study, we investigated the mechanistic role of nuclear factor of activated T cells 1 (NFATc1) in CRC metastasis. First, we explored the potential role of NFATc1 in CRC using bioinformatics and hypothesized that NFATc1 might play different roles at different stages of CRC development. Then, we examined the relative expression of NFATc1 in 25 CRC tissues and adjacent normal tissues, and further analyzed the correlation between NFATc1 expression levels and clinical stages in 120 CRC patients. The role of NFATc1 in CRC metastasis and the molecular mechanisms were investigated in both in vitro and in vivo models. Our results showed that the expression of NFATc1 was increased in metastatic CRC tissues and positively associated with clinical stages (stage I vs. stage II, III or IV) of CRC. Overexpression of NFATc1 promoted CRC cell migration, invasion, and epithelial-mesenchymal transition (EMT). Moreover, SNAI1 was verified as the direct transcriptional target of NFATc1 and interacted with SLUG to promote EMT. Remarkably, our lung and liver metastasis mouse model demonstrated that NFATc1 overexpression accelerated CRC metastasis, and treatment with FK506, a calcineurin-NFAT pathway inhibitor, could suppress CRC metastasis in vivo. Taken together, our findings suggest that NFATc1 could transcriptionally activate SNAI1, which in turn interacts with SLUG to mediate EMT to promote CRC metastasis. Thus, making NFATc1 a promising therapeutic target in the treatment of metastatic CRC.

60 APPLIED LIFE SCIENCES↗