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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 325 records · Page 18
All sourcesNASA NTRSDOE OSTI
DOE OSTI2023

Parallel Grid-Forming Inverter-Driven Black Start: Power-Hardware-in-the-Loop Validation: Preprint

With power systems encountering increasing deployment levels of inverter-based resources (IBRs), system restoration using grid-forming (GFM) IBRs has gained attention. Engineered to establish grid voltages in the absence of a stiff grid, black-start-capable GFM IBRs are expected to enhance power system resilience by playing a critical role in bottom-up system restoration. This paper experimentally studies the feasibility of the novel approach through power-hardware-in-the-loop (PHIL) testing and validation with a commercial GFM inverter. The PHIL test setup demonstrates an inverter-driven black start of a 5-MW unbalanced distribution feeder where two GFM inverters collectively black start the feeder: one is a commercial hardware GFM inverter interacting through the PHIL interface, and the other is a software GFM emulated by a real-time simulation with full electromagnetic transient (EMT) models. Both GFM inverters are equipped with negative-sequence voltage control to suppress the voltage imbalance resulting from the unbalanced loading, allowing us to study the dynamic interactions between the GFMs with their control parameters unknown. To evaluate the dynamic behavior of the GFM inverters under the entire black-start process, the EMT model of the distribution system details the transformer and motor dynamics to emulate their inrush and startup behaviors. It abstracts conventional grid-connected inverter dynamics, i.e., grid-following inverters. Oscilloscope measurements of the hardware GFM inverter are also presented for critical steps. Takeaways for further study and field deployment are provided.

grid-forming inverter↗
DOE OSTI2024

Equivalent-Circuit Models of Grid-Forming IBRs for Electromagnetic-Transient Simulations: Preprint

We derive equivalent-circuit models of control- and physical-layer subsystems of grid-forming (GFM) inverter-based resources (IBRs) for electromagnetic-transient (EMT) simulations. Three different primary controllers are considered: droop, virtual synchronous machine (VSM), and dispatchable virtual oscillator control (dVOC). In addition, the models include cascaded voltage- and current-control loops, and LCL output filters. Simulations for a single-inverter setup and for a network of five inverters in a modified IEEE 14-bus topology are presented. The equivalent-circuit models simulated with analog electronic circuit-simulator software (in our case, LTspice) offer the same accuracy with up to 150x lower computational burden compared to block-diagram-based implementations in commercial off-the-shelf EMT software (in our case, MATLAB-Simulink).

circuit-equivalent model↗
DOE OSTI2024

Studying the Impact of IBR Modeling on the Commonly Applied Transmission Line Protective Elements

It is a well-accepted fact that detailed inverter-based resource (IBR) models are needed for electromagnetic transient (EMT) studies, especially for protection studies and protection designs. However, it is not clear which modeling aspects should be included in the EMT model to accurately represent the IBR fault responses. Therefore, this paper addresses this gap by evaluating the impact of key modeling aspects (DC source, inverter model, power control, current/voltage control, and current limiting) on the response of protective relay elements both qualitatively and quantitatively. Both grid-following (GFL) and grid-forming (GFM) IBR models are comprehensively evaluated through a simplified real-world transmission network by varying the IBR modeling aspects, fault locations, and types. The insights and findings from this paper will benefit the power system protection community because this work provides modeling requirements and guidelines for IBR modeling so that correct IBR models will be used for protection scheme settings design.

grid-following inverter↗
DOE OSTI2026

Evaluation of a Reduced-Order Model for IBR Fault Response Representation via OEM Blackbox Models: Preprint

Driven by the need to capture the electromagnetic transients of transmission lines, inverter switching behavior, and detailed control systems, electromagnetic transient (EMT) studies have become increasingly important in industry, such as IBR interconnection study and fault study. However, original equipment manufacturer (OEM) inverter models typically include extensive parameters and proprietary settings that are unavailable to protection engineers. This paper introduces a data-driven, reduced-order model (ROM) developed as a PSCAD library component for use in EMT-based fault studies. The ROM replicates key OEM model behaviors without requiring detailed knowledge of control design or parameterization. The accompanying Python automation scripts streamline data generation, parameter fitting, and validation. The ROM's performance is demonstrated through comparison with both IEEE 2800-compliant and non-compliant OEM models in a real-world power system. Relay responses show nearly identical results, while simulation runtime is reduced by an average of 32.8\%, highlighting the ROM's practicality for protection engineers.

14 SOLAR ENERGY↗
DOE OSTI2024

Autonomous Inverter Controls for Resilient and Secure Grid Operation: Vector Control Design for Grid Forming

The project addresses both fundamental and practical challenges of GFM/GFL inverter control for the power grids with high inverter based resources (IBRs) penetration. A data- driven modeling technique is applied to accurately model dynamics of PWM inverters, including electromagnetic-transient (EMT). Systematic and integrative designs of grid- forming (GFM) and grid-following (GFL) primary controls are developed to guarantee system performance under either normal or abnormal operating conditions without violating constraints. This modeling and control framework provides black-start capability in case of an outage without relying on rotating generators, and its secondary control is also shown to enhance resilience against cyber-physical attacks.

14 SOLAR ENERGY↗
DOE OSTI2025

Modeling of Inductive Constant Power Load for Electromagnetic-Transient Simulations-Part II

This paper improves the dynamic constant power (CP) load model that was published in Part I, which is appropriate for electromagnetic-transient (EMT). The improved model conserves all features of its predecessor. For instance, it maintains a fixed power consumption (both active and reactive parts) and a fixed power factor for loads that are predominantly inductive. Furthermore, as the proposed model is a time-dependent system, it is applicable to both sinusoidal and non-sinusoidal case studies. However, the previous model cannot be easily integrated with numeric solvers because it simulated load data over one cycle all together, not sequentially in a time-step manner, due to the limitation involved with the power factor. The improved version, on the contrary, allows the load to be simulated at every time step, which would facilitate its integration with numeric solvers. The model's validity is confirmed by comparing its response with data that is synthesized from constant impedance load, and the result is satisfactory.

24 POWER TRANSMISSION AND DISTRIBUTION↗
DOE OSTI2023

Analytical Large-Signal Modeling of Inverter-Based Microgrids With Koopman Operator Theory for Autonomous Control

The microgrid (MG) plays a crucial role in the energy transition, but its nonlinearity presents a significant challenge for large-signal power systems studies in the electromagnetic transient (EMT) time scale. In this paper, we develop a large-signal linear MG model that considers the detailed dynamics of the primary and zero-control levels based on the Koopman operator (KO) theory. Firstly, a set of observable functions is carefully designed to capture the nonlinear dynamics of the MG. The corresponding linear KO is then analytically derived based on these observables, resulting in the linear representation of the original nonlinear MG with observables as the new coordinate. The influence of external input on the system dynamics is also considered during the derivation, enabling control of the MG. We solve the voltage control problem using the traditional linear quadratic integrator (LQI) method to demonstrate that textbook linear control techniques can accurately control the original nonlinear MG via the developed KO-linearized MG model. Our proposed KO linearization method is generic and can be easily extended for different control objectives and MG structures using our analytical derivation procedure. Here, we validate the effectiveness of our methodology through various case studies.

25 ENERGY STORAGE↗
DOE OSTI2024

Advanced grid-forming (GFM) inverter controls, modeling and system impact study for inverter dominated grids

Our main goals in this project are to understand: 1) the stability of the power system with very high penetration of PV or other inverter-based resources (IBR), 2) the interactions among IBRs and traditional generators, and 3) the impact of the GFM inverters on bulk power system. To achieve these goals, we took a holistic research and development approach. First, an impedance-based large system modeling and stability analysis tool was developed to aid the large IBR system small-signal stability analysis. Second, consensus-based control and transient overload ride through were developed to control and coordinate multiple GFM inverters in a large system to maintain transient stability during big grid events. Third, high fidelity electromagnetic transient (EMT) IBR models were developed and integrated into a large reduced WECC model to study the system impact from IBRs. Lastly, extensive validation tests of the GFM control which was developed in this project and implemented in two 1MW commercial solar inverters were performed using different validation platforms, e.g., control hardware-in-the-loop (CHIL) platform, power hardware- in-the-loop (PHIL) platform, and a real PV plant.

14 SOLAR ENERGY↗
DOE OSTI2026

Demonstration of Grid Services Using Mixed Grid-Forming and Grid-Following Technologies at the Wheatridge Renewable Energy Facility (Final Technical Report)

This Final Technical Report summarizes the analytical, modeling, and engineering work performed to evaluate grid-forming (GFM) inverter capabilities within a large hybrid renewable energy facility. The project focused on assessing the ability of advanced inverter-based resources to provide essential reliability services through coordinated operation of grid-forming (GFM) and grid-following (GFL) technologies. During Budget Period 1, the project developed a comprehensive framework of GFM performance metrics, including angle support, voltage regulation, frequency response, damping behavior, and current-limiting performance. Extensive electromagnetic transient (EMT) studies and hardware-in-the-loop (HIL) testing were conducted to validate GFM behavior under a range of operating conditions, including weak-grid scenarios, voltage disturbances, and multi-resource interactions. The project also established validated modeling approaches, plant-level control integration strategies, commissioning frameworks, and high-speed measurement infrastructure to support future field demonstration. Although the project concluded prior to field demonstration, the results provide a utility-scale foundation for evaluating, modeling, and deploying grid-forming technologies. The methodologies and tools developed contribute to industry understanding of inverter-based resource behavior and support future power system reliability under increasing renewable penetration.

14 SOLAR ENERGY↗
DOE OSTI2021

PV and Dynamic Load Modeling Update

This report documents the PV and dynamic load modeling update for transient stability, EMT, harmonics, and short circuit analyses during budget period one of the DOE PV-MOD research.

14 SOLAR ENERGY↗
DOE OSTI2013

miR-9 modulates the expression of interferon-regulated genes and MHC class I molecules in human nasopharyngeal carcinoma cells

Highlights: ► miR-9 can negatively or positively modulate interferon-induced gene expression. ► miR-9 can up-regulate major histocompatibility complex class I molecule expression. ► miR-9 can down-regulate the expression of interleukin-related genes. -- Abstract: The functions of miR-9 in some cancers are recently implicated in regulating proliferation, epithelial–mesenchymal transition (EMT), invasion and metastasis, apoptosis, and tumor angiogenesis, etc. miR-9 is commonly down-regulated in nasopharyngeal carcinoma (NPC), but the exact roles of miR-9 dysregulation in the pathogenesis of NPC remains unclear. Therefore, we firstly used miR-9-expressing CNE2 cells to determine the effects of miR-9 overexpression on global gene expression profile by microarray analysis. Microarray-based gene expression data unexpectedly demonstrated a significant number of up- or down-regulated immune- and inflammation-related genes, including many well-known interferon (IFN)-induced genes (e.g., IFI44L, PSMB8, IRF5, PSMB10, IFI27, PSB9{sub H}UMAN, IFIT2, TRAIL, IFIT1, PSB8{sub H}UMAN, IRF1, B2M and GBP1), major histocompatibility complex (MHC) class I molecules (e.g., HLA-B, HLA-C, HLA-F and HLA-H) and interleukin (IL)-related genes (e.g., IL20RB, GALT, IL7, IL1B, IL11, IL1F8, IL1A, IL6 and IL7R), which was confirmed by qRT-PCR. Moreover, the overexpression of miR-9 with the miRNA mimics significantly up- or down-regulated the expression of above-mentioned IFN-inducible genes, MHC class I molecules and IL-related genes; on the contrary, miR-9 inhibition by anti-miR-9 inhibitor in CNE2 and 5–8F cells correspondingly decreased or increased the aforementioned immune- and inflammation-related genes. Taken together, these findings demonstrate, for the first time, that miR-9 can modulate the expression of IFN-induced genes and MHC class I molecules in human cancer cells, suggesting a novel role of miR-9 in linking inflammation and cancer, which remains to be fully characterized.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

Gas6 induces cancer cell migration and epithelial–mesenchymal transition through upregulation of MAPK and Slug

Highlights: •We investigated the molecular mechanisms underlying Gas6-mediated cancer cell migration. •Gas6 treatment and subsequent Axl activation induce cell migration and EMT via upregulation of Slug. •Slug expression mediated by Gas6 is mainly through c-Jun and ATF-2 in an ERK1/2 and JNK-dependent manner. •The Gas6/Axl-Slug axis may be exploited as a target for anti-cancer metastasis therapy. -- Abstract: Binding of Gas6 to Axl (Gas6/Axl axis) alters cellular functions, including migration, invasion, proliferation, and survival. However, the molecular mechanisms underlying Gas6-mediated cell migration remain poorly understood. In this study, we found that Gas6 induced the activation of JNK and ERK1/2 signaling in cancer cells expressing Axl, resulting in the phosphorylation of activator protein-1 (AP-1) transcription factors c-Jun and ATF-2, and induction of Slug. Depletion of c-Jun or ATF-2 by siRNA attenuated the Gas6-induced expression of Slug. Slug expression was required for cell migration and E-cadherin reduction/vimentin induction induced by Gas6. These results suggest that Gas6 induced cell migration via Slug upregulation in JNK- and ERK1/2-dependent mechanisms. These data provide an important insight into the molecular mechanisms mediating Gas6-induced cell migration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

OTX1 promotes colorectal cancer progression through epithelial-mesenchymal transition

Highlights: • OTX1 is overexpression in colorectal cancer tissues. • Overexpression of OTX1 promotes colorectal cancer cell proliferation and invasion in vitro and tumor growth in vivo. • Depletion of OTX1 inhibits colorectal cancer cell proliferation and invasion in vitro. • Overexpression of OTX1 is linked to the EMT-like phenotype. - Abstract: Orthodenticle homeobox 1 (OTX1), a transcription factor containing a bicoid-like homeodomain, plays a role in brain and sensory organ development. In this study, we report that OTX1 is overexpressed in human colorectal cancer (CRC) and OTX1 overexpression is associated with higher stage. Functional analyses reveal that overexpression of OTX1 results in accumulation of CRC cell proliferation and invasion in vitro and tumor growth in vivo, whereas ablation of OTX1 expression significantly inhibits the proliferative and invasive capability of CRC cells in vitro. Together, our results indicate that OTX1 is involved in human colon carcinogenesis and may serve as a potential therapeutic target for human colorectal cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition

Highlights: • FOXD3 is down-regulated in breast cancer tissues. • FOXD3 inhibits breast cancer cell proliferation and invasion. • FoxD3 deficiency induces epithelial–mesenchymal transition. - Abstract: The transcription factor forkhead box D3 (FOXD3) plays an important role in the development of neural crest and gastric cancer cells. However, the function and mechanisms of FOXD3 in the breast tumorigenesis and progression is still limited. Here, we report that FOXD3 is a tumor suppressor of breast cancer tumorigenicity and aggressiveness. We found that FOXD3 is down-regulated in breast cancer tissues. Patients with low FOXD3 expression have a poor outcome. Depletion of FOXD3 expression promotes breast cancer cell proliferation and invasion in vitro, whereas overexpression of FOXD3 inhibits breast cancer cell proliferation and invasion both in vitro and in vivo. In addition, depletion of FOXD3 is linked to epithelial–mesenchymal transition (EMT)-like phenotype. Our results indicate FOXD3 exhibits tumor suppressive activity and may be useful for breast therapy.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Long non-coding RNA HOTAIR promotes carcinogenesis and invasion of gastric adenocarcinoma

Highlights: • HOTAIR expression was tested in fifty patients with gastric cancer. • Cell proliferation was measured after HOTAIR silencing in gastric cancer cell line. • siRNA–HOTAIR suppresses cell invasiveness and capacity of migration. • Knock down of HOTAR leads to decreased expression of EMT markers. • Inhibition of HOTAIR induces apoptosis and cell cycle arrest. - Abstract: Gastric cancer is one of the major causes of cancer death worldwide; however, the mechanism of carcinogenesis is complex and poorly understood. Long non-coding RNA HOTAIR (HOX transcript antisense RNA) recently emerged as a promoter of metastasis in various cancers including gastric cancer. Here we investigated the impact of HOTAIR on apoptosis, cell proliferation and cell cycle to dissect the carcinogenesis of gastric cancer. We examined the mechanism of invasion and metastasis and analyzed the clinical significance of HOTAIR. Downregulation of HOTAIR was confirmed by two different siRNAs. The expression of HOTAIR was significantly elevated in various gastric cancer cell lines and tissues compared to normal control. si-HOTAIR significantly reduced viability in MKN 28, MKN 74, and KATO III cells but not in AGS cells. si-HOTAIR induced apoptosis in KATO III cells. Lymphovascular invasion and lymph node metastasis were more common in the high level of HOTAIR group. si-HOTAIR significantly decreased invasiveness and migration. si-HOTAIR led to differential expression of epithelial to mesenchymal transition markers. We found that HOTAIR was involved in inhibition of apoptosis and promoted invasiveness, supporting a role for HOTAIR in carcinogenesis and progression of gastric cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

17β-Estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner

In bone, different concentration of estrogen leads to various of physiological processes in osteoblast, such as the proliferation, migration, and apoptosis in an estrogen receptor-dependent manner. But little was known about the estrogen effects on osteosarcoma (OS). In this study, OS cell MG-63 was treated with low (1 nM) or high (100 nM) dose of 17β-Estradiol (E2) with the presence or absence of estrogen receptor α (ERα), for evaluating the E2 effects on proliferation, migration, invasion, colony formation and apoptosis. Consistent with a previous study, high dose of E2 treatment dramatically downregulated expressing level of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1). The observation of upregulation of miR-9 after a high dose of E2 treatment indicated the cause of MALAT-1 reduction. Downregulation of MALAT-1 promoted the combination of SFPQ/PTBP2 complex. It was also observed that the proliferation, migration, invasion, colony formation and apoptosis of OS cells were remarkably affected by high dose of E2 treatment, but not by low dose, in an ERα independent manner. Furthermore, the abolishment of the effects on these physiological processes caused by ectopic expression of miR-9 ASOs suggested the necessity of miR-9 in MALAT-1 regulation. Here we found that the high dose of E2 treatment upregulated miR-9 thus posttranscriptionally regulated MALAT-1 RNA level in OS cells, and then the downregulation of MALAT-1 inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) processes in the E2-dose dependent and ER-independent ways. - Highlights: • E2 affects osteosarcoma cell MG-63 in an Estrogen receptor-independent way. • High dose of E2 treatment upregulates miR-9 which target to MALAT-1 RNA. • Upregulated miR-9 degrades MALAT-1 and thus affects combination of SFPQ/PTBP2. • E2 treatment block cell proliferation, colony formation, mobility, and enhance apoptosis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Stable knockdown of Kif5b in MDCK cells leads to epithelial–mesenchymal transition

Polarization of epithelial cells requires vectorial sorting and transport of polarity proteins to apical or basolateral domains. Kif5b is the mouse homologue of the human ubiquitous Kinesin Heavy Chain (uKHC). To investigate the function of Kif5b in epithelial cells, we examined the phenotypes of Kif5b-deficient MDCK cells. Stable knockdown of Kif5b in MDCK cells resulted in reduced cell proliferation rate, profound changes in cell morphology, loss of epithelial cell marker, and gain of mesenchymal marker, as well as increased cell migration, invasion, and tumorigenesis abilities. E-cadherin and NMMIIA could interact with Kif5b in polarized MDCK cells, and their expression levels were decreased in Kif5b-deficient MDCK cells. Overexpression of E-cadherin and NMMIIA in Kif5b depleted MDCK cells could decrease mesenchymal marker expression and cell migration ability. These results indicate that stable knockdown of Kif5b in MDCK cells can lead to epithelial–mesenchymal transition, which is mediated by defective E-cadherin and NMMIIA expression. - Highlights: • Knockdown of Kif5b in MDCK cells resulted in reduced cell proliferation rate. • Kif5b deficient MDCK cells underwent epithelial–mesenchymal transition. • E-cadherin and NMMIIA could interact with Kif5b in polarized MDCK cells. • Decreased E-cadherin and NMMIIA levels mediate EMT in Kif5b deficient MDCK cells. • Overexpression of E-cadherin and NMMIIA reverse the effects of Kif5b knockdown.

60 APPLIED LIFE SCIENCES↗