An Unsupervised Feature Learning Approach to Improve Automatic Incident Detection

Sophisticated automatic incident detection (AID) technology plays a key role in contemporary transportation systems. Though many papers were devoted to study incident classification algorithms, few study investigated how to enhance feature representation of incidents to improve AID performance. In this paper, we propose to use an unsupervised feature learning algorithm to generate higher level features to represent incidents. We used real incident data in the experiments and found that effective feature mapping function can be learnt from the data crosses the test sites. With the enhanced features, detection rate (DR), false alarm rate (FAR) and mean time to detect (MTTD) are significantly improved in all of the three representative cases. This approach also provides an alternative way to reduce the amount of labeled data, which is expensive to obtain, required in training better incident classifiers since the feature learning is unsupervised.Comment: The 15th IEEE International Conference on Intelligent Transportation Systems (ITSC 2012

The depth-profiled carrier concentration and scattering mechanism in undoped GaN film grown on sapphire

The carrier concentration and scattering mechanism in undoped GaN film grown on sapphire were investigated. The film was grown on sapphire using metal organic chemical vapor deposition (MOCVD). Confocal micro-Raman spectroscopic measurements and temperature-dependant Hall (TDH) measurements were performed for the study of the depth distribution of the carrier density across the GaN film. The existence of a nonuniform spatial distribution of free carriers in the film with a highly conductive layer of ∼1 μm thickness near the GaN sapphire boundary was confirmed from the study. The electron mobility limiting effect of nitrogen vacancies on GaN bulk film was also discussed.published_or_final_versio

Raman scattering and X-ray diffraction study of neutron irradiated GaN epilayers

Neutron irradiation induced defects and their effects on the carrier concentration of GaN epilayers are investigated with Raman scattering and X-ray diffraction techniques. Relative to the as-grown sample, the neutronirradiated samples exhibit a clear variation in the position and lineshape of the A 1(LO)-mode Raman peak as well as in the fullwidth at half-maximum height (FWHM) of the XRD rocking curves. Careful curve fitting and adequate calculations give the carrier concentrations of the irradiated GaN. It is found that the defects induced by neutron irradiation act as carrier trap centres which capture the electron carriers so that the carrier concentration of the irradiated GaN is reduced. © 2005 IEEE.published_or_final_versio

Reinforcement learning or active inference?

This paper questions the need for reinforcement learning or control theory when optimising behaviour. We show that it is fairly simple to teach an agent complicated and adaptive behaviours using a free-energy formulation of perception. In this formulation, agents adjust their internal states and sampling of the environment to minimize their free-energy. Such agents learn causal structure in the environment and sample it in an adaptive and self-supervised fashion. This results in behavioural policies that reproduce those optimised by reinforcement learning and dynamic programming. Critically, we do not need to invoke the notion of reward, value or utility. We illustrate these points by solving a benchmark problem in dynamic programming; namely the mountain-car problem, using active perception or inference under the free-energy principle. The ensuing proof-of-concept may be important because the free-energy formulation furnishes a unified account of both action and perception and may speak to a reappraisal of the role of dopamine in the brain

Theoretical basis and practical aspects of small specimen creep testing

Interest in and the application of small specimen creep test techniques are increasing. This is because it is only possible to obtain small samples of material in some situations, for example, the scoop samples that are removed from in-service components, the heat-affected zones that are created when welds are used to join components and the desire to produce only small amounts of material in alloy development programmes. It is therefore important to review and compare the theoretical basis and practical aspects of each of the small specimen creep testing methods, in order to clearly understand which of the methods is the best for any specific application. This article provides the theoretical basis for each commonly used test method

An essential function for the ATR-Activation-Domain (AAD) of TopBP1 in mouse development and cellular senescence

ATR activation is dependent on temporal and spatial interactions with partner proteins. In the budding yeast model, three proteins – Dpb11TopBP1, Ddc1Rad9 and Dna2 - all interact with and activate Mec1ATR. Each contains an ATR activation domain (ADD) that interacts directly with the Mec1ATR:Ddc2ATRIP complex. Any of the Dpb11TopBP1, Ddc1Rad9 or Dna2 ADDs is sufficient to activate Mec1ATR in vitro. All three can also independently activate Mec1ATR in vivo: the checkpoint is lost only when all three AADs are absent. In metazoans, only TopBP1 has been identified as a direct ATR activator. Depletion-replacement approaches suggest the TopBP1-AAD is both sufficient and necessary for ATR activation. The physiological function of the TopBP1 AAD is, however, unknown. We created a knock-in point mutation (W1147R) that ablates mouse TopBP1-AAD function. TopBP1-W1147R is early embryonic lethal. To analyse TopBP1-W1147R cellular function in vivo, we silenced the wild type TopBP1 allele in heterozygous MEFs. AAD inactivation impaired cell proliferation, promoted premature senescence and compromised Chk1 signalling following UV irradiation. We also show enforced TopBP1 dimerization promotes ATR-dependent Chk1 phosphorylation. Our data suggest that, unlike the yeast models, the TopBP1-AAD is the major activator of ATR, sustaining cell proliferation and embryonic development

PPAR? Downregulation by TGF in Fibroblast and Impaired Expression and Function in Systemic Sclerosis: A Novel Mechanism for Progressive Fibrogenesis

The nuclear orphan receptor peroxisome proliferator-activated receptor-gamma (PPAR-γ) is expressed in multiple cell types in addition to adipocytes. Upon its activation by natural ligands such as fatty acids and eicosanoids, or by synthetic agonists such as rosiglitazone, PPAR-γ regulates adipogenesis, glucose uptake and inflammatory responses. Recent studies establish a novel role for PPAR-γ signaling as an endogenous mechanism for regulating transforming growth factor-ß (TGF-ß)- dependent fibrogenesis. Here, we sought to characterize PPAR-γ function in the prototypic fibrosing disorder systemic sclerosis (SSc), and delineate the factors governing PPAR-γ expression. We report that PPAR-γ levels were markedly diminished in skin and lung biopsies from patients with SSc, and in fibroblasts explanted from the lesional skin. In normal fibroblasts, treatment with TGF-ß resulted in a time- and dose-dependent down-regulation of PPAR-γ expression. Inhibition occurred at the transcriptional level and was mediated via canonical Smad signal transduction. Genome-wide expression profiling of SSc skin biopsies revealed a marked attenuation of PPAR-γ levels and transcriptional activity in a subset of patients with diffuse cutaneous SSc, which was correlated with the presence of a ''TGF-ß responsive gene signature'' in these biopsies. Together, these results demonstrate that the expression and function of PPAR-γ are impaired in SSc, and reveal the existence of a reciprocal inhibitory cross-talk between TGF-ß activation and PPAR-γ signaling in the context of fibrogenesis. In light of the potent anti-fibrotic effects attributed to PPAR-γ, these observations lead us to propose that excessive TGF-ß activity in SSc accounts for impaired PPAR-γ function, which in turn contributes to unchecked fibroblast activation and progressive fibrosis. © 2010 Wei et al

Benefits and risks of the hormetic effects of dietary isothiocyanates on cancer prevention

The isothiocyanate (ITC) sulforaphane (SFN) was shown at low levels (1-5 µM) to promote cell proliferation to 120-143% of the controls in a number of human cell lines, whilst at high levels (10-40 µM) it inhibited such cell proliferation. Similar dose responses were observed for cell migration, i.e. SFN at 2.5 µM increased cell migration in bladder cancer T24 cells to 128% whilst high levels inhibited cell migration. This hormetic action was also found in an angiogenesis assay where SFN at 2.5 µM promoted endothelial tube formation (118% of the control), whereas at 10-20 µM it caused significant inhibition. The precise mechanism by which SFN influences promotion of cell growth and migration is not known, but probably involves activation of autophagy since an autophagy inhibitor, 3-methyladenine, abolished the effect of SFN on cell migration. Moreover, low doses of SFN offered a protective effect against free-radical mediated cell death, an effect that was enhanced by co-treatment with selenium. These results suggest that SFN may either prevent or promote tumour cell growth depending on the dose and the nature of the target cells. In normal cells, the promotion of cell growth may be of benefit, but in transformed or cancer cells it may be an undesirable risk factor. In summary, ITCs have a biphasic effect on cell growth and migration. The benefits and risks of ITCs are not only determined by the doses, but are affected by interactions with Se and the measured endpoint