Inferring Unusual Crowd Events From Mobile Phone Call Detail Records

The pervasiveness and availability of mobile phone data offer the opportunity of discovering usable knowledge about crowd behaviors in urban environments. Cities can leverage such knowledge in order to provide better services (e.g., public transport planning, optimized resource allocation) and safer cities. Call Detail Record (CDR) data represents a practical data source to detect and monitor unusual events considering the high level of mobile phone penetration, compared with GPS equipped and open devices. In this paper, we provide a methodology that is able to detect unusual events from CDR data that typically has low accuracy in terms of space and time resolution. Moreover, we introduce a concept of unusual event that involves a large amount of people who expose an unusual mobility behavior. Our careful consideration of the issues that come from coarse-grained CDR data ultimately leads to a completely general framework that can detect unusual crowd events from CDR data effectively and efficiently. Through extensive experiments on real-world CDR data for a large city in Africa, we demonstrate that our method can detect unusual events with 16% higher recall and over 10 times higher precision, compared to state-of-the-art methods. We implement a visual analytics prototype system to help end users analyze detected unusual crowd events to best suit different application scenarios. To the best of our knowledge, this is the first work on the detection of unusual events from CDR data with considerations of its temporal and spatial sparseness and distinction between user unusual activities and daily routines.Comment: 18 pages, 6 figure

Mutation Symmetries in BPS Quiver Theories: Building the BPS Spectra

We study the basic features of BPS quiver mutations in 4D $\mathcal{N}=2$ supersymmetric quantum field theory with $G=ADE$ gauge symmetries.\ We show, for these gauge symmetries, that there is an isotropy group $\mathcal{G}_{Mut}^{G}$ associated to a set of quiver mutations capturing information about the BPS spectra. In the strong coupling limit, it is shown that BPS chambers correspond to finite and closed groupoid orbits with an isotropy symmetry group $\mathcal{G}_{strong}^{G}$ isomorphic to the discrete dihedral groups $Dih_{2h_{G}}$ contained in Coxeter$(G)$ with $$ the Coxeter number of G. These isotropy symmetries allow to determine the BPS spectrum of the strong coupling chamber; and give another way to count the total number of BPS and anti-BPS states of $\mathcal{N}=2$ gauge theories. We also build the matrix realization of these mutation groups $\mathcal{G}_{strong}^{G}$ from which we read directly the electric-magnetic charges of the BPS and anti-BPS states of $\mathcal{N}=2$ QFT$_{4}$ as well as their matrix intersections. We study as well the quiver mutation symmetries in the weak coupling limit and give their links with infinite Coxeter groups. We show amongst others that $\mathcal{G}_{weak}^{su_{2}}$ is contained in ${GL}({2,}\mathbb{Z})$; and isomorphic to the infinite Coxeter ${I_{2}^{\infty}}$. Other issues such as building $\mathcal{G}$ and $\mathcal{G}_{weak}^{su_{3}}$ are also studied.Comment: LaTeX, 98 pages, 18 figures, Appendix I on groupoids adde

Modeling and improving the output power of terahertz master-oscillator power-amplifier quantum cascade lasers

A model based on carrier rate equations is proposed to evaluate the gain saturation and predict the dependence of the output power of a terahertz master-oscillator power-amplifier quantum cascade laser (THz-MOPA-QCL) on the material and structure parameters. The model reveals the design rules of the preamplifier and the power extractor to maximize the output power and the wall-plug efficiency. The correction of the model is verified by its agreement with the experiment results. The optimized MOPA devices exhibit single-mode emission at ∼ 2.6 THz with a side mode suppression ratio of 23 dB, a pulsed output power of 153 mW, a wall-plug efficiency of 0.22%, and a low divergence angle of ∼6°×16°, all measured at an operation temperature of 77 K. The model developed here is helpful for the design of MOPA devices and semiconductor optical amplifiers, in which the active region is based on intersubband transitions

Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial-mesenchymal transition

Introduction: Previous reports have shown epithelial–mesenchymal transition (EMT) as an active processthat contributes to small airway fibrotic pathology. Myofibroblasts are highly active pro-fibrotic cells thatsecrete excessive and altered extracellular matrix (ECM). Here we relate small airway myofibroblastpresence with airway remodelling, physiology and EMT activity in smokers and COPD patients.Methods: Lung resections from nonsmoker controls, normal lung function smokers and COPD currentand ex-smokers were stained with anti-human α-smooth muscle actin (SMA), collagen 1 and fibronectin.αSMA+ cells were computed in reticular basement membrane (Rbm), lamina propria and adventitia andpresented per mm of Rbm and mm2 of lamina propria. Collagen-1 and fibronectin are presented as apercentage change from normal. All analyses including airway thickness were measured using Image-proplus 7.0.Results: We found an increase in subepithelial lamina propria (especially) and adventitia thickness in allpathological groups compared to nonsmoker controls. Increases in αSMA+ myofibroblasts were observedin subepithelial Rbm, lamina propria and adventitia in both the smoker and COPD groups compared tononsmoker controls. Furthermore, the increase in the myofibroblast population in the lamina propria wasstrongly associated with decrease in lung function, lamina propria thickening, increase in ECM proteindeposition, and finally EMT activity in epithelial cells.Conclusions: This is the first systematic characterisation of small airway myofibroblasts in COPD based ontheir localisation, with statistically significant correlations between them and other pan-airway structural,lung function and ECM protein changes. Finally, we suggest that EMT may be involved in such changes

Genetic inhibition of neurotransmission reveals role of glutamatergic input to dopamine neurons in high-effort behavior

Midbrain dopamine neurons are crucial for many behavioral and cognitive functions. As the major excitatory input, glutamatergic afferents are important for control of the activity and plasticity of dopamine neurons. However, the role of glutamatergic input as a whole onto dopamine neurons remains unclear. Here we developed a mouse line in which glutamatergic inputs onto dopamine neurons are specifically impaired, and utilized this genetic model to directly test the role of glutamatergic inputs in dopamine-related functions. We found that while motor coordination and reward learning were largely unchanged, these animals showed prominent deficits in effort-related behavioral tasks. These results provide genetic evidence that glutamatergic transmission onto dopaminergic neurons underlies incentive motivation, a willingness to exert high levels of effort to obtain reinforcers, and have important implications for understanding the normal function of the midbrain dopamine system.Fil: Hutchison, M. A.. National Institutes of Health; Estados UnidosFil: Gu, X.. National Institutes of Health; Estados UnidosFil: Adrover, Martín Federico. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Lee, M. R.. National Institutes of Health; Estados UnidosFil: Hnasko, T. S.. University of California at San Diego; Estados UnidosFil: Alvarez, V. A.. National Institutes of Health; Estados UnidosFil: Lu, W.. National Institutes of Health; Estados Unido

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

PEP was a Wellcome Trust Clinical Research Training Fellow and this research was supported by the Wellcome Trust (Grant 098882/Z/12/Z). This research was also supported by the National Institute for Health Research (NIHR) Clinical Research Facility at Guy’s & St Thomas’ NHS Foundation Trust and NIHR Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London

Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.

To gain insight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths. We found repeat length-dependent transcriptional signatures to be prominent in the striatum, less so in cortex, and minimal in the liver. Coexpression network analyses revealed 13 striatal and 5 cortical modules that correlated highly with CAG length and age, and that were preserved in HD models and sometimes in patients. Top striatal modules implicated mHtt CAG length and age in graded impairment in the expression of identity genes for striatal medium spiny neurons and in dysregulation of cyclic AMP signaling, cell death and protocadherin genes. We used proteomics to confirm 790 genes and 5 striatal modules with CAG length-dependent dysregulation at the protein level, and validated 22 striatal module genes as modifiers of mHtt toxicities in vivo

Astrocytic Ion Dynamics: Implications for Potassium Buffering and Liquid Flow

We review modeling of astrocyte ion dynamics with a specific focus on the implications of so-called spatial potassium buffering, where excess potassium in the extracellular space (ECS) is transported away to prevent pathological neural spiking. The recently introduced Kirchoff-Nernst-Planck (KNP) scheme for modeling ion dynamics in astrocytes (and brain tissue in general) is outlined and used to study such spatial buffering. We next describe how the ion dynamics of astrocytes may regulate microscopic liquid flow by osmotic effects and how such microscopic flow can be linked to whole-brain macroscopic flow. We thus include the key elements in a putative multiscale theory with astrocytes linking neural activity on a microscopic scale to macroscopic fluid flow.Comment: 27 pages, 7 figure

Beclin-1 Expression is a Predictor of Clinical Outcome in Patients with Esophageal Squamous Cell Carcinoma and Correlated to Hypoxia-Inducible Factor (HIF)-1α Expression

In the present study, we examined the relationship between Beclin-1 expression and HIF-1α expression in esophageal squamous cell carcinoma(ESCC). There was a loss of Beclin-1 protein expression in 33% of ESCCs. Beclin-1 expression significantly correlated with depth of invasion, lymph node metastasis and clinical stage. Among the 54 patients, The survival rate of the Beclin-1-positive group was better than that of the Beclin-1-negative group. Twenty-five of the 54 (46%) tumor specimens showed high levels of HIF-1α immunoreactivity. Beclin-1 expression was associated with HIF-1α expression. The survival rate of patients with Beclin-1-positive and HIF-1α-low tumors was significantly higher than that of the other groups. These results suggest that Beclin-1 and HIF-1α expression are important determinants of survival in ESCCs