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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 19 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2019

Interaction and Regulation Between Lipid Mediator Phosphatidic Acid and Circadian Clock Regulators

Circadian clocks play important roles in regulating cellular metabolism, but the reciprocal effect that metabolism has on the clock is largely unknown in plants. Here we show that the central glycerolipid metabolite and lipid mediator phosphatidic acid (PA) interacts with and modulates the function of the core clock regulators LATE ELONGATED HYPOCOTYL (LHY) and CIRCADIAN CLOCK ASSOCIATED1 (CCA1) in Arabidopsis. PA reduced the ability of LHY and CCA1 to bind the promoter of their target gene TIMING OF CAB EXPRESSION1. Increased PA accumulation and inhibition of PA-producing enzymes had opposite effects on circadian clock outputs. Diurnal change in levels of several membrane phospholipid species, including PA, observed in wild-type was lost in the LHY and CCA1 double knockout mutant. Storage lipid accumulation was also affected in the clock mutants. These results indicate that the interaction of PA with the clock regulator may function as a cellular conduit to integrate the circadian clock with lipid metabolism.

bio-inspired↗
DOE OSTI2024

Experimental Analysis of Distribution Network Voltage Regulation Using Smart Inverters

Smart inverters (SIs) have demonstrated their potential to provide grid services for both transmission and distribution systems. One of these grid services, distribution network voltage regulation by SIs, has the potential to improve network voltage regulation through controlling the reactive and active power output of the SIs. Voltage regulation by SIs will be distributed and might be better suited to controlling local conditions to complement traditional voltage-regulating assets, e.g., tap-changing transformers, capacitor banks, and line voltage regulators. There is a gap in the literature on comparing the SI response characteristics when the SIs are controlled by a local controller or external control signals. This paper presents an experimental study to characterize SI reactive power regulation responses to two different control methods: autonomous control and remote dispatch. We found that SI reactive power regulation responses exhibit important differences between these methods in terms of delays and ramp rate. Finally, power-hardware-in-the-loop (PHIL) tests were conducted to evaluate the performance of these two methods. The PHIL test results show that the SI response characteristics for autonomous control and remote dispatch need to be considered when planning for distribution network voltage regulation using SIs.

autonomous control↗
DOE OSTI2014

A SiC NMOS Linear Voltage Regulator for High-Temperature Applications

The first SiC integrated circuit linear voltage regulator is reported. The voltage regulator uses a 20-V supply and generates an output of 15 V, adjustable down to 10 V. It was designed for loads of up to 2 A over a temperature range of 25-225 degrees C. It was, however, successfully tested up to 300 degrees C. The voltage regulator demonstrated load regulations of 1.49% and 9% for a 2-A load at temperatures of 25 and 300 degrees C, respectively. However, the load regulation is less than 2% up to 300 degrees C for a 1-A load. The line regulation with a 2-A load at 25 and 300 degrees C was 17 and 296 mV/V, respectively. The regulator was fabricated in a Cree 4H-SiC 2-mu m experimental process and consists of 1000, 32/2-mu m NMOS depletion MOSFETs as the pass device, an integrated error amplifier with enhancement MOSFETs, and resistor loads, and uses external feedback and compensation networks to ensure operational integrity. It was designed to be integrated with high-voltage vertical power MOSFETs on the same SiC substrate. It also serves as a guide to future attempts for voltage regulation in any type of integrated SiC circuitry.

Valle-Mayorga, JA↗
DOE OSTI2018

Sensitivity of Regulated Flow Regimes to Climate Change in the Western United States

Water management activities or flow regulations modify water fluxes at the land surface and affect water resources in space and time. We hypothesize that flow regulations change the sensitivity of river flow to climate change with respect to unmanaged water resources. Quantifying these changes in sensitivity could help elucidate the impacts of water management at different spatiotemporal scales and inform climate adaptation decisions. In this study, we compared the emergence of significant changes in natural and regulated river flow regimes across the Western United States from simulations driven by multiple climate models and scenarios. We find that significant climate change-induced alterations in natural flow do not cascade linearly through water management activities. At the annual time scale, 50% of the Hydrologic Unit Code 4 (HUC4) sub-basins over the Western U.S. regions tend to have regulated flow regime more sensitive to the climate change than natural flow regime. Seasonality analyses show that the sensitivity varies remarkably across the seasons. We also find that the sensitivity is related to the level of water management. For 35% of the HUC4 sub-basins with the highest level of water management, the summer and winter flows tend to show a heightened sensitivity to climate change due to the complexity of joint reservoir operations. We further demonstrate that the impacts of considering water management in models are comparable to those that arises from uncertainties across climate models and emission scenarios. This prompts further climate adaptation studies research about nonlinearity effects of climate change through water management activities.

Zhou, Tian↗
DOE OSTI2021

Utility Regulation Through Legislation: A Cautionary Tale for Legislators, Regulators, Stakeholders, and Utilities

State legislatures in the U.S. are becoming increasingly involved in utility regulation. While state utility legislation can expand regulator authority, for example in the case of renewable energy or energy efficiency standard administration, it can also reduce it. Given the challenging nature of for-profit monopoly regulation, state utility legislation often reduces regulator authority unintentionally. This editorial begins with an examination of the outcomes of state legislation related to baseload generation in the U.S. and the resulting impacts to customers, shareholders, and state economies. The record indicates that utility regulation through state legislation has caused significant economic harm, generally by encouraging for-profit utilities to make riskier investments. A description of more recent state legislation involving distribution grids is presented, along with evidence that increases in grid investment encouraged by state legislation has not improved the reliability of U.S. for-profit utilities. The authors claim that features common to state utility legislation, particularly the requirement that utilities provide investment plans to regulators in advance, practically eliminates cost disallowance risk. This, in turn, reduces regulator authority despite legislative provisions intended to protect consumers. The authors hypothesize that the practical elimination of cost disallowance risk, combined with information and expertise asymmetry among regulators and stakeholders, encourages for-profit monopoly utilities to make grid investments that are not cost effective. The editorial concludes that legislators should avoid utility regulation through legislation, thereby preserving regulator authority, whenever possible. The authors also present their fifth annual Customer Value Ranking of U.S. investor-owned electric utilities. The ranking represents a comparison of the benefits utilities deliver to customers (measured by reliability performance and customer satisfaction) to the costs customers pay (measured by O&M and capital spending per customer).

ENERGY PLANNING, POLICY, AND ECONOMY,POWER TRANSMI↗
DOE OSTI2016

Rapamycin regulates the proliferation of Huh7, a hepatocellular carcinoma cell line, by up-regulating p53 expression

Rapamycin, a specific inhibitor of mTOR used extensively as an immunosuppressant, has been expanded recently to cancer therapy, because the mTOR signal is known to be up-regulated in various cancer cells including hepatocellular carcinoma (HCC) cells. In spite of extensive efforts to employ mTOR inhibitors as anti-HCC therapy, they have not yet been approved by the FDA. Because of the heterogeneity and complexity of molecular signaling in HCC, suitable biomarkers should be identified or discovered to improve clinical efficacy of mTOR-specific inhibitors to HCC cells. In this study, the effect of rapamycin was investigated on two different HCC cell lines, Huh7 cells and HepG2 cells. Rapamycin was found to inhibit the proliferation of Huh7 cells but not of HepG2 cells. Moreover, it was found that rapamycin can up-regulate p53 at the protein level, but not affect its transcript. To understand the critical role of p53 in the rapamycin effect, knock-down experiments were performed using small-interfering RNAs (siRNAs). The anti-proliferative effect of rapamycin on Huh7 cells clearly disappeared after blocking p53 production with siRNA, which indicates that p53 is a critical factor in the anti-proliferative effect of rapamycin in HCC cells. The over-expression system of p53 was also employed to mimic the effect of rapamycin and found that cell proliferation was clearly down-regulated by p53 over-expression. Finally, we found that the extracellular signal-regulated kinase 1/2 (ERK1/2) signal was regulated by p53 whose expression was induced by rapamycin. Overall, this study demonstrates that rapamycin inhibited the proliferation of Huh7 cells by up-regulating the expression of p53 and down-regulating the ERK1/2 signal, indicating that p53 is a useful biomarker for anti-cancer therapy using the specific inhibitor of mTOR signal, rapamycin, against hepatocellular carcinoma cells. - Highlights: • Rapamycin inhibits the proliferation of hepatocellular carcinoma cells depending on the expression of p53. • Rapamycin up-regulates p53 at the protein level, but not affect its transcript. • The up-regulation of p53 expression by rapamycin inhibits ERK signal.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Down-regulation of miR-193a-3p promotes osteoblast differentiation through up-regulation of LGR4/ATF4 signaling

Highlights: • miR-193a-3p was decreased during osteoblast differentiation. • Inhibition of miR-193a-3p promoted osteoblast differentiation. • LRG4 was a target gene of miR-193a-3p. • miR-193a-3p regulates osteoblast differentiation by LGR4/ATF4. Emerging evidence indicates that microRNAs (miRNAs) are crucial regulators of osteoblast differentiation. A previous study has reported that miR-193a-3p expression is altered during the induction of osteoblast differentiation. However, the precise biological function and regulatory mechanism of miR-193a-3p during osteoblast differentiation remains unclear. In this study, we aimed to investigate the precise role and underlying mechanism of miR-193a-3p in regulating osteoblast differentiation. The results showed that miR-193a-3p expression was significantly down-regulated during the induction of osteoblast differentiation. Functional experiments demonstrated that the overexpression of miR-193a-3p impeded osteoblast differentiation while miR-193a-3p inhibition promoted osteoblast differentiation. Bioinformatics analysis and a luciferase assay revealed that leucine-rich repeat-containing G-protein coupled receptor 4 (LGR4), a critical regulator of osteoblast differentiation, was a target gene of miR-193a-3p. We showed that miR-193a-3p negatively regulated the expression of LGR4 and activating transcription factor 4 (ATF4). Moreover, the knockdown of LGR4 or ATF4 significantly reversed the promotion effect of miR-193a-3p inhibition on osteoblast differentiation. Overall, these findings demonstrate that miR-193a-3p regulates osteoblast differentiation by modulating LGR4/ATF4 signaling and suggests that the miR-193a-3p/LGR4/ATF4 regulation axis may play an important role in regulating bone remodeling.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Hydrogen monitoring requirements in the global technical regulation on hydrogen and fuel cell vehicles

Here, the United Nations Economic Commission for Europe Global Technical Regulation (GTR) Number 13 ( Global Technical Regulation on Hydrogen and Fuel Cell Vehicles ) is the defining document regulating safety requirements in hydrogen vehicles, and in particular, fuel cell electric vehicles (FCEVs). GTR Number 13 has been formally adopted and will serve as the basis for the national regulatory standards for FCEV safety in North America (led by the United States), Japan, Korea, and the European Union. The GTR defines safety requirements for these vehicles, including specifications on the allowable hydrogen levels in vehicle enclosures during in-use and post-crash conditions and on the allowable hydrogen emissions levels in vehicle exhaust during certain modes of normal operation. However, in order to be incorporated into national regulations, that is, to be legally binding, methods to verify compliance with the specific requirements must exist. In a collaborative program, the Sensor Laboratories at the National Renewable Energy Laboratory in the United States and the Joint Research Centre, Institute for Energy and Transport in the Netherlands have been evaluating and developing analytical methods that can be used to verify compliance with the hydrogen release requirements as specified in the GTR.

30 DIRECT ENERGY CONVERSION↗
DOE OSTI2017

Negative regulation of NOD1 mediated angiogenesis by PPARγ-regulated miR-125a

Infection with pathogens activates the endothelial cell and its sustained activation may result in impaired endothelial function. Endothelial dysfunction contributes to the pathologic angiogenesis that is characteristic of infection-induced inflammatory pathway activation. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is a protein receptor which recognizes bacterial molecules and stimulates an immune reaction in various cells; however, the underlying molecular mechanisms in the regulation of inflammation-triggered angiogenesis are not fully understood. Here we report that peroxisome proliferator-activated receptor gamma (PPARγ)-mediated miR-125a serves as an important regulator of NOD1 agonist-mediated angiogenesis in endothelial cells by directly targeting NOD1. Treatment of human umbilical vein endothelial cells with natural PPARγ ligand, 15-Deoxy-Delta12,14-prostaglandin J2, led to inhibition of NOD1 expression; contrarily, protein levels of NOD1 were significantly increased by PPARγ knockdown. We report that PPARγ regulation of NOD1 expression is a novel microRNA-mediated regulation in endothelial cells. MiR-125a expression was markedly decreased in human umbilical vein endothelial cells subjected to PPARγ knockdown while 15-Deoxy-Delta12,14-prostaglandin J2 treatment increased the level of miR-125a. In addition, NOD1 is closely regulated by miR-125a, which directly targets the 3′ untranslated region of NOD1. Moreover, both overexpression of miR-125a and PPARγ activation led to inhibition of NOD1 agonist-induced tube formation in endothelial cells. Finally, NOD1 agonist increased the formation of cranial and subintestinal vessel plexus in zebrafish, and this effect was abrogated by concurrent PPARγ activation. Overall, these findings identify a PPARγ-miR-125a-NOD1 signaling axis in endothelial cells that is critical in the regulation of inflammation-mediated angiogenesis. - Highlights: • Expression of NOD1 is regulated by PPARγ signaling in HUVECs. • PPARγ-regulated NOD1 expression is mediated at least in part by of miR-125a. • NOD1 is a novel target gene of miR-125. • miR-125a inhibits inflammation induced angiogenesis in HUVECs. • PPARγ activation inhibits inflammation mediated angiogenesis in vitro and in vivo.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Environmental contaminants and microRNA regulation: Transcription factors as regulators of toxicant-altered microRNA expression

MicroRNAs (miRNAs) regulate gene expression by binding mRNA and inhibiting translation and/or inducing degradation of the associated transcripts. Expression levels of miRNAs have been shown to be altered in response to environmental toxicants, thus impacting cellular function and influencing disease risk. Transcription factors (TFs) are known to be altered in response to environmental toxicants and play a critical role in the regulation of miRNA expression. To date, environmentally-responsive TFs that are important for regulating miRNAs remain understudied. In a state-of-the-art analysis, we utilized an in silico bioinformatic approach to characterize potential transcriptional regulators of environmentally-responsive miRNAs. Using the miRStart database, genomic sequences of promoter regions for all available human miRNAs (n = 847) were identified and promoter regions were defined as − 1000/+500 base pairs from the transcription start site. Subsequently, the promoter region sequences of environmentally-responsive miRNAs (n = 128) were analyzed using enrichment analysis to determine overrepresented TF binding sites (TFBS). While most (56/73) TFs differed across environmental contaminants, a set of 17 TFs was enriched for promoter binding among miRNAs responsive to numerous environmental contaminants. Of these, one TF was common to miRNAs altered by the majority of environmental contaminants, namely SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 3 (SMARCA3). These identified TFs represent candidate common transcriptional regulators of miRNAs perturbed by environmental toxicants. - Highlights: • Transcription factors that regulate environmentally-modulated miRNA expression are understudied • Transcription factor binding sites (TFBS) located within DNA promoter regions of miRNAs were identified. • Specific transcription factors may serve as master regulators of environmentally-mediated microRNA expression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Differential regulation of HIF-1α and HIF-2α in neuroblastoma: Estrogen-related receptor alpha (ERRα) regulates HIF2A transcription and correlates to poor outcome

Hypoxia-inducible factors (HIFs) are differentially regulated in tumor cells. While the current paradigm supports post-translational regulation of the HIF-α subunits, we recently showed that hypoxic HIF-2α is also transcriptionally regulated via insulin-like growth factor (IGF)-II in the childhood tumor neuroblastoma. Here, we demonstrate that transcriptional regulation of HIF-2α seems to be restricted to neural cell-derived tumors, while HIF-1α is canonically regulated at the post-translational level uniformly across different tumor forms. Enhanced expression of HIF2A mRNA at hypoxia is due to de novo transcription rather than increased mRNA stability, and chemical stabilization of the HIF-α proteins at oxygen-rich conditions unexpectedly leads to increased HIF2A transcription. The enhanced HIF2A levels do not seem to be dependent on active HIF-1. Using a transcriptome array approach, we identified members of the Peroxisome proliferator-activated receptor gamma coactivator (PGC)/Estrogen-related receptor (ERR) complex families as potential regulators of HIF2A. Knockdown or inhibition of one of the members, ERRα, leads to decreased expression of HIF2A, and high expression of the ERRα gene ESRRA correlates with poor overall and progression-free survival in a clinical neuroblastoma material consisting of 88 tumors. Thus, targeting of ERRα and pathways regulating transcriptional HIF-2α are promising therapeutic avenues in neuroblastoma. - Highlights: • Transcriptional control of HIF-2α is restricted to neural cell-derived tumors. • Enhanced transcription of HIF2A is not due to increased mRNA stability. • Chemical stabilization of the HIF-α subunits leads to increased HIF2A transcription. • ERRα regulates HIF2A mRNA expression in neuroblastoma. • High expression of ESRRA correlates to poor outcome in neuroblastoma.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2020

Two interacting ethylene response factors regulate heat stress response

Abstract The ethylene response factor (ERF) transcription factors are integral components of environmental stress signaling cascades, regulating a wide variety of downstream genes related to stress responses and plant development. However, the mechanisms by which ERF genes regulate the heat stress response are not well understood. Here, we uncover the positive role of ethylene signaling, ERF95 and ERF97 in basal thermotolerance of Arabidopsis thaliana. We demonstrate that ethylene signaling-defective mutants exhibit compromised basal thermotolerance, whereas plants with constitutively activated ethylene response show enhanced basal thermotolerance. EIN3 physically binds to the promoters of ERF95 and ERF97. Ectopic constitutive expression of ERF95 or ERF97 increases the basal thermotolerance of plants. In contrast, erf95 erf96 erf97 erf98 quadruple mutants exhibit decreased basal thermotolerance. ERF95 and ERF97 genetically function downstream of EIN3. ERF95 can physically interact with ERF97, and this interaction is heat inducible. ERF95 and ERF97 regulate a common set of target genes, including known heat-responsive genes and directly bind to the promoter of HSFA2. Thus, our study reveals that the EIN3-ERF95/ERF97-HSFA2 transcriptional cascade may play an important role in the heat stress response, thereby establishing a connection between ethylene and its downstream regulation in basal thermotolerance of plants.

Biochemistry & Molecular Biology↗
DOE OSTI2022

Design of a Combined Proportional Integral Derivative Controller to Regulate the Temperature Inside a High-Temperature Tubular Solar Reactor

Solar fuels are proven to be promising candidates for thermochemical energy storage. However, the transient nature of solar radiation is an obstacle to maintaining a stable operational temperature inside a solar reactor. To overcome this challenge, the temperature of a solar reactor can be regulated by controlling the incoming solar radiation or the feedstock flowrate inside the reactor. In this work, a combined proportional integral derivative (PID) controller is implemented to regulate the temperature inside a high-temperature tubular solar reactor with counter-current flowing gas/particles. The control model incorporates two control systems to regulate incoming solar radiation and gas flow simultaneously. The design of the controller is based on a reduced-order numerical model of a high-temperature tubular solar reactor that is vertically oriented with an upward gas flow and downward particle flow. The reactor receives heat circumferentially through its wall over a finite segment of its length. Formulation of the heat transfer model is presented by applying the energy balance for the reactor tube and considering heat and mass transfer inside. A set of governing differential equations are solved numerically by using the finite volume method to obtain reactor wall, particles, and gas temperatures along the reactor length with various boundary conditions. Simulation results are used to tune the PID controller parameters by utilizing the Ziegler–Nichols tuning method. Both the simulation results and the controller performance are visualized on the LABVIEW platform. The controller is challenged to track different temperature setpoints with different scenarios of transient solar radiation. Here, the performance of the PID controller was compared to experimental results obtained from an industrial PID controller embedded in a 7 kW electric furnace. Results show that the combined PID controller is successful in maintaining a stable temperature inside the reactor by regulating the incoming solar radiation and the flowrate via small steady-state error and reasonable settling time and overshoot.

14 SOLAR ENERGY↗
DOE OSTI2025

Polyyne production is regulated by the transcriptional regulators PgnC and GacA in Pseudomonas protegens Pf-5

ABSTRACT Polyynes produced by bacteria have promising applications in agriculture and medicine due to their potent antimicrobial activities. Polyyne biosynthetic genes have been identified inPseudomonasandBurkholderia. However, the molecular mechanisms underlying the regulation of polyyne biosynthesis remain largely unknown. In this study, we used a soil bacteriumPseudomonas protegensPf-5, which was recently reported to produce polyyne called protegenin, as a model to investigate the regulation of bacterial polyyne production. Our results show that Pf-5 controls polyyne production at both the pathway-specific level and a higher global level. Mutation ofpgnC, a transcriptional regulatory gene located in the polyyne biosynthetic gene cluster, abolished polyyne production. Gene expression analysis revealed that PgnC directly activates the promoter of polyyne biosynthetic genes. The production of polyyne also requires a global regulator GacA. Mutation ofgacAdecreased the translation of PgnC, which is consistent with the result thatpgnCleader mRNA bound directly to RsmE, an RNA-binding protein negatively regulated by GacA. These results suggest that GacA induces the expression of the PgnC regulator, which in turn activates polyyne biosynthesis. Additionally, the polyyne-producing strain of Pf-5, but not the polyyne-nonproducing strain, could inhibit a broad spectrum of bacteria including both Gram-negative and Gram-positive bacteria. IMPORTANCE Antimicrobial metabolites produced by bacteria are widely used in agriculture and medicine to control plant, animal, and human pathogens. Although bacteria-derived polyynes have been identified as potent antimicrobials for decades, the molecular mechanisms by which bacteria regulate polyyne biosynthesis remain understudied. In this study, we found that polyyne biosynthesis is directly activated by a pathway-specific regulator PgnC, which is induced by a global regulator GacA through the RNA-binding protein RsmE inPseudomonas protegens. To our knowledge, this work is the first comprehensive study of the regulatory mechanisms of bacterial polyyne biosynthesis at both pathway-specific level and global level. The discovered molecular mechanisms can help us optimize polyyne production for agricultural or medical applications.

Biotechnology & Applied Microbiology↗
DOE OSTI2018

Prediction of Metabolite Concentrations, Rate Constants and Post-Translational Regulation Using Maximum Entropy-Based Simulations with Application to Central Metabolism of Neurospora crassa

We report the application of a recently proposed approach for modeling biological systems using a maximum entropy production rate principle in lieu of having in vivo rate constants. The method is applied in four steps: (1) a new ordinary differential equation (ODE) based optimization approach based on Marcelin’s 1910 mass action equation is used to obtain the maximum entropy distribution; (2) the predicted metabolite concentrations are compared to those generally expected from experiments using a loss function from which post-translational regulation of enzymes is inferred; (3) the system is re-optimized with the inferred regulation from which rate constants are determined from the metabolite concentrations and reaction fluxes; and finally (4) a full ODE-based, mass action simulation with rate parameters and allosteric regulation is obtained. From the last step, the power characteristics and resistance of each reaction can be determined. The method is applied to the central metabolism of Neurospora crassa and the flow of material through the three competing pathways of upper glycolysis, the non-oxidative pentose phosphate pathway, and the oxidative pentose phosphate pathway are evaluated as a function of the NADP/NADPH ratio. It is predicted that regulation of phosphofructokinase (PFK) and flow through the pentose phosphate pathway are essential for preventing an extreme level of fructose 1,6-bisphophate accumulation. Such an extreme level of fructose 1,6-bisphophate would otherwise result in a glassy cytoplasm with limited diffusion, dramatically decreasing the entropy and energy production rate and, consequently, biological competitiveness.

Cannon, William R.↗