A wall interference assessment/correction system

A Wall Signature method originally developed by Hackett was selected to be adapted for the Ames 12-ft Wind Tunnel Wall Interference Assessment/Correction (WIAC) System in the project. This method uses limited measurements of the static pressure at the wall, in conjunction with the solid wall boundary condition, to determine the strength and distribution of singularities representing the test article. The singularities are used in turn for estimating wall interference at the model location. The lifting interference will be treated separately by representing in a horseshoe vortex system for the model's lifting effects. The development and implementation of a working prototype will be completed, delivered, and documented with a software manual. The WIAC code will be validated by conducting numerically simulated experiments rather than actual wind tunnel experiments. The simulations will be used to generate both free-air and confined wind-tunnel flow fields for each of the test articles over a range of test configurations. Specifically, the pressure signature at the test section wall will be computed for the tunnel case to provide the simulated 'measured' data. These data will serve as the input for the WIAC method - Wall Signature method. The performance of the WIAC method then may be evaluated by comparing the corrected parameters with those for the free-air simulation. The following two additional tasks are included in the supplement No. 1 to the basic Grant. On-line wall interference calculation: The developed wall signature method (modified Hackett's method) for Ames 12-ft Tunnel will be the pre-computed coefficients which facilitate the on-line calculation of wall interference; and support system effects estimation: The effects on the wall pressure measurements due to the presence of the model support systems will be evaluated

Development of an intelligent hypertext manual for the space shuttle hazardous gas detection system

A computer-based Integrated Knowledge System (IKS), the Intelligent Hypertext Manual (IHM), is being developed for the Space Shuttle Hazardous Gas Detection System (HGDS) at the Huntsville Operations Support Center (HOSC). The IHM stores all HGDS related knowledge and presents them in an interactive and intuitive manner. The IHM's purpose is to provide HGDS personnel with the capabilities of: enhancing the interpretation of real time data; recognizing and identifying possible faults in the Space Shuttle sub-system related to hazardous gas detections; locating applicable documentation related to procedures, constraints, and previous fault histories; and assisting in the training of personnel

A wall interference assessment/correction system

A Wall Signature method, the Hackett method, has been selected to be adapted for the 12-ft Wind Tunnel wall interference assessment/correction (WIAC) system in the present phase. This method uses limited measurements of the static pressure at the wall, in conjunction with the solid wall boundary condition, to determine the strength and distribution of singularities representing the test article. The singularities are used in turn for estimating wall interferences at the model location. The Wall Signature method will be formulated for application to the unique geometry of the 12-ft Tunnel. The development and implementation of a working prototype will be completed, delivered and documented with a software manual. The WIAC code will be validated by conducting numerically simulated experiments rather than actual wind tunnel experiments. The simulations will be used to generate both free-air and confined wind-tunnel flow fields for each of the test articles over a range of test configurations. Specifically, the pressure signature at the test section wall will be computed for the tunnel case to provide the simulated 'measured' data. These data will serve as the input for the WIAC method-Wall Signature method. The performance of the WIAC method then may be evaluated by comparing the corrected parameters with those for the free-air simulation. Each set of wind tunnel/test article numerical simulations provides data to validate the WIAC method. A numerical wind tunnel test simulation is initiated to validate the WIAC methods developed in the project. In the present reported period, the blockage correction has been developed and implemented for a rectangular tunnel as well as the 12-ft Pressure Tunnel. An improved wall interference assessment and correction method for three-dimensional wind tunnel testing is presented in the appendix

Supersonic laminar flow control research

The objective of this research is to understand supersonic laminar flow stability, transition and active control. Some prediction techniques will be developed or modified to analyze laminar flow stability. The effects of distributed heating and cooling as an active boundary layer control technique will be studied. The primary tasks of the research apply to the NASA/Ames PoC and LFSWT's nozzle design with laminar flow control and are listed as follows: (1) predictions of supersonic laminar boundary layer stability and transition; (2) effects of wall heating and cooling on supersonic laminar flow control; (3) performance evaluation of the PoC and LFSWT nozzle designs with wall heating and cooling applied at different locations and various lengths; and (4) effects of a conducted -vs- pulse wall temperature distribution for the LFSWT

A wall interference assessment/correction system

A Wall Signature method originally developed by Hackett has been selected to be adapted for the Ames 12-ft Wind Tunnel WIAC system in the project. This method uses limited measurements of the static pressure at the wall, in conjunction with the solid wall boundary condition, to determine the strength and distribution of singularities representing the test article. The singularities are used in turn for estimating blockage wall interference. The lifting interference will be treated separately by representing in a horseshoe vortex system for the model's lifting effects. The development and implementation of a working prototype will be completed, delivered and documented with a software manual. The WIAC code will be validated by conducting numerically simulated experiments rather than actual wind tunnel experiments. The simulations will be used to generate both free-air and confined wind-tunnel flow fields for each of the test articles over a range of test configurations. Specifically, the pressure signature at the test section wall will be computed for the tunnel case to provide the simulated 'measured' data. These data will serve as the input for the WIAC method--Wall Signature method. The performance of the WIAC method then may be evaluated by comparing the corrected data with those of the free-air simulation

Ordovician 40Ar/39Ar phengite ages from the blueschist-facies Ondor Sum subduction-accretion complex (Inner Mongolia) and implications for the early Paleozoic history of continental blocks in China and adjacent areas

We obtained 453.2 ± 1.8 Ma and 449.4 ± 1.8 Ma (2{sigma}) laser step-heating 40Ar/39Ar plateau ages for phengite from quartzite mylonites from the blueschist-facies Ondor Sum subduction-accretion complex in Inner Mongolia (northern China). These ages are within error of the inverse isochron ages calculated using the plateau steps and the weighted mean ages of total fusion of single grains. The compositional change from glaucophane in the cores to crossite in the rims of blue amphiboles, as revealed by electron microprobe analysis, points to decompression, probably caused by progressive exhumation of the subducted material. The Late Ordovician ages were not affected by excess argon incorporation because in all likelihood the oceanic sediments were wet on arrival at the trench and free of older detrital mica. The ca. 450 Ma ages are, hence, interpreted as the time of crystallization during mylonitization under high fluid activity at fairly low temperatures. This means that accretion of the quartzite mylonite unit occured about 200 Ma before final closure of the Paleo-Asian Ocean, amalgamation of the Siberian, Tarim and North China cratons, and formation of the end-Permian Solonker suture zone. We argue that the Early Paleozoic evolution of the Ondor Sum complex occurred along the northeastern Cimmerian margin of Gondwana, which was composed of micro-continents fringed by subduction-accretion complexes and island arcs. The later evolution took place during the building of the Eurasian continent following middle Devonian and younger rifting along the East Gondwanan margin and northward drift of the detached North China craton. An extensive review shows that this type of two-stage scenario probably also applies to the geodynamic evolution of other micro-continents like, South China, Tarim, a number of Kazakh terranes, Alashan, Qaidam and Kunlun, as well as South Kitakami and correlatives in Japan, and probably Indochina. Like the North China craton, these were bordered by Early Paleozoic subduction-accretion complexes, island arcs or contained calc-alkaline volcanic margins, like for example, the central Tienshan, North Qinling, North Qaidam-Altun, North Qilian and Kunlun belts in China, as well as the Oeyama and Miyamori ophiolites and Matsugadaira-Motai blueschist belt of Japan and the dismembered Sergeevka ophiolite of the southern part of the Russian Far East. This implies that a vast orogenic system, comprising an archipelago of micro-continents, seems to have existed along the Cimmerian margin of East Gondwana in Early Paleozoic time in which the ultrahigh-pressure metamorphism that characterizes the early evolution of many of the Asian micro-continents occurred

A positive feedback loop of IL-17B-IL-17RB activates ERK/β-catenin to promote lung cancer metastasis

Inflammation contributes to the development and progression of cancer. Interleukin-17 (IL-17) is an inflammatory cytokine that functions in inflammation and cancer, as well as several other cellular processes. In this study, we investigated the roles and the prognostic value of IL-17 and the IL-17 receptor (IL-17R) in lung cancer. Gene expression microarray analysis followed by Kaplan-Meier survival curve showed that IL-17B was associated with poor patient survival, and IL-17B receptor (IL-17RB) was up-regulated in lung cancer tissue compared with normal tissue. Expression of IL-17RB was associated with lymph node metastasis and distant metastasis, as well as poor patient survival. IL-17RB overexpression significantly increased cancer cell invasion/migration and metastasis in vitro and in vivo. IL-17RB induced ERK phosphorylation, resulting in GSK3β inactivation and leading to β-catenin up-regulation. IL-17RB also participated in IL-17B synthesis via the ERK pathway. IL-17RB activation is required for IL-17B-mediated ERK phosphorylation. Taken together, IL-17B-IL-17RB signaling and ERK participate in a positive feedback loop that enhances invasion/migration ability in lung cancer cell lines. IL-17RB may therefore serve as an independent prognostic factor and a therapeutic target for lung cancer

IMPAD1 functions as mitochondrial electron transport inhibitor that prevents ROS production and promotes lung cancer metastasis through the AMPK-Notch1-HEY1 pathway

The tumor microenvironment (TME) and metabolic reprogramming have been implicated in cancer development and progression. However, the link between TME, metabolism, and cancer progression in lung cancer is unclear. In the present study, we identified IMPAD1 from the conditioned medium of highly invasive CL1-5. High expression of IMPAD1 was associated with a poorer clinical phenotype in lung cancer patients, with reduced survival and increased lymph node metastasis. Knockdown of IMPAD1 significantly inhibited migration/invasion abilities and metastasis in vitro and in vivo. Upregulation of IMPAD1 and subsequent accumulation of AMP in cells increased the pAMPK, leading to Notch1 and HEY1 upregulation. As AMP is an ADORA1 agonist, treatment with ADORA1 inhibitor reduced the expression of pAMPK and HEY1 expression in IMPAD1-overexpressing cells. IMPAD1 caused mitochondria dysfunction by inhibiting mitochondrial Complex I activity, which reduced mitochondrial ROS levels and activated the AMPK-HEY1 pathway. Collectively this study supports the multipotent role of IMPAD1 in promotion of lung cancer metastasis by simultaneously increasing AMP levels, inhibition of Complex I activity to decrease ROS levels, thereby activating AMPK-Notch1-HEY1 signaling, and providing an alternative metabolic pathway in energy stress conditions

ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

The tumor microenvironment represents one of the main obstacles in breast cancer treatment owing to the presence of heterogeneous stromal cells, such as adipose-derived stem cells (ADSCs), that may interact with breast cancer cells and promote cancer development. Resistin is an adipocytokine associated with adverse breast cancer progression; however, its underlying mechanisms in the context of the breast tumor microenvironment remain largely unidentified. Here, we utilized a transwell co-culture model containing patient-derived ADSCs and breast cancer cell lines to investigate their potential interaction, and observed that breast cancer cells co-cultured with resistin-treated ADSCs (R-ADSCs) showed enhanced cancer cell growth and metastatic ability. Screening by proteome arrays revealed that C-X-C motif chemokine ligand 5 (CXCL5) was released in the conditioned medium of the co-culture system, and phosphorylated ERK was increased in breast cancer cells after co-culture with R-ADSCs. Breast cancer cells treated with the recombinant proteins of CXCL5 showed similarly enhanced cell migration and invasion ability as occurred in the co-culture model, whereas application of neutralizing antibodies against CXCL5 reversed these phenomena. The orthotopic xenograft in mice by breast cancer cells after co-culture with R-ADSCs had a larger tumor growth and more CXCL5 expression than control. In addition, clinical analysis revealed a positive correlation between the expression of resistin and CXCL5 in both tumor tissues and serum specimens of breast cancer patients. The current study suggests that resistin-stimulated ADSCs may interact with breast cancer cells in the tumor microenvironment via CXCL5 secretion, leading to breast cancer cell malignancy