Finitely presented wreath products and double coset decompositions

We characterize which permutational wreath products W^(X)\rtimes G are finitely presented. This occurs if and only if G and W are finitely presented, G acts on X with finitely generated stabilizers, and with finitely many orbits on the cartesian square X^2. On the one hand, this extends a result of G. Baumslag about standard wreath products; on the other hand, this provides nontrivial examples of finitely presented groups. For instance, we obtain two quasi-isometric finitely presented groups, one of which is torsion-free and the other has an infinite torsion subgroup. Motivated by the characterization above, we discuss the following question: which finitely generated groups can have a finitely generated subgroup with finitely many double cosets? The discussion involves properties related to the structure of maximal subgroups, and to the profinite topology.Comment: 21 pages; no figure. To appear in Geom. Dedicat

Comparison of K+K^+ and e−e^- Quasielastic Scattering

We formulate $K^+$-nucleus quasielastic scattering in a manner which closely parallels standard treatments of $e^-$-nucleus quasielastic scattering. For $K^+$ scattering, new responses involving scalar contributions appear in addition to the Coulomb (or longitudinal) and transverse $(e,e')$ responses which are of vector character. We compute these responses using both nuclear matter and finite nucleus versions of the Relativistic Hartree Approximation to Quantum Hadrodynamics including RPA correlations. Overall agreement with measured $(e,e')$ responses and new $K^+$ quasielastic scattering data for $^{40}$Ca at |\qs|=500 MeV/c is good. Strong RPA quenching is essential for agreement with the Coulomb response. This quenching is notably less for the $K^+$ cross section even though the new scalar contributions are even more strongly quenched than the vector contributions. We show that this ``differential quenching'' alters sensitive cancellations in the expression for the $K^+$ cross section so that it is reduced much less than the individual responses. We emphasize the role of the purely relativistic distinction between vector and scalar contributions in obtaining an accurate and consistent description of the $(e,e')$ and $K^+$ data within the framework of our nuclear structure model.Comment: 26 pages, 5 uuencoded figures appended to end of this fil

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Cerebellar Nuclear Neurons Use Time and Rate Coding to Transmit Purkinje Neuron Pauses

Copyright: © 2015 Sudhakar et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedNeurons of the cerebellar nuclei convey the final output of the cerebellum to their targets in various parts of the brain. Within the cerebellum their direct upstream connections originate from inhibitory Purkinje neurons. Purkinje neurons have a complex firing pattern of regular spikes interrupted by intermittent pauses of variable length. How can the cerebellar nucleus process this complex input pattern? In this modeling study, we investigate different forms of Purkinje neuron simple spike pause synchrony and its influence on candidate coding strategies in the cerebellar nuclei. That is, we investigate how different alignments of synchronous pauses in synthetic Purkinje neuron spike trains affect either time-locking or rate-changes in the downstream nuclei. We find that Purkinje neuron synchrony is mainly represented by changes in the firing rate of cerebellar nuclei neurons. Pause beginning synchronization produced a unique effect on nuclei neuron firing, while the effect of pause ending and pause overlapping synchronization could not be distinguished from each other. Pause beginning synchronization produced better time-locking of nuclear neurons for short length pauses. We also characterize the effect of pause length and spike jitter on the nuclear neuron firing. Additionally, we find that the rate of rebound responses in nuclear neurons after a synchronous pause is controlled by the firing rate of Purkinje neurons preceding it.Peer reviewedFinal Published versio

O período da contaminação com petróleo influencia a rebrota de Echinochloa polystachya (H.B.K.) Hitchcock em solo de várzea da Amazônia central?

Several factors may influence the impact of oil on the environment. However, although it is understood that the effect of pollutants may change throughout the year according to seasonal variations in environmental parameters, this effect is poorly studied in the tropical region. The effects of Urucu's crude oil on the vegetative propagation and growth of Echinochloa polystachya were evaluated in a 63 days period, in two experiments, "A" (July-September) and "B" (September-November) planting the species in a greenhouse. In both experiments parts of stems were placed in 2 L of várzea soil contaminated by 6 oil doses, ranging from 0 to 0.231 L oil m-2 soil. In response to dosage increase there was a decrease of total biomass, ratio of live /total biomass, the leaf length and number of leaves. The period of planting influenced the response of plants to the dosage applied due to climate change, with negative effects in the "B" period of higher temperatures. We concluded that the exposure period influence the vegetative propagation and growth of the seedlings, being a spill in the period of the higher temperatures more dangerous for this specie

Driver Fusions and Their Implications in the Development and Treatment of Human Cancers.

Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated fusions in 9,624 tumors across 33 cancer types using multiple fusion calling tools. We identified a total of 25,664 fusions, with a 63% validation rate. Integration of gene expression, copy number, and fusion annotation data revealed that fusions involving oncogenes tend to exhibit increased expression, whereas fusions involving tumor suppressors have the opposite effect. For fusions involving kinases, we found 1,275 with an intact kinase domain, the proportion of which varied significantly across cancer types. Our study suggests that fusions drive the development of 16.5% of cancer cases and function as the sole driver in more than 1% of them. Finally, we identified druggable fusions involving genes such as TMPRSS2, RET, FGFR3, ALK, and ESR1 in 6.0% of cases, and we predicted immunogenic peptides, suggesting that fusions may provide leads for targeted drug and immune therapy

Somatic Mutational Landscape of Splicing Factor Genes and Their Functional Consequences across 33 Cancer Types

Hotspot mutations in splicing factor genes have been recently reported at high frequency in hematological malignancies, suggesting the importance of RNA splicing in cancer. We analyzed whole-exome sequencing data across 33 tumor types in The Cancer Genome Atlas (TCGA), and we identified 119 splicing factor genes with significant non-silent mutation patterns, including mutation over-representation, recurrent loss of function (tumor suppressor-like), or hotspot mutation profile (oncogene-like). Furthermore, RNA sequencing analysis revealed altered splicing events associated with selected splicing factor mutations. In addition, we were able to identify common gene pathway profiles associated with the presence of these mutations. Our analysis suggests that somatic alteration of genes involved in the RNA-splicing process is common in cancer and may represent an underappreciated hallmark of tumorigenesis

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although the MYC oncogene has been implicated in cancer, a systematic assessment of alterations of MYC, related transcription factors, and co-regulatory proteins, forming the proximal MYC network (PMN), across human cancers is lacking. Using computational approaches, we define genomic and proteomic features associated with MYC and the PMN across the 33 cancers of The Cancer Genome Atlas. Pan-cancer, 28% of all samples had at least one of the MYC paralogs amplified. In contrast, the MYC antagonists MGA and MNT were the most frequently mutated or deleted members, proposing a role as tumor suppressors. MYC alterations were mutually exclusive with PIK3CA, PTEN, APC, or BRAF alterations, suggesting that MYC is a distinct oncogenic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such as immune response and growth factor signaling; chromatin, translation, and DNA replication/repair were conserved pan-cancer. This analysis reveals insights into MYC biology and is a reference for biomarkers and therapeutics for cancers with alterations of MYC or the PMN. We present a computational study determining the frequency and extent of alterations of the MYC network across the 33 human cancers of TCGA. These data, together with MYC, positively correlated pathways as well as mutually exclusive cancer genes, will be a resource for understanding MYC-driven cancers and designing of therapeutics