Exploiting Sparse Representations for Robust Analysis of Noisy Complex Video Scenes

Abstract. Recent works have shown that, even with simple low level visual cues, complex behaviors can be extracted automatically from crowded scenes, e.g. those depicting public spaces recorded from video surveillance cameras. However, low level features as optical flow or fore-ground pixels are inherently noisy. In this paper we propose a novel unsupervised learning approach for the analysis of complex scenes which is specifically tailored to cope directly with features ’ noise and uncer-tainty. We formalize the task of extracting activity patterns as a matrix factorization problem, considering as reconstruction function the robust Earth Mover’s Distance. A constraint of sparsity on the computed basis matrix is imposed, filtering out noise and leading to the identification of the most relevant elementary activities in a typical high level behavior. We further derive an alternate optimization approach to solve the pro-posed problem efficiently and we show that it is reduced to a sequence of linear programs. Finally, we propose to use short trajectory snippets to account for object motion information, in alternative to the noisy optical flow vectors used in previous works. Experimental results demonstrate that our method yields similar or superior performance to state-of-the arts approaches.

X-Ray Cone Beam Tomography with Two Tilted Circular Trajectories

Recently 3-D cone-beam tomography has become of interest for the nondestructive evaluation of advanced materials. The main field of application in nondestructive testing is the evaluation of structural ceramics. Study of such materials implies high density resolution and high sensitivity to cracks. In fact, with a single circular source trajectory, when the cone-beam aperture increases, density is underestimated and cone shaped artifacts may appear at interfaces in the sample even at relatively small aperture [1–3]. These artifacts limit the thickness we can examine with a planar source trajectory. To maintain optimal reconstruction accuracy with a circular source trajectory, the angular aperture must remain within ±10°. However Kudo and Saito [4] showed that this limit can be slightly overcome by using a special interpolation of the shadow area. But to examine greater thicknesses and to maintain resolution, we must widen the cone-beam aperture thereby decreasing accuracy. To overcome these aperture limitations, Tuy [5] introduced the double circular source trajectory idea

Mutation of the Diamond-Blackfan Anemia Gene Rps7 in Mouse Results in Morphological and Neuroanatomical Phenotypes

The ribosome is an evolutionarily conserved organelle essential for cellular function. Ribosome construction requires assembly of approximately 80 different ribosomal proteins (RPs) and four different species of rRNA. As RPs co-assemble into one multi-subunit complex, mutation of the genes that encode RPs might be expected to give rise to phenocopies, in which the same phenotype is associated with loss-of-function of each individual gene. However, a more complex picture is emerging in which, in addition to a group of shared phenotypes, diverse RP gene-specific phenotypes are observed. Here we report the first two mouse mutations (Rps7(Mtu) and Rps7(Zma)) of ribosomal protein S7 (Rps7), a gene that has been implicated in Diamond-Blackfan anemia. Rps7 disruption results in decreased body size, abnormal skeletal morphology, mid-ventral white spotting, and eye malformations. These phenotypes are reported in other murine RP mutants and, as demonstrated for some other RP mutations, are ameliorated by Trp53 deficiency. Interestingly, Rps7 mutants have additional overt malformations of the developing central nervous system and deficits in working memory, phenotypes that are not reported in murine or human RP gene mutants. Conversely, Rps7 mouse mutants show no anemia or hyperpigmentation, phenotypes associated with mutation of human RPS7 and other murine RPs, respectively. We provide two novel RP mouse models and expand the repertoire of potential phenotypes that should be examined in RP mutants to further explore the concept of RP gene-specific phenotypes.This research was supported in part by the Intramural Research Program of NHGRI, NIH, and the Wellcome Trust and by NHMRC Australia grant 366746. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Energy-efficient precoding in multicell networks with full-duplex base stations

© 2017, The Author(s). This paper considers multi-input multi-output (MIMO) multicell networks, where the base stations (BSs) are full-duplex transceivers, while uplink and downlink users are equipped with multiple antennas and operate in a half-duplex mode. The problem of interest is to design linear precoders for BSs and users to optimize the network’s energy efficiency. Given that the energy efficiency objective is not a ratio of concave and convex functions, the commonly used Dinkelbach-type algorithms are not applicable. We develop a low-complexity path-following algorithm that only invokes one simple convex quadratic program at each iteration, which converges at least to the local optimum. Numerical results demonstrate the performance advantage of our proposed algorithm in terms of energy efficiency

Optimisation of whole-body PET/CT scanning protocols

Positron emission tomography (PET) has become one of the major tools for the in vivo localisation of positron-emitting tracers and now is performed routinely using 18F-fluorodeoxyglucose (FDG) to answer important clinical questions including those in cardiology, neurology, psychiatry, and oncology. The latter application contributed largely to the wide acceptance of this imaging modality and its use in clinical diagnosis, staging, restaging, and assessment of tumour response to treatment. Dual-modality PET/CT systems have been operational for almost a decade since their inception. The complementarity between anatomic (CT) and functional or metabolic (PET) information provided in a “one-stop shop” has been the driving force of this technology. Although combined anato-metabolic imaging is an obvious choice, the way to perform imaging is still an open issue. The tracers or combinations of tracers to be used, how the imaging should be done, when contrast-enhanced CT should be performed, what are the optimal acquisition and processing protocols, are all unanswered questions. Moreover, each data acquisition–processing combination may need to be independently optimised and validated. This paper briefly reviews the basic principles of dual-modality imaging and addresses some of the practical issues involved in optimising PET/CT scanning protocols in a clinical environment

Mice with Mutation in Dynein Heavy Chain 1 Do Not Share the Same Tau Expression Pattern with Mice with SOD1-Related Motor Neuron Disease

Due to controversy about the involvement of Dync1h1 mutation in pathogenesis of motor neuron disease, we investigated expression of tau protein in transgenic hybrid mice with Dync1h1 (so-called Cra1/+), SOD1G93A (SOD1/+), double (Cra1/SOD1) mutations and wild-type controls. Total tau-mRNA and isoforms 0, 1 and 2 N expression was studied in frontal cortex, hippocampus, spinal cord and cerebellum of presymptomatic and symptomatic animals (age 70, 140 and 365 days). The most significant differences were found in brain cortex and cerebellum, but not in hippocampus and spinal cord. There were less changes in Cra1/SOD1 double heterozygotes compared to mice harboring single mutations. The differences in total tau expression and in profile of its isoforms between Cra1/+ and SOD1/+ transgenics indicate a distinct pathogenic entity of these two conditions

Therapeutic targeting of CK2 in acute and chronic leukemias

Phosphorylation can regulate almost every property of a protein and is involved in all fundamental cellular processes. Thus, proper regulation of phosphorylation events is critical to the homeostatic functions of cell signaling. Indeed, deregulation of signaling pathways underlies many human diseases, including cancer.[1] The importance of phosphorylation makes protein kinases and phosphatases promising therapeutic targets for a wide variety of disorders.[2] CK2, formerly known as casein kinase II, was discovered in 1954, [3] although only recently, and especially over the last two decades, it has become one of the most studied protein kinases, due to its ubiquity, pleiotropy and constitutive activity. In particular, appreciation of its pleiotropy has completely changed our vision of CK2 biology, from an ordinary cell homeostasis-maintaining enzyme to a master kinase potentially implicated in many human physiological and pathological events. CK2 is responsible for about 25% of the phosphoproteome,[4] as it catalyzes the phosphorylation of >300 substrates.[5] This partly explains the CK2 interconnected roles that underlie its involvement in many signaling pathways. However, CK2 prevalent roles are promotion of cell growth and suppression of apoptosis. Accordingly, several lines of evidence support the notion that CK2 is a key player in the pathogenesis of cancer. High levels of CK2 transcript and protein expression, as well as increased kinase activity are associated with the pathological functions of CK2 in a number of neoplasias.[6] It was only over the last decade, after extensive analyses in solid tumors, that basic and translational studies have provided evidence for a pivotal role of CK2 in driving the growth of different blood cancers as well, although the first report demonstrating increased CK2 expression in acute myelogenous leukemia (AML) dates back to 1985.[7] Since then, CK2 overexpression/activity has been demonstrated in other hematological malignancies, including acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and chronic myelogenous leukemia (CML). [8] With the notable exceptions of CML and pediatric ALL, many patients with leukemias still have a poor outcome, despite the development of protocols with optimized chemotherapy combinations. Insufficient response to first-line therapy and unsalvageable relapses present major therapeutic challenges. Moreover, chemotherapy, even if successful, could have deleterious long-term biological and psychological effects, especially in children.[9] Furthermore, CML patients can develop resistance to tyrosine kinase inhibitors (TKIs), while both primary chemoresistant and relapsed pediatric ALL cases still remain an unresolved issue.[9