419 research outputs found
Micro-manufacturing : research, technology outcomes and development issues
Besides continuing effort in developing MEMS-based manufacturing techniques, latest effort in Micro-manufacturing is also in Non-MEMS-based manufacturing. Research and technological development (RTD) in this field is encouraged by the increased demand on micro-components as well as promised development in the scaling down of the traditional macro-manufacturing processes for micro-length-scale manufacturing. This paper highlights some EU funded research activities in micro/nano-manufacturing, and gives examples of the latest development in micro-manufacturing methods/techniques, process chains, hybrid-processes, manufacturing equipment and supporting technologies/device, etc., which is followed by a summary of the achievements of the EU MASMICRO project. Finally, concluding remarks are given, which raise several issues concerning further development in micro-manufacturing
uPA is upregulated by high dose celecoxib in women at increased risk of developing breast cancer
<p>Abstract</p> <p>Background</p> <p>While increased urokinase-type plasminogen activator (uPA) expression in breast cancer tissue is directly associated with poor prognosis, recent evidence suggests that uPA overexpression may suppress tumor growth and prolong survival. Celecoxib has been shown to have antiangiogenic and antiproliferative properties. We sought to determine if uPA, PA inhibitor (PAI)-1 and prostaglandin (PG)E<sub>2 </sub>expression in nipple aspirate fluid (NAF) and uPA and PGE<sub>2 </sub>expression in plasma were altered by celecoxib dose and concentration in women at increased breast cancer risk.</p> <p>Methods</p> <p>NAF and plasma samples were collected in women at increased breast cancer risk before and 2 weeks after taking celecoxib 200 or 400 mg twice daily (bid). uPA, PAI-1 and PGE<sub>2 </sub>were measured before and after intervention.</p> <p>Results</p> <p>Celecoxib concentrations trended higher in women taking 400 mg (median 1025.0 ng/mL) compared to 200 mg bid (median 227.3 ng/mL), and in post- (534.6 ng/mL) compared to premenopausal (227.3 ng/mL) women. In postmenopausal women treated with the higher (400 mg bid) celecoxib dose, uPA concentrations increased, while PAI-1 and PGE<sub>2 </sub>decreased. In women taking the higher dose, both PAI-1 (r = -.97, p = .0048) and PGE<sub>2 </sub>(r = -.69, p = .019) in NAF and uPA in plasma (r = .45, p = .023) were correlated with celecoxib concentrations.</p> <p>Conclusion</p> <p>Celecoxib concentrations after treatment correlate inversely with the change in PAI-1 and PGE<sub>2 </sub>in the breast and directly with the change in uPA in the circulation. uPA upregulation, in concert with PAI-1 and PGE<sub>2 </sub>downregulation, may have a cancer preventive effect.</p
Unique Structure and Dynamics of the EphA5 Ligand Binding Domain Mediate Its Binding Specificity as Revealed by X-ray Crystallography, NMR and MD Simulations
10.1371/journal.pone.0074040PLoS ONE89-POLN
Greedy Shortest Common Superstring Approximation in Compact Space
Given a set of strings, the shortest common superstring problem is to find the shortest possible string that contains all the input strings. The problem is NP-hard, but a lot of work has gone into designing approximation algorithms for solving the problem. We present the first time and space efficient implementation of the classic greedy heuristic which merges strings in decreasing order of overlap length. Our implementation works in O(n log σ) time and bits of space, where n is the total length of the input strings in characters, and σσ is the size of the alphabet. After index construction, a practical implementation of our algorithm uses roughly 5n log σ bits of space and reasonable time for a real dataset that consists of DNA fragments.Peer reviewe
Functional Promoter -31G>C Variant in Survivin Gene Is Associated with Risk and Progression of Renal Cell Cancer in a Chinese Population
BACKGROUND: Survivin is an inhibitor of apoptosis protein and is involved in the occurrence and progression of human malignancies. Recently, a functional polymorphism (-31G>C, rs9904341) in the promoter of survivin has been shown to influence its expression and confer susceptibility to different types of cancer. The present study was aimed to investigate whether the polymorphism also influences susceptibility and progression of renal cell cancer (RCC) in a Chinese population. METHODS: We genotyped this polymorphism using the TaqMan assay in a case-control study comprised of 710 RCC patients and 760 controls. The logistic regression was used to assess the genetic association with occurrence and progression of RCC. RESULTS: Compared with the genotypes containing G allele (GG and GC), we found a statistically significant increased occurrence of RCC associated with the CC genotype [P = 0.006, adjusted odds ratio (OR) = 1.38, 95% confidence interval (CI) = 1.08-1.76]. The polymorphism was associated with risk of developing advanced stage (OR = 2.02, 95%CI = 1.34-3.07) and moderately differentiated (OR = 1.75; 95%CI = 1.20-2.54) RCC. Furthermore, the patients carrying the CC genotype had a significantly greater prevalence of high clinical stage disease (P(trend) = 0.003). Similar results were also observed when we restricted the analysis to clear cell RCC, a major histological type of RCC. CONCLUSIONS: Our results suggest that the functional -31G>C polymorphism in the promoter of survivin may influence the susceptibility and progression of RCC in the Chinese population. Large population-based prospective studies are required to validate our findings
Measurement of the proton form factor by studying
Using data samples collected with the BESIII detector at the BEPCII collider,
we measure the Born cross section of at 12
center-of-mass energies from 2232.4 to 3671.0 MeV. The corresponding effective
electromagnetic form factor of the proton is deduced under the assumption that
the electric and magnetic form factors are equal . In
addition, the ratio of electric to magnetic form factors, , and
are extracted by fitting the polar angle distribution of the proton
for the data samples with larger statistics, namely at 2232.4 and
2400.0 MeV and a combined sample at = 3050.0, 3060.0 and 3080.0 MeV,
respectively. The measured cross sections are in agreement with recent results
from BaBar, improving the overall uncertainty by about 30\%. The
ratios are close to unity and consistent with BaBar results in
the same region, which indicates the data are consistent with the
assumption that within uncertainties.Comment: 13 pages, 24 figure
An amplitude analysis of the system produced in radiative decays
An amplitude analysis of the system produced in radiative
decays is presented. In particular, a piecewise function that
describes the dynamics of the system is determined as a
function of from an analysis of the
decays collected by the BESIII detector.
The goal of this analysis is to provide a description of the scalar and tensor
components of the system while making minimal assumptions about
the properties or number of poles in the amplitude. Such a model-independent
description allows one to integrate these results with other related results
from complementary reactions in the development of phenomenological models,
which can then be used to directly fit experimental data to obtain parameters
of interest. The branching fraction of is
determined to be , where the uncertainty is
systematic only and the statistical uncertainty is negligible.Comment: Submitted to Phys. Rev. D 19 pages, 4 figure
Observation of the isospin-violating decay
Using a sample of 1.31 billion events collected with the BESIII
detector at the BEPCII collider, the decays and are
investigated. The isospin violating decay
with , is observed for the first time. The width of the
obtained from the dipion mass spectrum is found to be much smaller
than the world average value. In the mass spectrum, there
is evidence of production. By studying the decay , the branching fractions of and
, as well as their ratio, are also measured.Comment: 10 pages, 10 figures, published in Phys. Rev.
Microglial activation and chronic neurodegeneration
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurode-generative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson’s disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype
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