507 research outputs found

    A 100-m-Scale Modeling Study of a Gale Event on the Lee Side of a Long Narrow Mountain

    Get PDF
    In this study, a gale event that occurred on the lee side of a long narrow mountain was investigated, together with the associated mountain flows, using a realistic-case large-eddy simulation (LES) that is based on the Weather Research and Forecasting Model. The mountain is located on the southeastern Tibetan Plateau, where approximately 58 gales occur annually, mostly in the afternoons during the winter season. Benefitting from realistic topography and high horizontal resolution as fine as 111 m, the LES can replicate features similar to the wind fields observed during the gale period. Investigation of the early morning wind structure over the mountain revealed that weak inflows were blocked, reversed, and divided in the upstream area and that some weak lee waves, rotors, and two clear lee vortices were evident downstream. As the upstream wind accelerated and the boundary layer developed during the daytime, the lee waves became amplified with severe downslope wind and rotors. The interaction and coherent structure of the downslope wind, rotor, and vortices were investigated to show the severe wind distribution. The mountain drags associated with blocking and amplified lee waves are displayed to show the potential impact on the large-scale model. The linear lee-wave theory was adopted to explain the wave evolution during this event together with a discussion of the uncertainty around low-level nonlinear processes

    GPU Accelerated High Intensity Ultrasound Acoustical Power Computation

    No full text
    International audienceThe simulation of the hepatocellular carcinoma therapy effects is often used for the intervention planning. As the physical-based model of the simulation is very time-consuming, the speed of this method becomes an obstacle during the clinical application simulation. In order to accelerate the simulation, a GPU-based (Graphic Processing Unit) acceleration method of the pressure field estimation is proposed in this paper. The results demonstrate that the proposed acceleration method can solve the time-consuming problem

    Re-Expression of AKAP12 Inhibits Progression and Metastasis Potential of Colorectal Carcinoma In Vivo and In Vitro

    Get PDF
    Background: AKAP12/Gravin (A kinase anchor protein 12) is one of the A-kinase scaffold proteins and a potential tumor suppressor gene in human primary cancers. Our recent study demonstrated the highly recurrent loss of AKAP12 in colorectal cancer and AKAP12 reexpression inhibited proliferation and anchorage-independent growth in colorectal cancer cells, implicating AKAP12 in colorectal cancer pathogenesis. Methods: To evaluate the effect of this gene on the progression and metastasis of colorectal cancer, we examined the impact of overexpressing AKAP12 in the AKAP12-negative human colorectal cancer cell line LoVo, the single clone (LoVo-AKAP12) compared to mock-transfected cells (LoVo-CON). Results: pCMV6-AKAP12-mediated AKAP12 re-expression induced apoptosis (3 % to 12.7%, p,0.01), migration (89.667.5 cells to 31.064.1 cells, p,0.01) and invasion (82.765.2 cells to 24.763.3 cells, p,0.01) of LoVo cells in vitro compared to control cells. Nude mice injected with LoVo-AKAP12 cells had both significantly reduced tumor volume (p,0.01) and increased apoptosis compared to mice given AKAP12-CON. The quantitative human-specific Alu PCR analysis showed overexpression of AKAP12 suppressed the number of intravasated cells in vivo (p,0.01). Conclusion: These results demonstrate that AKAP12 may play an important role in tumor growth suppression and the survival of human colorectal cancer

    Insulin signaling regulates neurite growth during metamorphic neuronal remodeling

    Get PDF
    From the publisher (Biology Open): Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.Although the growth capacity of mature neurons is often limited, some neurons can shift through largely unknown mechanisms from stable maintenance growth to dynamic, organizational growth (e.g. to repair injury, or during development transitions). During insect metamorphosis, many terminally differentiated larval neurons undergo extensive remodeling, involving elimination of larval neurites and outgrowth and elaboration of adult-specific projections. Here, we show in the fruit fly, Drosophila melanogaster (Meigen), that a metamorphosis-specific increase in insulin signaling promotes neuronal growth and axon branching after prolonged stability during the larval stages. FOXO, a negative effector in the insulin signaling pathway, blocked metamorphic growth of peptidergic neurons that secrete the neuropeptides CCAP and bursicon. RNA interference and CCAP/bursicon cell-targeted expression of dominant-negative constructs for other components of the insulin signaling pathway (InR, Pi3K92E, Akt1, S6K) also partially suppressed the growth of the CCAP/bursicon neuron somata and neurite arbor. In contrast, expression of wild-type or constitutively active forms of InR, Pi3K92E, Akt1, Rheb, and TOR, as well as RNA interference for negative regulators of insulin signaling (PTEN, FOXO), stimulated overgrowth. Interestingly, InR displayed little effect on larval CCAP/bursicon neuron growth, in contrast to its strong effects during metamorphosis. Manipulations of insulin signaling in many other peptidergic neurons revealed generalized growth stimulation during metamorphosis, but not during larval development. These findings reveal a fundamental shift in growth control mechanisms when mature, differentiated neurons enter a new phase of organizational growth. Moreover, they highlight strong evolutionarily conservation of insulin signaling in neuronal growth regulation.This work was supported by National Science Foundation grant IOS-0744447 (http://nsf.gov/) to R.S.H.YesAnonymous peer review by three experts in this fiel
    • …
    corecore