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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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4 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2023

Comparison of ozone formation attribution techniques in the northeastern United States

The Integrated Source Apportionment Method (ISAM) has been revised in the Community Multiscale Air Quality (CMAQ) model. This work updates ISAM to maximize its flexibility, particularly for ozone (O 3 ) modeling, by providing multiple attribution options, including products inheriting attribution fully from nitrogen oxide reactants, fully from volatile organic compound (VOC) reactants, equally from all reactants, or dynamically from NO x or VOC reactants based on the indicator gross production ratio of hydrogen peroxide (H 2 O 2 ) to nitric acid (HNO 3 ). The updated ISAM has been incorporated into the most recent publicly accessible versions of CMAQ (v5.3.2 and beyond). This study's primary objective is to document these ISAM updates and demonstrate their impacts on source apportionment results for O 3 and its precursors. Additionally, the ISAM results are compared with the Ozone Source Apportionment Technology (OSAT) in the Comprehensive Air-quality Model with Extensions (CAMx) and the brute-force method (BF). All comparisons are performed for a 4 km horizontal grid resolution application over the northeastern US for a selected 2 d summer case study (9 and 10 August 2018). General similarities among ISAM, OSAT, and BF results add credibility to the new ISAM algorithms. However, some discrepancies in magnitude or relative proportions among tracked sources illustrate the distinct features of each approach, while others may be related to differences in model formulation of chemical and physical processes. Despite these differences, OSAT and ISAM still provide useful apportionment data by identifying the geographical and temporal contributions of O 3 and its precursors. Both OSAT and ISAM attribute the majority of O 3 and NO x contributions to boundary, mobile, and biogenic sources, whereas the top three contributors to VOCs are found to be biogenic, boundary, and area sources.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2022

The Terrestrial Biosphere Model Farm

Model Intercomparison Projects (MIPs) are fundamental to our understanding of how the land surface responds to changes in climate. However, MIPs are challenging to conduct, requiring the organization of multiple, decentralized modeling teams throughout the world running common protocols. We explored centralizing these models on a single supercomputing system. We ran nine offline terrestrial biosphere models through the Terrestrial Biosphere Model Farm: CABLE, CENTURY, HyLand, ISAM, JULES, LPJ-GUESS, ORCHIDEE, SiB-3, and SiB-CASA. All models were wrapped in a software framework driven with common forcing data, spin-up, and run protocols specified by the Multi-scale Synthesis and Terrestrial Model Intercomparison Project (MsTMIP) for years 1901–2100. We ran more than a dozen model experiments. We identify three major benefits and three major challenges. The benefits include: (a) processing multiple models through a MIP is relatively straightforward, (b) MIP protocols are run consistently across models, which may reduce some model output variability, and (c) unique multimodel experiments can provide novel output for analysis. The challenges are: (a) technological demand is large, particularly for data and output storage and transfer; (b) model versions lag those from the core model development teams; and (c) there is still a need for intellectual input from the core model development teams for insight into model results. A merger with the open-source, cloud-based Predictive Ecosystem Analyzer (PEcAn) ecoinformatics system may be a path forward to overcoming these challenges.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2017

The effect of O-GlcNAcylation on hnRNP A1 translocation and interaction with transportin1

The heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) is a major pre-mRNA binding protein involved in transcription and translation. Although predominantly nuclear, hnRNP A1 shuttles rapidly between the nucleus and the cytosol, delivering its anchored pre-mRNA for further processing. Translocation is important for hnRNP A1 to accomplish its transcriptional and translational roles. Transportin1 (Trn1), a translocation protein, facilitates the translocation of hnRNP A1 back to the nucleus. Moreover, phosphorylation of serine residues at hnRNP A1 C-terminal domain affects its translocation. In this study, we found that phosphorylation is not the only modification that hnRNP A1 undergoes, but also O-linked N-acetylglucosaminylation (O-GlcNAcylation) could occur. Several putative novel O-GlcNAcylation and phosphorylation sites in hnRNP A1 were mapped. Whereas enhanced O-GlcNAcylation increased hnRNP A1 interaction with Trn1, enhanced phosphorylation reduced the interaction between the proteins. In addition, elevated O-GlcNAcylation resulted in hnRNP A1 seclusion in the nucleus, whereas elevated phosphorylation resulted in its accumulation in the cytosol. These findings suggest that a new player, i.e., O-GlcNAcylation, regulates hnRNP A1 translocation and interaction with Trn1, possibly affecting its function. There is a need for further study, to elucidate the role of O-GlcNAcylation in the regulation of the specific activities of hnRNP A1 in transcription and translation. - Highlights: • O-GlcNAcylation regulates hnRNP A1 translocation and interaction with Trn1. • Reciprocity between phosphorylation and O-GlcNAcylation in hnRNP A1 is proposed. • Novel O-GlcNAcylation and phosphorylation sites on hnRNPA1 were identified.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

O-GlcNAcylation affects β-catenin and E-cadherin expression, cell motility and tumorigenicity of colorectal cancer

O-GlcNAcylation, the addition of β-N-acetylglucosamine (O-GlcNAc) moiety to Ser/Thr residues, is a sensor of the cell metabolic state. Cancer diseases such as colon, lung and breast cancer, possess deregulated O-GlcNAcylation. Studies during the last decade revealed that O-GlcNAcylation is implicated in cancer tumorigenesis and proliferation. The Wnt/β-catenin signaling pathway and cadherin-mediated adhesion are also implicated in epithelial-mesenchymal transition (EMT), a key cellular process in invasion and cancer metastasis. Often, deregulation of the Wnt pathway is caused by altered phosphorylation of its components. Specifically, phosphorylation of Ser or Thr residues of β-catenin affects its location and interaction with E-cadherin, thus facilitating cell-cell adhesion. Consistent with previous studies, the current study indicates that β-catenin is O-GlcNAcylated. To test the effect of O-GlcNAcylation on cell motility and how O-GlcNAcylation might affect β-catenin and E-cadherin functions, the enzyme machinery of O-GlcNAcylation was modulated either with chemical inhibitors or by gene silencing. When O-GlcNAcase (OGA) was inhibited, a global elevation of protein O-GlcNAcylation and increase in the expression of E-cadherin and β-catenin were noted. Concomitantly with enhanced O-GlcNAcylation, β-catenin transcriptional activity were elevated. Additionally, fibroblast cell motility was enhanced. Stable silenced cell lines with adenoviral OGA or adenoviral O-GlcNAc transferase (OGT) were established. Consistent with the results obtained by OGA chemical inhibition by TMG, OGT-silencing led to a significant reduction in β-catenin level. In vivo, murine orthotropic colorectal cancer model indicates that elevated O-GlcNAcylation leads to increased mortality rate, tumor and metastasis development. However, reduction in O-GlcNAcylation promoted survival that could be attributed to attenuated tumor and metastasis development. The results described herein provide circumstantial clues that O-GlcNAcylation deregulates β-catenin and E-cadherin expression and activity in fibroblast cell lines and this might influence EMT and cell motility, which may further influence tumor development and metastasis.

60 APPLIED LIFE SCIENCES↗