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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

Low-speed wind-tunnel investigation of forward-located spoilers and trailing splines as trailing-vortex hazard-alleviation devices on an aspect-ratio-8 wing model

An investigation was made in the Langley V/STOL tunnel in order to determine, by the trailing-wing sensor technique, the effectiveness of either a forward-mounted spoiler or a tip-mounted spline as trailing-vortex attenuation devices on an unswept aspect-ratio-8 wing model. The trailing-wing rolling-moment data taken in the tunnel diffuser section show good agreement with the data taken in the tunnel test section. This agreement indicates that reasonable results may be obtained in the Langley V/STOL tunnel in experimental investigations of the trailing-vortex hazard at relatively great distances behind aircraft models.

Croom, D. R.↗

Equations and charts for the rapid estimation of hinge-moment and effectiveness parameters for trailing-edge controls having leading and trailing edges swept ahead of the Mach lines

Existing conical-flow solutions have been used to calculate the hinge-moments and effectiveness parameters of trailing-edge controls having leading and trailing edges swept ahead of the Mach lines and having streamwise root and tip chords. Equations and detailed charts are presented for the rapid estimation of these parameters. Also included is an approximate method by which these parameters may be corrected for airfoil-section thickness.

Goin, Kennith L↗

Cold-air annular-cascade investigation of aerodynamic performance of core-engine-cooled turbine vanes. 2: Pressure surface trailing edge ejection and split trailing edge ejection

The aerodynamic performance of two trailing edge ejection cooling configurations of a core-engine stator vane were experimentally determined in an ambient inlet-air full-annular cascade where three-dimensional effects could be obtained. The tests were conducted at the design mean-radius ideal aftermixed critical velocity ratio of 0.778. Overall vane aftermixed thermodynamic and primary efficiencies were obtained over a range of coolant flows to about 10 percent of the primary flow at a primary to coolant total temperature ratio of 1.0. The radial variation in efficiency and the circumferential and radial variations in vane-exit total pressure were determined. Comparisons are made with the solid (uncooled) vane.

Mclallin, K. L.↗

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↗

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↗

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↗

Effect of trailing edge geometry and thickness on the performance of certain turbine stator blading

The experimental and analytical investigation included solid blades with five different trailing-edge thicknesses and four different trailing-edge geometries. One of the geometries was round, one was square, one was tapered from the suction surface, and the other tapered from the pressure surface. One of the trailing-edge thicknesses was sharp edged; the other four thicknesses were equivalent to about 5, 11, 16, and 20 percent of the blade throat width. The experimental results show increased efficiency loss for increased trailing-edge thickness for all trailing-edge geometries. The blade with round trailing edge, equal to about 11 percent of the blade throat width, had 60 percent more loss than the sharp-edged blade. For the same trailing-edge thickness, square trailing edges caused more loss than round trailing edges, and the tapered trailing edges caused about the same loss as the round trailing edges.

Prust, H. W., Jr.↗

Global Variation of Meteor Trail Plasma Turbulence

We present the first global simulations on the occurrence of meteor trail plasma irregularities. These results seek to answer the following questions: when a meteoroid disintegrates in the atmosphere will the resulting trail become plasma turbulent, what are the factors influencing the development of turbulence, and how do they vary on a global scale. Understanding meteor trail plasma turbulence is important because turbulent meteor trails are visible as non-specular trails to coherent radars, and turbulence influences the evolution of specular radar meteor trails, particularly regarding the inference of mesospheric temperatures from trail diffusion rates, and their usage for meteor burst communication. We provide evidence of the significant effect that neutral atmospheric winds and density, and ionospheric plasma density have on the variability of meteor trail evolution and the observation of nonspecular meteor trails, and demonstrate that trails are far less likely to become and remain turbulent in daylight, explaining several observational trends using non-specular and specular meteor trails.

Dyrud, L. P.↗

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↗

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↗

The Effect of Nozzle Trailing Edge Thickness on Jet Noise

The effect of nozzle trailing edge thickness on broadband acoustic radiation and the production of tones is investigated for coannular nozzles. Experiments were performed for a core nozzle trailing edge thickness between 0.38 mm and 3.17 mm. The on-set of discrete tones was found to be predominantly affected by the velocity ratio, the ratio of the fan velocity to the core velocity, although some dependency on trailing edge thickness was also noted. For a core nozzle trailing edge thickness greater than or equal to 0.89 mm, tones were produced for velocity ratios between 0.91 and 1.61. For a constant nozzle trailing edge thickness, the frequency varied almost linearly with the core velocity. The Strouhal number based on the core velocity changed with nozzle trailing edge thickness and varied between 0.16 and 0.2 for the core nozzles used in the experiments. Increases in broadband noise with increasing trailing edge thickness were observed for tone producing and non-tone producing conditions. A variable thickness trailing edge (crenellated) nozzle resulted in no tonal production and a reduction of the broadband trailing edge noise relative to that of the corresponding constant thickness trailing edge.

Henderson, Brenda↗