59,493 research outputs found

    From non-semisimple Hopf algebras to correlation functions for logarithmic CFT

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    We use factorizable finite tensor categories, and specifically the representation categories of factorizable ribbon Hopf algebras H, as a laboratory for exploring bulk correlation functions in local logarithmic conformal field theories. For any ribbon Hopf algebra automorphism omega of H we present a candidate for the space of bulk fields and endow it with a natural structure of a commutative symmetric Frobenius algebra. We derive an expression for the corresponding bulk partition functions as bilinear combinations of irreducible characters; as a crucial ingredient this involves the Cartan matrix of the category. We also show how for any candidate bulk state space of the type we consider, correlation functions of bulk fields for closed oriented world sheets of any genus can be constructed that are invariant under the natural action of the relevant mapping class group.Comment: 41 pages, several figures. version 2: typos corrected, bibliography updated, introduction extended, a few minor clarifications adde

    Müller glia activation in response to inherited retinal degeneration is highly varied and disease-specific

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    Despite different aetiologies, most inherited retinal disorders culminate in photoreceptor loss, which induces concomitant changes in the neural retina, one of the most striking being reactive gliosis by Müller cells. It is typically assumed that photoreceptor loss leads to an upregulation of glial fibrilliary acidic protein (Gfap) and other intermediate filament proteins, together with other gliosis-related changes, including loss of integrity of the outer limiting membrane (OLM) and deposition of proteoglycans. However, this is based on a mix of both injury-induced and genetic causes of photoreceptor loss. There are very few longitudinal studies of gliosis in the retina and none comparing these changes across models over time. Here, we present a comprehensive spatiotemporal assessment of features of gliosis in the degenerating murine retina that involves Müller glia. Specifically, we assessed Gfap, vimentin and chondroitin sulphate proteoglycan (CSPG) levels and outer limiting membrane (OLM) integrity over time in four murine models of inherited photoreceptor degeneration that encompass a range of disease severities (Crb1rd8/rd8, Prph2+/Δ307, Rho-/-, Pde6brd1/rd1). These features underwent very different changes, depending upon the disease-causing mutation, and that these changes are not correlated with disease severity. Intermediate filament expression did indeed increase with disease progression in Crb1rd8/rd8 and Prph2+/Δ307, but decreased in the Prph2+/Δ307 and Pde6brd1/rd1 models. CSPG deposition usually, but not always, followed the trends in intermediate filament expression. The OLM adherens junctions underwent significant remodelling in all models, but with differences in the composition of the resulting junctions; in Rho-/- mice, the adherens junctions maintained the typical rod-Müller glia interactions, while in the Pde6brd1/rd1 model they formed predominantly between Müller cells in late stage of degeneration. Together, these results show that gliosis and its associated processes are variable and disease-dependent

    Instanton-soliton loops in 5D super-Yang-Mills

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    C.P. is a Royal Society Research Fellow and is partly supported by U.S. DOE Grants DOESC0010008, DOE-ARRA-SC0003883 and DOE-DE-SC000789

    OBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency

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    Studies of the functional consequences of DCM-causing mutations have been limited to a few cases where patients with known mutations had heart transplants. To increase the number of potential tissue samples for direct investigation we performed whole exon sequencing of explanted heart muscle samples from 30 patients that had a diagnosis of familial dilated cardiomyopathy and screened for potentially disease-causing mutations in 58 HCM or DCM-related genes.We identified 5 potentially disease-causing OBSCN mutations in 4 samples; one sample had two OBSCN mutations and one mutation was judged to be not disease-related. Also identified were 6 truncating mutations in TTN, 3 mutations in MYH7, 2 in DSP and one each in TNNC1, TNNI3, MYOM1, VCL, GLA, PLB, TCAP, PKP2 and LAMA4. The mean level of obscurin mRNA was significantly greater and more variable in healthy donor samples than the DCM samples but did not correlate with OBSCN mutations. A single obscurin protein band was observed in human heart myofibrils with apparent mass 960 ± 60 kDa. The three samples with OBSCN mutations had significantly lower levels of obscurin immunoreactive material than DCM samples without OBSCN mutations (45±7, 48±3, and 72±6% of control level).Obscurin levels in DCM controls, donor heart and myectomy samples were the same.OBSCN mutations may result in the development of a DCM phenotype via haploinsufficiency. Mutations in the obscurin gene should be considered as a significant causal factor of DCM, alone or in concert with other mutations

    Uterine sarcoma – current perspectives

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    Uterine sarcomas comprise a group of rare tumors with differing tumor biology, natural history and response to treatment. Diagnosis is often made following surgery for presumed benign disease. Currently, preoperative imaging does not reliably distinguish between benign leiomyomas and other malignant pathology. Uterine leiomyosarcoma is the most common sarcoma, but other subtypes include endometrial stromal sarcoma (low grade and high grade), undifferentiated uterine sarcoma and adenosarcoma. Clinical trials have shown no definite survival benefit of adjuvant radiotherapy or chemotherapy and have been hampered by the rarity and heterogeneity of these disease types. There is a role of adjuvant treatment in carefully selected cases following multidisciplinary discussion at sarcoma reference centers. In patients with metastatic disease, systemic chemotherapy can then be considered. There is activity of a number of agents, including doxorubicin, trabectedin, gemcitabine-based chemotherapy, eribulin and pazopanib. Patients should be considered for clinical trial entry where possible. Close international collaboration is important to allow progress in this group of diseases

    Bioethanol from Germinated Grains.

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    The most well-known way to produce bioethanol is by the enzymatic hydrolysis and fermentation of starch. In a new project “BioConcens” (2007) sponsored by DARCOF (DAnish Research Center for Organic Food and farming) one aim is to develop a combined ethanol and biogas production for use in organic farming using starch containing biomass. Natural enzymes from cereals will be used for hydrolysis of starch to glucose in accordance with technology in brewing technology. Commercial enzymes are often produced from gene-modified organisms and will therefore not be used in the suggested organic context or process. A preliminary study was performed in which grains of wheat, rye, and barley were germinated using traditional methods applied in malting for beer production. During malting the amylase enzymes present in the grain are activated (autoamylolytic effect). Three steps were applied in the malting process; steeping, germination, and drying of the grains. After malting the grains were milled and mixed with water to 13% DM, cooked at 57.5C for 2 hours (to activate the enzymes), and cooled to 30C before adding Bakers Yeast. The results of this study indicate that efficient hydrolysis of starch can be achieved by activation of autoamylolytic enzymes in cereal grains after a malting process. The ethanol yields obtained in the autoamylolytic hydrolysis was comparable (or slightly higher) to that of reference experiments using commercial enzymes (amylases). The highest ethanol yield was obtained with wheat (0.34 g/g DM grain), followed by barley (0.31 g/g DM grain), and rye (0.29 g/g DM grain)

    An integrated approach to the interpretation of Single Amino Acid Polymorphisms within the framework of CATH and Gene3D

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    Background: The phenotypic effects of sequence variations in protein-coding regions come about primarily via their effects on the resulting structures, for example by disrupting active sites or affecting structural stability. In order better to understand the mechanisms behind known mutant phenotypes, and predict the effects of novel variations, biologists need tools to gauge the impacts of DNA mutations in terms of their structural manifestation. Although many mutations occur within domains whose structure has been solved, many more occur within genes whose protein products have not been structurally characterized.Results: Here we present 3DSim (3D Structural Implication of Mutations), a database and web application facilitating the localization and visualization of single amino acid polymorphisms (SAAPs) mapped to protein structures even where the structure of the protein of interest is unknown. The server displays information on 6514 point mutations, 4865 of them known to be associated with disease. These polymorphisms are drawn from SAAPdb, which aggregates data from various sources including dbSNP and several pathogenic mutation databases. While the SAAPdb interface displays mutations on known structures, 3DSim projects mutations onto known sequence domains in Gene3D. This resource contains sequences annotated with domains predicted to belong to structural families in the CATH database. Mappings between domain sequences in Gene3D and known structures in CATH are obtained using a MUSCLE alignment. 1210 three-dimensional structures corresponding to CATH structural domains are currently included in 3DSim; these domains are distributed across 396 CATH superfamilies, and provide a comprehensive overview of the distribution of mutations in structural space.Conclusion: The server is publicly available at http://3DSim.bioinfo.cnio.es/. In addition, the database containing the mapping between SAAPdb, Gene3D and CATH is available on request and most of the functionality is available through programmatic web service access

    On Hierarchy and Equivalence of Relativistic Equations for Massive Fields

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    A non-canonical correspondence of the complete sets of solutions to the Dirac and Klein-Gordon free equations in Minkowski space-time is established. This allows for a novel viewpoint on the relationship of relativistic equations for different spins and on the origin of spinor transformations. In particular, starting from a solution to the Dirac equation, one obtains a chain of other solutions to both Dirac and Klein-Gordon equations. A comparison with the massless case is performed, and examples of non-trivial singular solutions are presented. A generalization to Riemannian space-time and inclusion of interactions are briefly discussed.Comment: 7 pages, twocolumn. Problem of construction the hierarchy of solutions in the massive case reformulate
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