854 research outputs found
Effective Vector Data Transmission and Visualization Using HTML5
In this paper we evaluate the potential of the next major revision of HTML (Hypertext
Markup Language), that is HTML5, to provide an effective platform for the transmission
and visualization of vector based geographical data. Relative to the current version of HTML,
HTML 4.01, HTML5 offers an improved platform to perform these tasks through greater interoperability
with existing technologies and the introduction of many new API’s. Visualization of
vector data can be achieved using the new methods of inline-SVG and the Canvas API. An analysis
of the pros and cons of each method is presented. HTML5 introduces a novel WebSocket
API which defines a full-duplex communication channel between client and server. This provides
improved data communication both in terms of bandwidth utilization and network latency
relative to existing push technologies. To demonstrate the effectiveness of HTML5 for vector
data delivery a novel selective progressive transmission methodology is implemented using the
WebSocket and Canvas API’s
Serum neurofilament light chain levels in healthy individuals: A proposal of cut-off values for use in multiple sclerosis clinical practice
Engineering, Characterization, and Biological Evaluation of an Antibody Targeting the HGF Receptor
Myostatin mediates abdominal aortic atherosclerosis progression by inducing vascular smooth muscle cell dysfunction and monocyte recruitment
Myostatin (Mstn) is a skeletal muscle growth inhibitor involved in metabolic disorders and heart fibrosis. In this study we sought to verify whether Mstn is also operative in atherosclerosis of abdominal aorta. In human specimens, Mstn expression was almost absent in normal vessels, became detectable in the media of non-progressive lesions and increased with the severity of the damage. In progressive atherosclerotic lesions, Mstn was present in the media, neointima, plaque shoulder and in infiltrating macrophages. Mstn co-localized with \uce\ub1-smooth muscle actin (\uce\ub1-SMA) staining and with some CD45+ cells, indicating Mstn expression in VSMCs and bloodstream-derived leukocytes. In vitro, Mstn was tested in VSMCs and monocytes. In A7r5 VSMCs, Mstn downregulated proliferation and Smoothelin mRNA, induced cytoskeletal rearrangement, increased migratory rate and MCP-1/CCR2 expression. In monocytes (THP-1 cells and human monocytes), Mstn acted as a chemoattractant and increased the MCP-1-dependent chemotaxis, F-actin, \uce\ub1-SMA, MCP-1 and CCR2 expression; in turn, MCP-1 increased Mstn mRNA. Mstn induced JNK phosphorylation both in VSMCs and monocytes. Our results indicate that Mstn is overexpressed in abdominal aortic wall deterioration, affects VSMCs and monocyte biology and sustains a chronic inflammatory milieu. These findings propose to consider Mstn as a new playmaker in atherosclerosis progression
Partial wave analysiss of pbar-p -> piminus-piplus, pizero-pizero, eta-eta and eta-etaprime
A partial wave analysis is presented of Crystal Barrel data on pbar-p ->
pizero-pizero, eta-eta and eta-etaprime from 600 to 1940 MeV/c, combined with
earlier data on d\sigma /d\Omega and P for pbar-p->piminus-piplus. The
following s-channel I=0 resonances are identified: (i) J^{PC} = 5^{--} with
mass and width (M,\Gamma) at (2295+-30,235^{+65}_{-40}) MeV, (ii) J^{PC} =
4^{++} at (2020+-12, 170+-15) MeV and (2300+-25, 270+-50) MeV, (iii) 3D3 JPC =
3^{--} at (1960+-15, 150+-25) MeV and (2210+-4$, 360+-55) MeV, and a 3G3 state
at (2300 ^{+50}_{-80}, 340+-150) MeV, (iv) JPC = 2^{++} at (1910+-30, 260+-40)
MeV, (2020+-30, 275+-35) MeV, (2230+-30, 245+-45) MeV, and (2300+-35, 290+-50)
MeV, (v) JPC = 1^{--} at (2005+-40, 275+-75) MeV, and (2165+-40, 160
^{+140}_{-70}) MeV, and (vi) JPC = 0^{++} at (2005+-30, 305+-50) MeV,
(2105+-15, 200+-25) MeV, and (2320+-30, 175+-45) MeV. In addition, there is a
less well defined 6^{++} resonance at 2485+-40 MeV, with Gamma = 410+-90 MeV.
For every JP, almost all these resonances lie on well defined linear
trajectories of mass squared v. excitation number. The slope is 1.10+-0.03
Gev^2 per excitation. The f_0(2105) has strong coupling to eta-\eta, but much
weaker coupling to pizero-pizero. Its flavour mixing angle between q-qbar and
s-sbar is (59-71.6)deg, i.e. dominant decays to s-sbar. Such decays and its
strong production in pbar-p interactions strongly suggest exotic character.Comment: Makes available the combined fit to Crystal Barrel data on pbar-p ->
2-body final states. 29 pages, 11 figures. Typo corrected in version
Testicular microlithiasis imaging and follow-up: guidelines of the ESUR scrotal imaging subcommittee
The subcommittee on scrotal imaging, appointed by the board of the European Society of Urogenital Radiology (ESUR), have produced guidelines on imaging and follow-up in testicular microlithiasis (TML)
SIRT1 promotes proliferation and inhibits the senescence-like phenotype in human melanoma cells
SIRT1 operates as both a tumor suppressor and oncogenic factor depending on the cell context. Whether SIRT1 plays a role in melanoma biology remained poorly elucidated. Here, we demonstrate that SIRT1 is a critical regulator of melanoma cell proliferation. SIRT1 suppression by genetic or pharmacological approaches induces cell cycle arrest and a senescence-like phenotype. Gain and loss of function experiments show that M-MITF regulates SIRT1 expression, thereby revealing a melanocyte-specific control of SIRT1. SIRT1 over-expression relieves the senescence-like phenotype and the proliferation arrest caused by MITF suppression, demonstrating that SIRT1 is an effector of MITF-induced proliferation in melanoma cells. Interestingly, SIRT1 level and activity are enhanced in the PLX4032-resistant BRAF(V600E)-mutated melanoma cells compared with their sensitive counterpart. SIRT1 inhibition decreases melanoma cell growth and rescues the sensibility to PLX4032 of PLX4032-resistant BRAF(V600E)-mutated melanoma cells. In conclusion, we provide the first evidence that inhibition of SIRT1 warrants consideration as an anti-melanoma therapeutic option
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