Total irredundance in graphs

AbstractA set S of vertices in a graph G is called a total irredundant set if, for each vertex v in G,v or one of its neighbors has no neighbor in S−{v}. We investigate the minimum and maximum cardinalities of maximal total irredundant sets

Building a reduced dictionary of relevant perfusion patterns from CEUS data for the classification of testis lesions

Radical orchifunicolectomy has traditionally been the main clinical treatment for small testicular masses (STMs); however STMs represent a constantly increasing and often incidental finding. Since many of them result benign, a more conservative testis-sparing surgery was proposed, but it requires a preliminary differentiation between benign and malignant masses: this however remains challenging. Although common understanding in radiology and oncology is that perfusion patterns might provide a useful information about the type of masses, no guidelines or consensus is available for the differentiation of STMs. We propose to build a dictionary of relevant perfusion patterns, extracted using non-negative matrix factorization on pixel-wise time-intensity curves from contrast-enhanced ultrasound data. When data from a lesion are reconstructed using this dictionary, a vector containing the frequency of utilization of each pattern can be used as a tissue signature. Using this signature, a support vector machine classifier has been trained, and the cross validated accuracy reached 100% in our pilot cohort

On the (parameterized) complexity of recognizing well-covered (r,l)-graphs.

An (r,ℓ)(r,ℓ)-partition of a graph G is a partition of its vertex set into r independent sets and ℓℓ cliques. A graph is (r,ℓ)(r,ℓ) if it admits an (r,ℓ)(r,ℓ)-partition. A graph is well-covered if every maximal independent set is also maximum. A graph is (r,ℓ)(r,ℓ)-well-covered if it is both (r,ℓ)(r,ℓ) and well-covered. In this paper we consider two different decision problems. In the (r,ℓ)(r,ℓ)-Well-Covered Graph problem ((r,ℓ)(r,ℓ) wcg for short), we are given a graph G, and the question is whether G is an (r,ℓ)(r,ℓ)-well-covered graph. In the Well-Covered (r,ℓ)(r,ℓ)-Graph problem (wc (r,ℓ)(r,ℓ) g for short), we are given an (r,ℓ)(r,ℓ)-graph G together with an (r,ℓ)(r,ℓ)-partition of V(G) into r independent sets and ℓℓ cliques, and the question is whether G is well-covered. We classify most of these problems into P, coNP-complete, NP-complete, NP-hard, or coNP-hard. Only the cases wc(r, 0)g for r≥3r≥3 remain open. In addition, we consider the parameterized complexity of these problems for several choices of parameters, such as the size αα of a maximum independent set of the input graph, its neighborhood diversity, or the number ℓℓ of cliques in an (r,ℓ)(r,ℓ)-partition. In particular, we show that the parameterized problem of deciding whether a general graph is well-covered parameterized by αα can be reduced to the wc (0,ℓ)(0,ℓ) g problem parameterized by ℓℓ, and we prove that this latter problem is in XP but does not admit polynomial kernels unless coNP⊆NP/polycoNP⊆NP/poly

Intracranial V. cholerae Sialidase Protects against Excitotoxic Neurodegeneration

Converging evidence shows that GD3 ganglioside is a critical effector in a number of apoptotic pathways, and GM1 ganglioside has neuroprotective and noötropic properties. Targeted deletion of GD3 synthase (GD3S) eliminates GD3 and increases GM1 levels. Primary neurons from GD3S−/− mice are resistant to neurotoxicity induced by amyloid-β or hyperhomocysteinemia, and when GD3S is eliminated in the APP/PSEN1 double-transgenic model of Alzheimer's disease the plaque-associated oxidative stress and inflammatory response are absent. To date, no small-molecule inhibitor of GD3S exists. In the present study we used sialidase from Vibrio cholerae (VCS) to produce a brain ganglioside profile that approximates that of GD3S deletion. VCS hydrolyzes GD1a and complex b-series gangliosides to GM1, and the apoptogenic GD3 is degraded. VCS was infused by osmotic minipump into the dorsal third ventricle in mice over a 4-week period. Sensorimotor behaviors, anxiety, and cognition were unaffected in VCS-treated mice. To determine whether VCS was neuroprotective in vivo, we injected kainic acid on the 25th day of infusion to induce status epilepticus. Kainic acid induced a robust lesion of the CA3 hippocampal subfield in aCSF-treated controls. In contrast, all hippocampal regions in VCS-treated mice were largely intact. VCS did not protect against seizures. These results demonstrate that strategic degradation of complex gangliosides and GD3 can be used to achieve neuroprotection without adversely affecting behavior

Evidence for a Common Toolbox Based on Necrotrophy in a Fungal Lineage Spanning Necrotrophs, Biotrophs, Endophytes, Host Generalists and Specialists

The Sclerotiniaceae (Ascomycotina, Leotiomycetes) is a relatively recently evolved lineage of necrotrophic host generalists, and necrotrophic or biotrophic host specialists, some latent or symptomless. We hypothesized that they inherited a basic toolbox of genes for plant symbiosis from their common ancestor. Maintenance and evolutionary diversification of symbiosis could require selection on toolbox genes or on timing and magnitude of gene expression. The genes studied were chosen because their products have been previously investigated as pathogenicity factors in the Sclerotiniaceae. They encode proteins associated with cell wall degradation: acid protease 1 (acp1), aspartyl protease (asps), and polygalacturonases (pg1, pg3, pg5, pg6), and the oxalic acid (OA) pathway: a zinc finger transcription factor (pac1), and oxaloacetate acetylhydrolase (oah), catalyst in OA production, essential for full symptom production in Sclerotinia sclerotiorum. Site-specific likelihood analyses provided evidence for purifying selection in all 8 pathogenicity-related genes. Consistent with an evolutionary arms race model, positive selection was detected in 5 of 8 genes. Only generalists produced large, proliferating disease lesions on excised Arabidopsis thaliana leaves and oxalic acid by 72 hours in vitro. In planta expression of oah was 10–300 times greater among the necrotrophic host generalists than necrotrophic and biotrophic host specialists; pac1 was not differentially expressed. Ability to amplify 6/8 pathogenicity related genes and produce oxalic acid in all genera are consistent with the common toolbox hypothesis for this gene sample. That our data did not distinguish biotrophs from necrotrophs is consistent with 1) a common toolbox based on necrotrophy and 2) the most conservative interpretation of the 3-locus housekeeping gene phylogeny – a baseline of necrotrophy from which forms of biotrophy emerged at least twice. Early oah overexpression likely expands the host range of necrotrophic generalists in the Sclerotiniaceae, while specialists and biotrophs deploy oah, or other as-yet-unknown toolbox genes, differently

Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders

There is a long-standing paradox that N-methyl-D-aspartate receptors (NMDARs) can both promote neuronal health and kill neurons. Recent studies show that NMDAR-induced responses depend on the receptor location: stimulation of synaptic NMDARs, acting primarily through nuclear Ca(2+) signaling, leads to the build-up of a neuroprotective ‘shield’, whereas stimulation of extrasynaptic NMDARs promotes cell death. These differences result from the activation of distinct genomic programmes and opposing actions on intracellular signalling pathways. Perturbations in the balance between synaptic and extrasynaptic NMDAR activity contribute to neuronal dysfunction in acute ischaemia and Huntington’s disease and could be a common theme in the aetiology of neurodegenerative diseases. Neuroprotective therapies should aim to both enhance the effect of synaptic activity and disrupt extrasynaptic NMDAR-dependent death signalling