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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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DOE OSTI2017

SAHA-induced TRAIL-sensitisation of Multiple Myeloma cells is enhanced in 3D cell culture

Background: Multiple Myeloma (MM) is currently incurable despite many novel therapies. Tumour Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) is a potential anti-tumour agent although effects as a single agent are limited. In this study, we investigated whether the Histone Deacetylase (HDAC) inhibitor SAHA can enhance TRAIL-induced apoptosis and target TRAIL resistance in both suspension culture, and 3D cell culture as a model of disseminated MM lesions that form in bone. Methods: The effects of SAHA and/or TRAIL in 6 Multiple Myeloma cell lines were assessed in both suspension cultures and in an Alginate-based 3D cell culture model. The effect of SAHA and/or TRAIL was assessed on apoptosis by assessment of nuclear morphology using Hoechst 33342/Propidium Iodide staining. Viable cell number was assessed by CellTiter-Glo luminescence assay, Caspase-8 and -9 activities were measured by Caspase-Glo™ assay kit. TRAIL-resistant cells were generated by culture of RPMI 8226 and NCI-H929 by acute exposure to TRAIL followed by selection of TRAIL-resistant cells. Results: TRAIL significantly induced apoptosis in a dose-dependent manner in OPM-2, RPMI 8226, NCI-H929, U266, JJN-3 MM cell lines and ADC-1 plasma cell leukaemia cells. SAHA amplified TRAIL responses in all lines except OPM-2, and enhanced TRAIL responses were both via Caspase-8 and -9. SAHA treatment induced growth inhibition that further increased in the combination treatment with TRAIL in MM cells. The co-treatment of TRAIL and SAHA reduced viable cell numbers all cell lines. TRAIL responses were further potentiated by SAHA in 3D cell culture in NCI-H929, RPMI 8226 and U266 at lower TRAIL + SAHA doses than in suspension culture. However TRAIL responses in cells that had been selected for TRAIL resistance were not further enhanced by SAHA treatment. Conclusions: SAHA is a potent sensitizer of TRAIL responses in both TRAIL sensitive and resistant cell lines, in both suspension and 3D culture, however SAHA did not sensitise TRAIL-sensitive cell populations that had been selected for TRAIL-resistance from initially TRAIL-sensitive populations. SAHA may increase TRAIL sensitivity in insensitive cells, but not in cells that have specifically been selected for acquired TRAIL-resistance. - Highlights: • The HDAC inhibitor SAHA sensitised Myeloma cells to TRAIL-induced apoptosis. • TRAIL, SAHA and combination apoptotic responses are potentiated in 3D cell culture. • TRAIL-resistant cells are not further sensitised to TRAIL-induced apoptosis by SAHA.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2024

Heparan sulfate promotes TRAIL-induced tumor cell apoptosis

TRAIL (TNF-related apoptosis-inducing ligand) is a potent inducer of tumor cell apoptosis through TRAIL receptors. While it has been previously pursued as a potential anti-tumor therapy, the enthusiasm subsided due to unsuccessful clinical trials and the fact that many tumors are resistant to TRAIL. In this report, we identified heparan sulfate (HS) as an important regulator of TRAIL-induced apoptosis. TRAIL binds HS with high affinity (K D = 73 nM) and HS induces TRAIL to form higher-order oligomers. The HS-binding site of TRAIL is located at the N-terminus of soluble TRAIL, which includes three basic residues. Binding to cell surface HS plays an essential role in promoting the apoptotic activity of TRAIL in both breast cancer and myeloma cells, and this promoting effect can be blocked by heparin, which is commonly administered to cancer patients. We also quantified HS content in several lines of myeloma cells and found that the cell line showing the most resistance to TRAIL has the least expression of HS, which suggests that HS expression in tumor cells could play a role in regulating sensitivity towards TRAIL. We also discovered that death receptor 5 (DR5), TRAIL, and HS can form a ternary complex and that cell surface HS plays an active role in promoting TRAIL-induced cellular internalization of DR5. Combined, our study suggests that TRAIL-HS interactions could play multiple roles in regulating the apoptotic potency of TRAIL and might be an important point of consideration when designing future TRAIL-based anti-tumor therapy.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Antihypertensive drug-candesartan attenuates TRAIL resistance in human lung cancer via AMPK-mediated inhibition of autophagy flux

Highlights: • Candesartan sensitizes lung adenocarcinoma to TRAIL via targeting TRAIL-DR5. • Autophagy inhibition by candesartan recruit DR5, induces TRAIL mediated caspase cascade. • Candesartan down regulate cFLIP, attenuates TRAIL resistance to lung adenocarcinoma. • Candesartan synergistic to TRAIL for patients presenting both hypertension and cancer. Angiotensin II type 1 receptor blockers (ARBs) are widely used as antihypertensive drugs. Candesartan is an ARB that has also been known for its anticancer effects but the exact molecular mechanism is remaining elusive. In this research, we showed for the first time that candesartan treatment significantly sensitized human lung adenocarcinoma cells to Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis by targeting TRAIL-DR5. TRAIL selectively kills cancer cells by binding to death receptors on the cell membrane, beyond the levels causing minimal toxicity in normal cells. However, some non-small-cell lung carcinoma (NSCLC) patients are resistant to TRAIL treatment in clinical trials due to inactivation of the death receptors during cytoprotective autophagy. The molecular mechanisms underlying candesartan-induced TRAIL-mediated apoptosis involved the downstream of AMPK phosphorylation resulting inhibition of autophagy flux, recruitment of death receptor 5 (DR5) and activation of apoptotic caspase cascade. Candesartan treatment also inhibits the expression of anti-apoptotic protein c-FLIP. Furthermore, blocking DR5 signaling using DR5 siRNA negatively regulated the apoptotic pathway and also induced autophagy flux, demonstrating the cytoprotective role of autophagy responsible for treatment resistance. This suggests that candesartan can be used to sensitize tumors to TRAIL treatment and may represent a useful strategy for human adenocarcinoma patients to overcome TRAIL resistance. Candesartan in combination with TRAIL also could be a novel therapeutic treatment for patients presenting both conditions of hypertension and lung cancer.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2017

CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis

Highlights: • EAC cells express all three decoy receptors of TRAIL. • CCN1 is barely detectable in EAC cells. • CCN1 inhibits expression of TRAIL decoy receptors in EAC cells. • CCN1 induces apoptosis in EAC cells. • TRAIL mediates CCN1-induced EAC cell apoptosis. TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors. A second molecule is needed to help TRAIL to complete its mission. Finding such molecules now becomes a top priority in cancer research. Our study shows that CCN1 is such a molecule. CCN1 was highly expressed in the esophageal epithelium of the patients suffering from gastroesophageal reflux disease, but faded away as the situation worsened towards adenocarcinoma. Treating the tumor cells with CCN1 resulted in apoptosis, while the same treatment to the normal cells only nourished cell growth. It was TRAIL that mediated this process. Apparently, CCN1 altered the expression profile of TRAIL and its receptors in tumor cells, namely, activating TRAIL and its death receptors and shutting down its decoy receptors. CCN1 and TRAIL worked as a team to put the cancer cells to death, as elimination of either one failed apoptosis.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2014

Electricity Transmission, Pipelines, and National Trails: An Analysis of Current and Potential Intersections on Federal Lands in the Eastern United States, Alaska, and Hawaii

As has been noted in many reports and publications, acquiring new or expanded rights-of-way for transmission is a challenging process, because numerous land use and land ownership constraints must be overcome to develop pathways suitable for energy transmission infrastructure. In the eastern U.S., more than twenty federally protected national trails (some of which are thousands of miles long, and cross many states) pose a potential obstacle to the development of new or expanded electricity transmission capacity. However, the scope of this potential problem is not well-documented, and there is no baseline information available that could allow all stakeholders to study routing scenarios that could mitigate impacts on national trails. This report, Electricity Transmission, Pipelines, and National Trails: An Analysis of Current and Potential Intersections on Federal Lands in the Eastern United States, was prepared by the Environmental Science Division of Argonne National Laboratory (Argonne). Argonne was tasked by DOE to analyze the “footprint” of the current network of National Historic and Scenic Trails and the electricity transmission system in the 37 eastern contiguous states, Alaska, and Hawaii; assess the extent to which national trails are affected by electrical transmission; and investigate the extent to which national trails and other sensitive land use types may be affected in the near future by planned transmission lines. Pipelines are secondary to transmission lines for analysis, but are also within the analysis scope in connection with the overall directives of Section 368 of the Energy Policy Act of 2005, and because of the potential for electrical transmission lines being collocated with pipelines. Based on Platts electrical transmission line data, a total of 101 existing intersections with national trails on federal land were found, and 20 proposed intersections. Transmission lines and pipelines are proposed in Alaska; however there are no locations that intersect national trails. Source data did not indicate any planned transmission lines or pipelines in Hawaii. A map atlas provides more detailed mapping of the topics investigated in this study, and the accompanying GIS database provides the baseline information for further investigating locations of interest. In many cases the locations of proposed transmission lines are not accurately mapped (or a specific route may not yet be determined), and accordingly the specific crossing locations are speculative. However since both national trails and electrical transmission lines are long linear systems, the characteristics of the crossings reported in this study are expected to be similar to both observed characteristics of the existing infrastructure provided in this report, and of the new infrastructure if these proposed projects are built. More focused study of these siting challenges is expected to mitigate some of potential impacts by choosing routes that minimize or eliminate them. The current study primarily addresses a set of screening-level characterizations that provide insights into how the National Trail System may influence the siting of energy transport facilities in the states identified under Section 368(b) of the Energy Policy Act of 2005. As such, it initializes gathering and beginning analysis of the primary environmental and energy data, and maps the contextual relationships between an important national environmental asset and how this asset intersects with energy planning activities. Thus the current study sets the stage for more in-depth analyses and data development activities that begin to solve key transmission siting constraints. Our recommendations for future work incorporate two major areas: (1) database development and analytics and (2) modeling and scenario analysis for energy planning. These recommendations provide a path forward to address key issues originally developed under the Energy Policy Act of 2005 that are now being carried forward under the President’s Climate Action Plan.

29 ENERGY PLANNING, POLICY, AND ECONOMY↗

DOE OSTI2018

Chaetospirolactone reverses the apoptotic resistance towards TRAIL in pancreatic cancer

Highlights: • CSL reverses TRAIL-mediated apoptotic resistance. • DR4 is induced by CSL. • H3 lysine 27 trimethylation by EZH2 is inhibited by CSL. The pancreatic cancer is one of the most aggressive tumors. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can trigger apoptosis by interaction with death receptors. However, in TRAIL-resistant pancreatic cancer, responsiveness to TRAIL treatment is terribly poor. In current work, we have demonstrated that a natural product chaetospirolactone (CSL) isolated from an endophytic fungus Chaetomium sp. NF00754 can enhance the susceptibility of TRAIL-resistant pancreatic cancer cells to apoptosis. CSL can induce apoptosis in TRAIL-treated pancreatic cancer cells. Furthermore, combined CSL and TRAIL treatment significantly inhibits viability and migration of pancreatic cancer cells. Combinatorial TRAIL and CSL treatment repressed xenograft tumor growth without substantially toxic side effects. CSL can specifically upregulate expression of death receptor 4 (DR4). Further study revealed that CSL represses the activities of an epigenetic regulator enhancer of zeste homolog 2 (EZH2) and consistently reduces histone H3 lysine 27 trimethylation (H3K27me3) to allow DR4 transcription. Taken together, CSL treatment may reverse TRAIL resistance in pancreatic cancer cells via epigenetic regulation of DR4 implying that administration of CSL might represent a putative strategy for pancreatic cancer therapy.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2014

Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells

Glioblastoma multiforme (GBM) is the most lethal and aggressive astrocytoma of primary brain tumors in adults. Although there are many clinical trials to induce the cell death of glioblastoma cells, most glioblastoma cells have been reported to be resistant to TRAIL-induced apoptosis. Here, we showed that gingerol as a major component of ginger can induce TRAIL-mediated apoptosis of glioblastoma. Gingerol increased death receptor (DR) 5 levels in a p53-dependent manner. Furthermore, gingerol decreased the expression level of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and increased pro-apoptotic protein, Bax and truncate Bid, by generating reactive oxygen species (ROS). We also found that the sensitizing effects of gingerol in TRAIL-induced cell death were blocked by scavenging ROS or overexpressing anti-apoptotic protein (Bcl-2). Therefore, we showed the functions of gingerol as a sensitizing agent to induce cell death of TRAIL-resistant glioblastoma cells. This study gives rise to the possibility of applying gingerol as an anti-tumor agent that can be used for the purpose of combination treatment with TRAIL in TRAIL-resistant glioblastoma tumor therapy. - Highlights: • Most GBM cells have been reported to be resistant to TRAIL-induced apoptosis. • Gingerol enhances the expression level of anti-apoptotic proteins by ROS. • Gingerol enhances TRAIL-induced apoptosis through actions on the ROS–Bcl2 pathway.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2015

Autophagy-mediated degradation of IAPs and c-FLIP L potentiates apoptosis induced by combination of TRAIL and Chal-24

Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. In this paper, we report that combination of the recently identified novel chalcone derivative, chalcone-24 (Chal-24), and TNF-related apoptosis-inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal-24 treatment significantly enhanced TRAIL-induced activation of caspase-8 and caspase-3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan-caspase inhibitor z-VAD-fmk. Chal-24 and TRAIL combination suppressed expression of cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein large (c-FLIPL) and cellular inhibitor of apoptosis proteins (c-IAPs), and ectopic expression of c-FLIPL and c-IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal-24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal-24 and TRAIL combination, which was associated with attenuation of c-FLIPL and c-IAPs degradation. In conclusion, these results suggest that Chal-24 potentiates the anticancer activity of TRAIL through autophagy-mediated degradation of c-FLIPL and c-IAPs, and that combination of Chal-24 and TRAIL could be an effective approach in improving chemotherapy efficacy.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2015

Fiscal Year 2013 Trails Management Program Mitigation Action Plan Annual Report, October 2013

This Trails Management Program Mitigation Action Plan Annual Report (Trails MAPAR) has been prepared for the Department of Energy (DOE)/National Nuclear Security Administration (NNSA) as part of implementing the 2003 Final Environmental Assessment for the Proposed Los Alamos National Laboratory Trails Management Program (DOE 2003). The Trails Mitigation Action Plan (MAP) is now a part of the Site-Wide Environmental Impact Statement for the Continued Operation of Los Alamos National Laboratory (DOE/EIS 0380) Mitigation Action Plan (2008 SWEIS MAP) (DOE 2008). The MAP provides guidance for the continued implementation of the Trails Management Program at Los Alamos National Laboratory (LANL) and integration of future mitigation actions into the 2008 SWEIS MAP to decrease impacts associated with recreational trails use at LANL. This eighth MAPAR includes a summary of Trails Management Program activities and actions during Fiscal Year (FY) 2013, from October 2012 through September 2013.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2014

Development of TRAIL Resistance by Radiation-Induced Hypermethylation of DR4 CpG Island in Recurrent Laryngeal Squamous Cell Carcinoma

Purpose: There are limited therapeutic options for patients with recurrent head and neck cancer after radiation therapy failure. To assess the use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) as a salvage chemotherapeutic agent for recurrent cancer after radiation failure, we investigated the effect of clinically relevant cumulative irradiation on TRAIL-induced apoptosis. Methods and Materials: Using a previously established HN3 cell line from a laryngeal carcinoma patient, we generated a chronically irradiated HN3R isogenic cell line. Viability and apoptosis in HN3 and HN3R cells treated with TRAIL were analyzed with MTS and PI/annexin V-FITC assays. Western blotting and flow cytometry were used to determine the underlying mechanism of TRAIL resistance. DR4 expression was semiquantitatively scored in a tissue microarray with 107 laryngeal cancer specimens. Methylation-specific polymerase chain reaction and bisulfite sequencing for DR4 were performed for genomic DNA isolated from each cell line. Results: HN3R cells were more resistant than HN3 cells to TRAIL-induced apoptosis because of significantly reduced levels of the DR4 receptor. The DR4 staining score in 37 salvage surgical specimens after radiation failure was lower in 70 surgical specimens without radiation treatment (3.03 ± 2.75 vs 5.46 ± 3.30, respectively; P<.001). HN3R cells had a methylated DR4 CpG island that was partially demethylated by the DNA demethylating agent 5-aza-2′-deoxycytidine. Conclusion: Epigenetic silencing of the TRAIL receptor by hypermethylation of a DR4 CpG island might be an underlying mechanism for TRAIL resistance in recurrent laryngeal carcinoma treated with radiation.

62 RADIOLOGY AND NUCLEAR MEDICINE↗

DOE OSTI2015

α-Hispanolol sensitizes hepatocellular carcinoma cells to TRAIL-induced apoptosis via death receptor up-regulation

Hispanolone derivatives have been previously described as anti-inflammatory and antitumoral agents. However, their effects on overcoming Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance remain to be elucidated. In this study, we analyzed the cytotoxic effects of the synthetic hispanolone derivative α-hispanolol (α-H) in several tumor cell lines, and we evaluated the induction of apoptosis, as well as the TRAIL-sensitizing potential of α-H in the hepatocellular carcinoma cell line HepG2. Our data show that α-H decreased cell viability in a dose-dependent manner in HeLa, MDA-MB231, U87 and HepG2 cell lines, with a more prominent effect in HepG2 cells. Interestingly, α-H had no effect on non-tumoral cells. α-H induced activation of caspase-8 and caspase-9 and also increased levels of the proapoptotic protein Bax, decreasing antiapoptotic proteins (Bcl-2, X-IAP and IAP-1) in HepG2 cells. Specific inhibition of caspase-8 abrogated the cascade of caspase activation, suggesting that the extrinsic pathway has a critical role in the apoptotic events induced by α-H. Furthermore, combined treatment of α-H with TRAIL enhanced apoptosis in HepG2 cells, activating caspase-8 and caspase-9. This correlated with up-regulation of both the TRAIL death receptor DR4 and DR5. DR4 or DR5 neutralizing antibodies abolished the effect of α-H on TRAIL-induced apoptosis, suggesting that sensitization was mediated through the death receptor pathway. Our results demonstrate that α-H induced apoptosis in the human hepatocellular carcinoma cell line HepG2 through activation of caspases and induction of the death receptor pathway. In addition, we describe a novel function of α-H as a sensitizer on TRAIL-induced apoptotic cell death in HepG2 cells. - Highlights: • α-Hispanolol induced apoptosis in the human hepatocellular carcinoma cell line HepG2. • α-Hispanolol induced activation of caspases and the death receptor pathway. • α-Hispanolol enhanced TRAIL-induced apoptosis through upregulation of death receptors.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2015

Interferon-α and cyclooxygenase-2 inhibitor cooperatively mediates TRAIL-induced apoptosis in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. Interferon-alpha (IFN-α) has recently been recognized to harbor therapeutic potential in the prevention and treatment of HCC, but it remains controversial as to whether IFN-α exerts direct cytotoxicity against HCC. Cyclooxygenase-2 (COX-2) is overexpressed in HCC and is considered to play a role in hepatocarcinogenesis. Therefore, we aimed to elucidate the combined effect of a COX-2 inhibitor, celecoxib, and IFN-α on in vitro growth suppression of HCC using the hepatoma cell line HLCZ01 and the in vivo nude mouse xenotransplantation model using HLCZ01 cells. Treatment with celecoxib and IFN-α synergistically inhibited cell proliferation in a dose- and time-dependent manner. Apoptosis was identified by 4',6-diamidino-2-phenylindole dihydrochloride and fluorescent staining. IFN-α upregulated the expression of TRAIL, while celecoxib increased the expression of TRAIL receptors. The combined regimen with celecoxib and IFN-α reduced the growth of xenotransplanted HCCs in nude mice. The regulation of IFN-α- and COX-2 inhibitor-induced cell death is impaired in a subset of TRAIL-resistant cells. The molecular mechanisms of HCC cells resistant to TRAIL-induced apoptosis were explored using molecular biological and immunological methods. Interferon-α and the COX-2 inhibitor celecoxib synergistically increased TRAIL-induced apoptosis in hepatocellular carcinoma. These data suggest that IFN-α and celecoxib may offer a novel role with important implications in designing new therapeutics for TRAIL-resistant tumors. - Highlights: ●The cytotoxic effect of TRAIL on a developed HCC HLCZ01 cells infected with HBV. ●IFN-α and celecoxib induced apoptosis in HLCZ01 cells infected with HBV. ●The combined regime reduced the growth of xenotransplanted HCCs in nude mice model.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2014

DRBE comet trails

Re-examination of the Cosmic Background Explorer Diffuse Infrared Background Experiment (DIRBE) data reveals the thermal emission of several comet dust trails. The dust trails of 1P/Halley, 169P/NEAT, and 3200 Phaethon have not been previously reported. The known trails of 2P/Encke and 73P/Schwassmann–Wachmann 3 are also seen. The dust trails have 12 and 25 μm surface brightnesses of <0.1 and <0.15 MJy sr{sup −1}, respectively, which is <1% of the zodiacal light intensity. The trails are very difficult to see in any single daily image of the sky, but are evident as rapidly moving linear features in movies of the DIRBE data. Some trails are clearest when crossing through the orbital plane of the parent comet, but others are best seen at high ecliptic latitudes as the Earth passes over or under the dust trail. All these comets have known associations with meteor showers. This re-examination also reveals 1 additional comet and 13 additional asteroids that had not previously been recognized in the DIRBE data.

79 ASTRONOMY AND ASTROPHYSICS↗

DOE OSTI2017

Aggregation-fragmentation-diffusion model for trail dynamics

We investigate statistical properties of trails formed by a random process incorporating aggregation, fragmentation, and diffusion. In this stochastic process, which takes place in one spatial dimension, two neighboring trails may combine to form a larger one, and also one trail may split into two. In addition, trails move diffusively. The model is defined by two parameters which quantify the fragmentation rate and the fragment size. In the long-time limit, the system reaches a steady state, and our focus is the limiting distribution of trail weights. We find that the density of trail weight has power-law tail P(w)~w –γ for small weight w. We obtain the exponent γ analytically and find that it varies continuously with the two model parameters. In conclusion, the exponent γ can be positive or negative, so that in one range of parameters small-weight trails are abundant and in the complementary range they are rare.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗

DOE OSTI2016

Electricity Transmission, Pipelines, and National Trails: An Analysis of Current and Potential Intersections on Federal Lands in the Eastern United States, Alaska, and Hawaii

24 POWER TRANSMISSION AND DISTRIBUTION↗

DOE OSTI2015

Trails Management at LANL - A Presentation to the Los Alamos County Parks and Recreation Board

Los Alamos National Laboratory’s (LANL) trail management program goals include reduce risk of damage and injury to property, human life, and health, and sensitive natural and cultural resources from social trail use at LANL, facilitate the establishment of a safe viable network of linked trails, maintain security of LANL operations, and many more, respect the wishes of local Pueblos, adapt trail use to changing conditions in a responsive manner, and maintain the recreational functionality of the DOE lands. There are approximately 30 miles of LANL trails. Some are open to the public and allow bicycles, horses, hikers, and runners. Know the rules of the trails to stay safe.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2016

Trails at LANL - Public Meeting and Forum - July 26, 2016

These are the slides of a meeting about trails at Los Alamos National Laboratory. The meeting goals are the folllowing: to inform and educate citizens about LANL trails management issues that include resource protection, safety, security and trails etiquette; to explain how and why LANL trails can be closed and reopened; and to understand your concerns and ideas about LANL trails use.

99 GENERAL AND MISCELLANEOUS↗

DOE OSTI2023

Demonstration of object location, classification, and characterization by developed deep learning dust ablation trail analysis code package using plasma jets

Based on deep learning, a Dust Ablation Trail Analysis (DATA) code package is developed to detect dust ablation trails in tokamaks, which is intended to analyze a large amount data of tokamak dusts. To validate and benchmark the DATA code package, 2440 plasma jet images are exploited for the training and test of the deep learning DATA code package, since plasma jets resemble the shape and size of dust ablation clouds in tokamaks. After being trained by 1920 plasma jet images, the DATA code package is able to locate 100% plasma jets, classify plasma jets with the accuracy of >99.9%, and output image skeleton information for classified plasma jets. The DATA code package trained by the plasma jet images is also used to analyze the dust ablation trails captured in the Experimental Advanced Superconducting (EAST) tokamak with the satisfactory performance, further verifying its applicability in the fusion dust ablation investigation. Based on its excellent performance presented here, it is demonstrated that our DATA code package is able to automatically identify and analyze dust ablation trails in tokamaks, which can be used for further detailed investigations, such as the three-dimensional reconstruction of dusts and their ablation trails.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗