Drum Transcription via Classification of Bar-level Rhythmic Patterns

acceptedMatthias Mauch is supported by a Royal Academy of Engineering Research Fellowshi

The Stripe 82 1-2 GHz Very Large Array Snapshot Survey: Multiwavelength Counterparts

We have combined spectrosopic and photometric data from the Sloan Digital Sky Survey (SDSS) with $1.4$ GHz radio observations, conducted as part of the Stripe 82 $1-2$ GHz Snapshot Survey using the Karl G. Jansky Very Large Array (VLA), which covers $\sim100$ sq degrees, to a flux limit of 88 $\mu$Jy rms. Cross-matching the $11\,768$ radio source components with optical data via visual inspection results in a final sample of $4\,795$ cross-matched objects, of which $1\,996$ have spectroscopic redshifts and $2\,799$ objects have photometric redshifts. Three previously undiscovered Giant Radio Galaxies (GRGs) were found during the cross-matching process, which would have been missed using automated techniques. For the objects with spectroscopy we separate radio-loud Active Galactic Nuclei (AGN) and star-forming galaxies (SFGs) using three diagnostics and then further divide our radio-loud AGN into the HERG and LERG populations. A control matched sample of HERGs and LERGs, matched on stellar mass, redshift and radio luminosity, reveals that the host galaxies of LERGs are redder and more concentrated than HERGs. By combining with near-infrared data, we demonstrate that LERGs also follow a tight $K-z$ relationship. These results imply the LERG population are hosted by population of massive, passively evolving early-type galaxies. We go on to show that HERGs, LERGs, QSOs and star-forming galaxies in our sample all reside in different regions of a WISE colour-colour diagram. This cross-matched sample bridges the gap between previous `wide but shallow' and `deep but narrow' samples and will be useful for a number of future investigations.Comment: 17 pages, 19 figures. Resubmitted to MNRAS after the initial comment

Subcellular immunocytochemical analysis detects the highest concentrations of glutathione in mitochondria and not in plastids

The tripeptide glutathione is a major antioxidant and redox buffer with multiple roles in plant metabolism. Glutathione biosynthesis is restricted to the cytosol and the plastids and the product is distributed to the various organelles by unknown mechanisms. In the present study immunogold cytochemistry based on anti-glutathione antisera and transmission electron microscopy was used to determine the relative concentration of glutathione in different organelles of Arabidopsis thaliana leaf and root cells. Glutathione-specific labelling was detected in all cellular compartments except the apoplast and the vacuole. The highest glutathione content was surprisingly not found in plastids, which have been described before as a major site of glutathione accumulation, but in mitochondria which lack the capacity for glutathione biosynthesis. Mitochondria of both leaf and root cells contained 7-fold and 4-fold, respectively, higher glutathione levels than plastids while the density of glutathione labelling in the cytosol, nuclei, and peroxisomes was intermediate. The accuracy of the glutathione labelling is supported by two observations. First, pre-adsorption of the anti-glutathione antisera with glutathione reduced the density of the gold particles in all organelles to background levels. Second, the overall glutathione-labelling density was reduced by about 90% in leaves of the glutathione-deficient Arabidopsis mutant pad2-1 and increased in transgenic plants with enhanced glutathione accumulation. Hence, there was a strong correlation between immunocytochemical and biochemical data of glutathione accumulation. Interestingly, the glutathione labelling of mitochondria in pad2-1 remained very similar to wild-type plants thus suggesting that the high mitochondrial glutathione content is maintained in a situation of permanent glutathione-deficiency at the expense of other glutathione pools. High and constant levels of glutathione in mitochondria appear to be particularly important in cell survival strategies and it is predicted that mitochondria must have highly competitive mitochondrial glutathione uptake systems. The present results underline the suggestion that subcellular glutathione concentrations are not controlled by a global mechanism but are controlled on an individual basis and it is therefore not possible to conclude from global biochemical glutathione analysis on the status of the various organellar pool

Análise técnico-econômica de dois sistemas de produção de cebola: orgânico e convencional - estudo de caso.

bitstream/item/31481/1/comunicado-210.pd

Evidence of a link between the evolution of clusters and their AGN fraction

‘The definitive version is available at www3.interscience.wiley.com .' Copyright Blackwell Publishing / Royal Astronomical Society. DOI: 10.1111/j.1365-2966.2009.14513.xPeer reviewe

Association between Antibodies to the MR 67,000 Isoform of Glutamate Decarboxylase (GAD) and Type 1 (Insulin-Dependent) Diabetes Mellitus with Coexisting Autoimmune Polyendocrine Syndrome Type II

By using an immunoprecipitation assay, we analysed reactivity of autoantibodies to human recombinant GAD65 and GAD67 in sera from patients with autoimmune polyendocrine syndrome Type II (APS II) with and without Type 1 (insulin-dependent) diabetes mellitus (IDDM) compared to patients with organ-specific autoimmunity. Overall antibodies to GAD65 were correlated with IDDM in all study groups, whereas GAD67 antibodies were associated with IDDM when APS II coexists. Antibodies to GAD65 and GAD67 were detected in 13 (44.8%) and 7 (24.1%) out of 29 APS II patients with IDDM, but in only 4 (13.8%) and 2 (6.9%) out of 29 APS II patients without IDDM, respectively (p < 0.05). In short-standing IDDM (< 1 year), antibodies to GAD67 were significantly more frequent in patients with APS II (5 of 9 [55.6%] subjects) compared to matched diabetic patients without coexisting polyendocrinopathy (1 of 18 [5.6%] subjects) (p < 0.02). The levels of GAD65 (142 ± 90 AU) and GAD67 antibodies (178 ± 95 AU) were significantly higher in patients with polyglandular disease than in patients with isolated IDDM (91 ± 85 AU and 93 ± 57 AU) (p < 0.02). Interestingly, all 11 GAD67 antibody positive subjects also had GAD65 antibodies (p < 0.0001), and in 10 of 11 anti-GAD67 positive sera the GAD67 antibodies could be blocked by either GAD67 or GAD65, suggesting the presence of cross-reactive autoantibodies. No correlation was observed between GAD antibodies and age, sex or any particular associated autoimmune disease, besides IDDM. GAD antibodies were present in only 1 of 6 (16.7%) patients with APS Type I, in 1 of 26 (3.9%) patients with autoimmune thyroid disease but in none of the patients with Addison's disease (n = 16), pernicious anaemia (n = 7) or normal controls (n = 50). Our data suggest distinct antibody specificities reactive to GAD isoforms in APS II and IDDM, which might reflect different mechanisms of autoimmune response in IDDM with coexisting autoimmune polyendocrine autoimmunity

Gad65 is recognized by t-cells, but not by antibodies from nod-mice

Since the 64kDa-protein glutamic acid decarboxylase (GAD) is one of the major autoantigens in T-cell mediated Type 1 diabetes, its relevance as a T-cell antigen needs to be clarified. After isolation of splenic T-cells from non-obese diabetic (NOD) mice, a useful model for human Type 1 diabetes, we found that these T-cells proliferate spontaneously when incubated with human GAD65, but only marginally after incubation with GAD67, both recombinated in the baculovirus system. No effect was observed with non-diabetic NOD mice or with T-cells from H-2 identical NON-NOD-H-2g7 control mice. It has been published previously that NOD mice develop autoantibodies against a 64kDa protein detected with mouse beta cells. In immunoprecipitation experiments with sera from the same NOD mice and 33S-methionine-labelled GAD, no autoantibody binding could be detected. We conclude firstly that GAD65 is an important T-cell antigen which is relevant early in the development of Type 1 diabetes and secondly that there is an antigenic epitope in the human GAD65 molecule recognized by NOD T-cells, but not by NOD autoantibodies precipitating conformational epitopes. Our results therefore provide further evidence that GAD65 is a T-cell antigen in NOD mice, being possibly also involved in very early processes leading to the development of human Type 1 diabetes