Local calibrations for minimizers of the Mumford-Shah functional with rectilinear discontinuity sets

Using a calibration method, we prove that, if $w$ is a function which satisfies all Euler conditions for the Mumford-Shah functional on a two-dimensional open set $\Omega$, and the discontinuity set of $w$ is a segment connecting two boundary points, then for every point $(x_0, y_0)$ of $\Omega$ there exists a neighbourhood $U$ of $(x_0, y_0)$ such that $w$ is a minimizer of the Mumford-Shah functional on $U$ with respect to its own boundary values on $\partial U$.Comment: 22 pages, 4 figure

Sampling-based optimal kinodynamic planning with motion primitives

This paper proposes a novel sampling-based motion planner, which integrates in RRT* (Rapidly exploring Random Tree star) a database of pre-computed motion primitives to alleviate its computational load and allow for motion planning in a dynamic or partially known environment. The database is built by considering a set of initial and final state pairs in some grid space, and determining for each pair an optimal trajectory that is compatible with the system dynamics and constraints, while minimizing a cost. Nodes are progressively added to the tree {of feasible trajectories in the RRT* by extracting at random a sample in the gridded state space and selecting the best obstacle-free motion primitive in the database that joins it to an existing node. The tree is rewired if some nodes can be reached from the new sampled state through an obstacle-free motion primitive with lower cost. The computationally more intensive part of motion planning is thus moved to the preliminary offline phase of the database construction at the price of some performance degradation due to gridding. Grid resolution can be tuned so as to compromise between (sub)optimality and size of the database. The planner is shown to be asymptotically optimal as the grid resolution goes to zero and the number of sampled states grows to infinity

Learning the dynamics of articulated tracked vehicles

In this work, we present a Bayesian non-parametric approach to model the motion control of ATVs. The motion control model is based on a Dirichlet Process-Gaussian Process (DP-GP) mixture model. The DP-GP mixture model provides a flexible representation of patterns of control manoeuvres along trajectories of different lengths and discretizations. The model also estimates the number of patterns, sufficient for modeling the dynamics of the ATV

Effects of lactation stage, parity, beta-lactoglobulin genotype and milk SCC on whey protein composition in Sarda dairy ewes

In 90 Sarda dairy ewes the effects of lactation stage, parity, beta-lactoglobulin genotypes, and somatic cell count (SCC) on the milk content of total protein (TP), casein (CN), whey protein (WP) and its fractions alpha-lactalbumin (ALA), beta-lactoglobulin (BLG), serum albumin (SA), immunoglobulin (IG) and lactoferrin (LF) were analysed using a linear mixed model. Mean values of variables (g/l) were: TP (54.0), CN (43.0), WP (11.0), BLG (4.78), ALA (1.37), SA (0.61), IG (3.83) and LF (0.28). The lactation stage significantly affected all the variables analysed. TP, CN and WP concentrations tended to increase throughout lactation, with the increase of WP being more pronounced than the corresponding variation in CN. There was no definite trend in BLG content, whereas ALA concentration decreased as lactation progressed. The parity affected almost all variables studied. WP concentration differed significantly only between the second and fourth parity (10.45 vs 11.44 g/l). BLG and SA concentrations were significantly lower in the youngest ewes. The BLG genotype affected milk yield, but no effects were observed on the components of the milk. The SCC influenced almost all variables studied. The TP concentration was significantly higher in milk with SCC >1,000,000 (55.0 g/l) than in milk with lower SCC (53.4 g/l). This was mainly due to the increase of WP (12.52 and 10.24 g/l in milk with SCC above and below 1,000,000/ml respectively), especially in those WP fractions originating from blood

The Multifaceted Activity of the VirF Regulatory Protein in the Shigella Lifestyle

Shigella is a highly adapted human pathogen, mainly found in the developing world and causing a severe enteric syndrome. The highly sophisticated infectious strategy of Shigella banks on the capacity to invade the intestinal epithelial barrier and cause its inflammatory destruction. The cellular pathogenesis and clinical presentation of shigellosis are the sum of the complex action of a large number of bacterial virulence factors mainly located on a large virulence plasmid (pINV). The expression of pINV genes is controlled by multiple environmental stimuli through a regulatory cascade involving proteins and sRNAs encoded by both the pINV and the chromosome. The primary regulator of the virulence phenotype is VirF, a DNA-binding protein belonging to the AraC family of transcriptional regulators. The virF gene, located on the pINV, is expressed only within the host, mainly in response to the temperature transition occurring when the bacterium transits from the outer environment to the intestinal milieu. VirF then acts as anti-H-NS protein and directly activates the icsA and virB genes, triggering the full expression of the invasion program of Shigella. In this review we will focus on the structure of VirF, on its sophisticated regulation, and on its role as major player in the path leading from the non-invasive to the invasive phenotype of Shigella. We will address also the involvement of VirF in mechanisms aimed at withstanding adverse conditions inside the host, indicating that this protein is emerging as a global regulator whose action is not limited to virulence systems. Finally, we will discuss recent observations conferring VirF the potential of a novel antibacterial target for shigellosis

Beyond motor neurons: expanding the clinical spectrum in Kennedy's disease

Kennedy's disease, or spinal and bulbar muscular atrophy (SBMA), is an X-linked neuromuscular condition clinically characterised by weakness, atrophy and fasciculations of the limb and bulbar muscles, as a result of lower motor neuron degeneration. The disease is caused by an abnormally expanded triplet repeat expansions in the ubiquitously expressed androgen receptor gene, through mechanisms which are not entirely elucidated. Over the years studies from both humans and animal models have highlighted the involvement of cell populations other than motor neurons in SBMA, widening the disease phenotype. The most compelling aspect of these findings is their potential for therapeutic impact: muscle, for example, which is primarily affected in the disease, has been recently shown to represent a valid alternative target for therapy to motor neurons. In this review, we discuss the emerging study of the extra-motor neuron involvement in SBMA, which, besides increasingly pointing towards a multidisciplinary approach for affected patients, deepens our understanding of the pathogenic mechanisms and holds potential for providing new therapeutic targets for this disease

Beta-agonist stimulation ameliorates the phenotype of spinal and bulbar muscular atrophy mice and patient-derived myotubes

Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease characterized by the loss of lower motor neurons. SBMA is caused by expansions of a polyglutamine tract in the gene coding for androgen receptor (AR). Expression of polyglutamine-expanded AR causes damage to motor neurons and skeletal muscle cells. Here we investigated the effect of β-agonist stimulation in SBMA myotube cells derived from mice and patients, and in knock-in mice. We show that treatment of myotubes expressing polyglutamine-expanded AR with the β-agonist clenbuterol increases their size. Clenbuterol activated the phosphatidylinositol-3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) pathway and decreased the accumulation of polyglutamine-expanded AR. Treatment of SBMA knock-in mice with clenbuterol, which was started at disease onset, ameliorated motor function and extended survival. Clenbuterol improved muscle pathology, attenuated the glycolytic-to-oxidative metabolic alterations occurring in SBMA muscles and induced hypertrophy of both glycolytic and oxidative fibers. These results indicate that β-agonist stimulation is a novel therapeutic strategy for SBMA

Treatment timing and multidisciplinary approach in Apert syndrome

Apert syndrome is a rare congenital disorder characterized by craniosynostosis, midface hypoplasia and symmetric syndactyly of hands and feet. Abnormalities associated with Apert syndrome include premature fusion of coronal sutures system (coronal sutures and less frequently lambdoid suture) resulting in brachiturricephalic dismorphism and impaired skull base growth. After this brief explanation it is clear that these anatomical abnormalities may have a negative impact on the ability to perform essential functions. Due to the complexity of the syndrome a multidisciplinary (respiratory, cerebral, maxillo-mandibular, dental, ophthalmic and orthopaedic) approach is necessary in treating the psychological, aesthetic and functional issues. The aim of this paper is to analyse the different functional issues and surgical methods trying to enhance results through a treatment plan which includes different specialities involved in Apert syndrome treatment. Reduced intellectual capacity is associated to the high number of general anaesthesia the small patients are subject to. Therefore the diagnostic and therapeutic treatment plan in these patients has established integrated and tailored surgical procedures based on the patients’ age in order to reduce the number of general anaesthesia, thus simplifying therapy for both Apert patients and their family members