Fitting a 3D Morphable Model to Edges: A Comparison Between Hard and Soft Correspondences

We propose a fully automatic method for fitting a 3D morphable model to single face images in arbitrary pose and lighting. Our approach relies on geometric features (edges and landmarks) and, inspired by the iterated closest point algorithm, is based on computing hard correspondences between model vertices and edge pixels. We demonstrate that this is superior to previous work that uses soft correspondences to form an edge-derived cost surface that is minimised by nonlinear optimisation.Comment: To appear in ACCV 2016 Workshop on Facial Informatic

Duckietown: An Innovative Way to Teach Autonomy

Teaching robotics is challenging because it is a multidisciplinary, rapidly evolving and experimental discipline that integrates cutting-edge hardware and software. This paper describes the course design and first implementation of Duckietown, a vehicle autonomy class that experiments with teaching innovations in addition to leveraging modern educational theory for improving student learning. We provide a robot to every student, thanks to a minimalist platform design, to maximize active learning; and introduce a role-play aspect to increase team spirit, by modeling the entire class as a fictional start-up (Duckietown Engineering Co.). The course formulation leverages backward design by formalizing intended learning outcomes (ILOs) enabling students to appreciate the challenges of: (a) heterogeneous disciplines converging in the design of a minimal self-driving car, (b) integrating subsystems to create complex system behaviors, and (c) allocating constrained computational resources. Students learn how to assemble, program, test and operate a self-driving car (Duckiebot) in a model urban environment (Duckietown), as well as how to implement and document new features in the system. Traditional course assessment tools are complemented by a full scale demonstration to the general public. The “duckie” theme was chosen to give a gender-neutral, friendly identity to the robots so as to improve student involvement and outreach possibilities. All of the teaching materials and code is released online in the hope that other institutions will adopt the platform and continue to evolve and improve it, so to keep pace with the fast evolution of the field.National Science Foundation (U.S.) (Award IIS #1318392)National Science Foundation (U.S.) (Award #1405259

The interplay of intrinsic and extrinsic bounded noises in genetic networks

After being considered as a nuisance to be filtered out, it became recently clear that biochemical noise plays a complex role, often fully functional, for a genetic network. The influence of intrinsic and extrinsic noises on genetic networks has intensively been investigated in last ten years, though contributions on the co-presence of both are sparse. Extrinsic noise is usually modeled as an unbounded white or colored gaussian stochastic process, even though realistic stochastic perturbations are clearly bounded. In this paper we consider Gillespie-like stochastic models of nonlinear networks, i.e. the intrinsic noise, where the model jump rates are affected by colored bounded extrinsic noises synthesized by a suitable biochemical state-dependent Langevin system. These systems are described by a master equation, and a simulation algorithm to analyze them is derived. This new modeling paradigm should enlarge the class of systems amenable at modeling. We investigated the influence of both amplitude and autocorrelation time of a extrinsic Sine-Wiener noise on: $(i)$ the Michaelis-Menten approximation of noisy enzymatic reactions, which we show to be applicable also in co-presence of both intrinsic and extrinsic noise, $(ii)$ a model of enzymatic futile cycle and $(iii)$ a genetic toggle switch. In $(ii)$ and $(iii)$ we show that the presence of a bounded extrinsic noise induces qualitative modifications in the probability densities of the involved chemicals, where new modes emerge, thus suggesting the possibile functional role of bounded noises

How managers can build trust in strategic alliances: a meta-analysis on the central trust-building mechanisms

Trust is an important driver of superior alliance performance. Alliance managers are influential in this regard because trust requires active involvement, commitment and the dedicated support of the key actors involved in the strategic alliance. Despite the importance of trust for explaining alliance performance, little effort has been made to systematically investigate the mechanisms that managers can use to purposefully create trust in strategic alliances. We use Parkhe’s (1998b) theoretical framework to derive nine hypotheses that distinguish between process-based, characteristic-based and institutional-based trust-building mechanisms. Our meta-analysis of 64 empirical studies shows that trust is strongly related to alliance performance. Process-based mechanisms are more important for building trust than characteristic- and institutional-based mechanisms. The effects of prior ties and asset specificity are not as strong as expected and the impact of safeguards on trust is not well understood. Overall, theoretical trust research has outpaced empirical research by far and promising opportunities for future empirical research exist

A Dual Inhibitory Mechanism Sufficient to Maintain Cell-Cycle-Restricted CENP-A Assembly

Chromatin featuring the H3 variant CENP-A at the centromere is critical for its mitotic function and epigenetic maintenance. Assembly of centromeric chromatin is restricted to G1 phase through inhibitory action of Cdk1/2 kinases in other phases of the cell cycle. Here, we identify the two key targets sufficient to maintain cell-cycle control of CENP-A assembly. We uncovered a single phosphorylation site in the licensing factor M18BP1 and a cyclin A binding site in the CENP-A chaperone, HJURP, that mediated specific inhibitory phosphorylation. Simultaneous expression of mutant proteins lacking these residues results in complete uncoupling from the cell cycle. Consequently, CENP-A assembly is fully recapitulated under high Cdk activities, indistinguishable from G1 assembly. We find that Cdk-mediated inhibition is exerted by sequestering active factors away from the centromere. Finally, we show that displacement of M18BP1 from the centromere is critical for the assembly mechanism of CENP-A

Effect of sampling effort and sampling frequency on the composition of the planktonic crustacean assemblage: a case study of the river Danube

Although numerous studies have focused on the seasonal dynamics of riverine zooplankton, little is known about its short-term variation. In order to examine the effects of sampling frequency and sampling effort, microcrustacean samples were collected at daily intervals between 13 June and 21 July of 2007 in a parapotamal side arm of the river Danube, Hungary. Samples were also taken at biweekly intervals from November 2006 to May 2008. After presenting the community dynamics, the effect of sampling effort was evaluated with two different methods; the minimal sample size was also estimated. We introduced a single index (potential dynamic information loss; to determine the potential loss of information when sampling frequency is reduced. The formula was calculated for the total abundance, densities of the dominant taxa, adult/larva ratios of copepods and for two different diversity measures. Results suggest that abundances may experience notable fluctuations even within 1 week, as do diversities and adult/larva ratios

Intraoperative device closure of atrial septal defects in the Older Population

<p>Abstract</p> <p>Objective</p> <p>This study sought to prove the safety and feasibility of intraoperative device closure of atrial septal defect (ASD) with transthoracic minimal invasion in the older patients.</p> <p>Methods</p> <p>From January 2006 to December 2009, 47 patients aged 50 years or more and suffered from atrial septal defect were enrolled in our institution. Patients were divided into two groups, 27 of which in group I with intraoperative device closure and the other 20 in group II with surgical closure. In group I, the method involved a minimal intercostal incision, which was performed after full evaluation of the atrial septal defect by transthoracic echocardiography, and the insertion of the device through the delivery sheath to occlude the atrial septal defect.</p> <p>Results</p> <p>In group I, implantation was ultimately successful in all patients. The complete closure rate at 24 hours and 1 year were 81.5% and 100% respectively. In 6 of 27 patients, minor complications occurred: transient arrhythmia (n = 5) and blood transfusion (n = 3). In group II, all patients were closured successfully; almost all of them needed blood transfusion and suffered from various minor complications though. During a follow-up period of 1 to 5 years, no residual shunt, noticeable mitral regurgitation, significant arrhythmias, thrombosis, or device failure were found. In our comparative studies, group II had significantly longer ICU stay and hospital stay than group I (p < 0.05). The cost of group I was less than that of group II(p < 0.05).</p> <p>Conclusions</p> <p>Minimally invasive transthoracic device closure of the atrial septal defect at advanced age with a domestically made device without cardiopulmonary bypass is safe and feasible under transthoracic echocardiographic guidance. It was cost-savings, yielding better cosmetic results and leaving fewer traumas than surgical closure. Early and mid-term results are encouraging. However, it is necessary to evaluate the long-term results.</p

Morphine induces preconditioning via activation of mitochondrial KCa channels

PURPOSE: Mitochondrial calcium sensitive potassium (mK(Ca)) channels are involved in cardioprotection induced by ischemic preconditioning. In the present study we investigated whether morphine-induced preconditioning also involves activation of mK(Ca) channels. METHODS: Isolated rat hearts (six groups; each n = 8) underwent global ischemia for 30 min followed by a 60-min reperfusion. Control animals were not further treated. Morphine preconditioning (MPC) was initiated by two five-minute cycles of morphine 1 muM infusion with one five-minute washout and one final ten-minute washout period before ischemia. The mK(Ca) blocker, paxilline 1 muM, was administered, with and without morphine administration (MPC + Pax and Pax). As a positive control, we added an ischemic preconditioning group (IPC) alone and combined with paxilline (IPC + Pax). At the end of reperfusion, infarct sizes were determined by triphenyltetrazoliumchloride staining. RESULTS: Infarct size was (mean +/- SD) 45 +/- 9% of the area at risk in the Control group. The infarct size was less in the morphine or ischemic preconditioning groups (MPC: 23 +/- 8%, IPC: 20 +/- 5%; each P < 0.05 vs Control). Infarct size reduction was abolished by paxilline (MPC + Pax: 37 +/- 7%, P < 0.05 vs MPC and IPC + Pax: 36 +/- 6%, P < 0.05 vs IPC), whereas paxilline alone had no effect (Pax: 46 +/- 7%, not significantly different from Control). CONCLUSION: Cardioprotection by morphine-induced preconditioning is mediated by activation of mK(Ca) channel

Biallelic mutations in IRF8 impair human NK cell maturation and function

Human NK cell deficiencies are rare yet result in severe and often fatal disease, particularly as a result of viral susceptibility. NK cells develop from hematopoietic stem cells, and few monogenic errors that specifically interrupt NK cell development have been reported. Here we have described biallelic mutations in IRF8, which encodes an interferon regulatory factor, as a cause of familial NK cell deficiency that results in fatal and severe viral disease. Compound heterozygous or homozygous mutations in IRF8 in 3 unrelated families resulted in a paucity of mature CD56dim NK cells and an increase in the frequency of the immature CD56bright NK cells, and this impairment in terminal maturation was also observed in Irf8–/–, but not Irf8+/–, mice. We then determined that impaired maturation was NK cell intrinsic, and gene expression analysis of human NK cell developmental subsets showed that multiple genes were dysregulated by IRF8 mutation. The phenotype was accompanied by deficient NK cell function and was stable over time. Together, these data indicate that human NK cells require IRF8 for development and functional maturation and that dysregulation of this function results in severe human disease, thereby emphasizing a critical role for NK cells in human antiviral defense