Log-Euclidean Bag of Words for Human Action Recognition

Representing videos by densely extracted local space-time features has recently become a popular approach for analysing actions. In this paper, we tackle the problem of categorising human actions by devising Bag of Words (BoW) models based on covariance matrices of spatio-temporal features, with the features formed from histograms of optical flow. Since covariance matrices form a special type of Riemannian manifold, the space of Symmetric Positive Definite (SPD) matrices, non-Euclidean geometry should be taken into account while discriminating between covariance matrices. To this end, we propose to embed SPD manifolds to Euclidean spaces via a diffeomorphism and extend the BoW approach to its Riemannian version. The proposed BoW approach takes into account the manifold geometry of SPD matrices during the generation of the codebook and histograms. Experiments on challenging human action datasets show that the proposed method obtains notable improvements in discrimination accuracy, in comparison to several state-of-the-art methods

A primate virus generates transformed human cells by fusion

A model that explains both the origin and sporadic nature of cancer argues that cancer cells are a chance result of events that cause genomic and epigenetic variability. The prevailing view is that these events are mutations that affect chromosome segregation or stability. However, genomic and epigenetic variability is also triggered by cell fusion, which is often caused by viruses. Yet, cells fused by viruses are considered harmless because they die. We provide evidence that a primate virus uses both viral and exosomal proteins involved in cell fusion to produce transformed proliferating human cells. Although normal cells indeed fail to proliferate after fusion, expression of an oncogene or a mutated tumor suppressor p53 in just one of the fusion partners is sufficient to produce heterogeneous progeny. We also show that this virus can produce viable oncogenically transformed cells by fusing cells that are otherwise destined to die. Therefore, we argue that viruses can contribute to carcinogenesis by fusing cells

Antiapoptotic herpesvirus Bcl-2 homologs escape caspase-mediated conversion to proapoptotic proteins

The antiapoptotic Bcl-2 and Bcl-x(L) proteins of mammals are converted into potent proapoptotic factors when they are cleaved by caspases, a family of apoptosis-inducing proteases (E. H.-Y. Cheng, D. G. Kirsch, R. J. Clem, R. Ravi, M. B. Kastan, A. Bedi, K. Ueno, and J. M. Hardwick, Science 278:1966-1968, 1997; R. J. Clem, E. H.-Y. Cheng, C. L. Karp, D. G. Kirsch, K. Ueno, A. Takahashi, M. B. Kastan, D. E. Griffin, W. C. Earnshaw, M. A. Veliuona, and J. M. Hardwick, Proc. Natl. Acad. Sci. USA 95:554-559, 1998). Gamma herpesviruses also encode homologs of the Bcl-2 family. All tested herpesvirus Bcl-2 homologs possess antiapoptotic activity, including the more distantly related homologs encoded by murine gammaherpesvirus 68 (gammaHV68) and bovine herpesvirus 4 (BHV4), as described here. To determine if viral Bcl-2 proteins can be converted into death factors, similar to their cellular counterparts, five herpesvirus Bcl-2 homologs from five different viruses were tested for their susceptibility to caspases. Only the viral Bcl-2 protein encoded by gammaHV68 was susceptible to caspase digestion. However, unlike the caspase cleavage products of cellular Bcl-2, Bcl-x(L), and Bid, which are potent inducers of apoptosis, the cleavage product of gammaHV68 Bcl-2 lacked proapoptotic activity. KSBcl-2, encoded by the Kaposi's sarcoma-associated herpesvirus, was the only viral Bcl-2 homolog that was capable of killing cells when expressed as an N-terminal truncation. However, because KSBcl-2 was not cleavable by caspases, the latent proapoptotic activity of KSBcl-2 apparently cannot be released. The Bcl-2 homologs encoded by herpesvirus saimiri, Epstein-Barr virus, and BHV4 were not cleaved by apoptotic cell extracts and did not possess latent proapoptotic activities. Thus, herpesvirus Bcl-2 homologs escape negative regulation by retaining their antiapoptotic activities and/or failing to be converted into proapoptotic proteins by caspases during programmed cell death

Oncogene-dependent apoptosis in extracts from drug-resistant cells

Many genotoxic agents kill tumor cells by inducing apoptosis; hence, mutations that suppress apoptosis produce resistance to chemotherapy. Although directly activating the apoptotic machinery may bypass these mutations, how to achieve this activation in cancer cells selectively is not clear. In this study, we show that the drug-resistant 293 cell line is unable to activate components of the apoptotic machinery-the ICE-like proteases (caspases)-following treatment with an anticancer drug. Remarkably, extracts from untreated cells spontaneously activate caspases and induce apoptosis in a cell-free system, indicating that drug-resistant cells have not only the apoptotic machinery but also its activator. Comparing extracts from cells with defined genetic differences, we show that this activator is generated by the adenovirus E1A oncogene and is absent from normal cells. We provide preliminary characterization of this oncogene generated activity (OGA) and show that partially purified OGA activates caspases when added to extracts from untransformed cells. We suggest that agents that link OGA to caspases in cells would kill tumor cells otherwise resistant to conventional cancer therapy. As this killing relies on an activity generated by an oncogene, the effect of these agents should be selective for transformed cells

Salient Objects in Clutter: Bringing Salient Object Detection to the Foreground

We provide a comprehensive evaluation of salient object detection (SOD) models. Our analysis identifies a serious design bias of existing SOD datasets which assumes that each image contains at least one clearly outstanding salient object in low clutter. The design bias has led to a saturated high performance for state-of-the-art SOD models when evaluated on existing datasets. The models, however, still perform far from being satisfactory when applied to real-world daily scenes. Based on our analyses, we first identify 7 crucial aspects that a comprehensive and balanced dataset should fulfill. Then, we propose a new high quality dataset and update the previous saliency benchmark. Specifically, our SOC (Salient Objects in Clutter) dataset, includes images with salient and non-salient objects from daily object categories. Beyond object category annotations, each salient image is accompanied by attributes that reflect common challenges in real-world scenes. Finally, we report attribute-based performance assessment on our dataset.Comment: ECCV 201

Studies of the lamin proteinase reveal multiple parallel biochemical pathways during apoptotic execution

Although specific proteinases play a critical role in the active phase of apoptosis, their substrates are largely unknown. We previously identified poly(ADP-ribose) polymerase (PARP) as an apoptosis-associated substrate for proteinase(s) related to interleukin 1 beta-converting enzyme (ICE). Now we have used a cell-free system to characterize proteinase(s) that cleave the nuclear lamins during apoptosis. Lamin cleavage during apoptosis requires the action of a second ICE-like enyzme, which exhibits kinetics of cleavage and a profile of sensitivity to specific inhibitors that is distinct from the PARP proteinase. Thus, multiple ICE-like enzymes are required for apoptotic events in these cell-free extracts. Inhibition of the lamin proteinase with tosyllysine "chloromethyl ketone" blocks nuclear apoptosis prior to the packaging of condensed chromatin into apoptotic bodies. Under these conditions, the nuclear DNA is fully cleaved to a nucleosomal ladder. Our studies reveal that the lamin proteinase and the fragmentation nuclease function in independent parallel pathways during the final stages of apoptotic execution. Neither pathway alone is sufficient for completion of nuclear apoptosis. Instead, the various activities cooperate to drive the disassembly of the nucleus

Organometallic iridium(III) anticancer complexes with new mechanisms of action: NCI-60 screening, mitochondrial targeting, and apoptosis

Platinum complexes related to cisplatin, cis-[PtCl2(NH3)2], are successful anticancer drugs; however, other transition metal complexes offer potential for combating cisplatin resistance, decreasing side effects, and widening the spectrum of activity. Organometallic half-sandwich iridium (IrIII) complexes [Ir(Cpx)(XY)Cl]+/0 (Cpx = biphenyltetramethylcyclopentadienyl and XY = phenanthroline (1), bipyridine (2), or phenylpyridine (3)) all hydrolyze rapidly, forming monofunctional G adducts on DNA with additional intercalation of the phenyl substituents on the Cpx ring. In comparison, highly potent complex 4 (Cpx = phenyltetramethylcyclopentadienyl and XY = N,N-dimethylphenylazopyridine) does not hydrolyze. All show higher potency toward A2780 human ovarian cancer cells compared to cisplatin, with 1, 3, and 4 also demonstrating higher potency in the National Cancer Institute (NCI) NCI-60 cell-line screen. Use of the NCI COMPARE algorithm (which predicts mechanisms of action (MoAs) for emerging anticancer compounds by correlating NCI-60 patterns of sensitivity) shows that the MoA of these IrIII complexes has no correlation to cisplatin (or oxaliplatin), with 3 and 4 emerging as particularly novel compounds. Those findings by COMPARE were experimentally probed by transmission electron microscopy (TEM) of A2780 cells exposed to 1, showing mitochondrial swelling and activation of apoptosis after 24 h. Significant changes in mitochondrial membrane polarization were detected by flow cytometry, and the potency of the complexes was enhanced ca. 5× by co-administration with a low concentration (5 μM) of the γ-glutamyl cysteine synthetase inhibitor L-buthionine sulfoximine (L-BSO). These studies reveal potential polypharmacology of organometallic IrIII complexes, with MoA and cell selectivity governed by structural changes in the chelating ligands

Asymptotic Limits and Zeros of Chromatic Polynomials and Ground State Entropy of Potts Antiferromagnets

We study the asymptotic limiting function $W({G},q) = \lim_{n \to \infty}P(G,q)^{1/n}$, where $P(G,q)$ is the chromatic polynomial for a graph $G$ with $n$ vertices. We first discuss a subtlety in the definition of $W({G},q)$ resulting from the fact that at certain special points $q_s$, the following limits do not commute: $\lim_{n \to \infty} \lim_{q \to q_s} P(G,q)^{1/n} \ne \lim_{q \to q_s} \lim_{n \to \infty} P(G,q)^{1/n}$. We then present exact calculations of $W({G},q)$ and determine the corresponding analytic structure in the complex $q$ plane for a number of families of graphs ${G}$, including circuits, wheels, biwheels, bipyramids, and (cyclic and twisted) ladders. We study the zeros of the corresponding chromatic polynomials and prove a theorem that for certain families of graphs, all but a finite number of the zeros lie exactly on a unit circle, whose position depends on the family. Using the connection of $P(G,q)$ with the zero-temperature Potts antiferromagnet, we derive a theorem concerning the maximal finite real point of non-analyticity in $W({G},q)$, denoted $q_c$ and apply this theorem to deduce that $q_c(sq)=3$ and $q_c(hc) = (3+\sqrt{5})/2$ for the square and honeycomb lattices. Finally, numerical calculations of $W(hc,q)$ and $W(sq,q)$ are presented and compared with series expansions and bounds.Comment: 33 pages, Latex, 5 postscript figures, published version; includes further comments on large-q serie

The history of degenerate (bipartite) extremal graph problems

This paper is a survey on Extremal Graph Theory, primarily focusing on the case when one of the excluded graphs is bipartite. On one hand we give an introduction to this field and also describe many important results, methods, problems, and constructions.Comment: 97 pages, 11 figures, many problems. This is the preliminary version of our survey presented in Erdos 100. In this version 2 only a citation was complete