100 research outputs found

    Epilithic diatoms (Bacillariophycae) from streams in Ramsar, Iran

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    Epilithic diatoms were identified from five small streams and one canal in Ramsar, northwest Iran. Atotal of 155 diatom taxa belonging to 37 genera were found and only two species remained unidentified (Fragilaria sp. and Nitzschia sp.). Achnanthes, Nitzschia, Navicula, Cocconeis, Melosira, Amphora, Craticula, Diatoma, Surirella, Cymbella, Diploneis and Entomoneis were among the most abundant genera. Eighty seven taxa were recorded for the first time in Iran. Thirty two of the genera belong to the Pennales and 5 to the Centrales. Species richness was rather high ranging from 66 to 95 taxa at the six sites studied. The epilithic diatom species found in Ramsar were dominated by cosmopolitan taxa found in meso- to fairly eutrophic waters with high conductivity and high nutrient concentrations. The abundances found at all six sites were compiled in order to estimate the overall abundance of each taxon in Ramsar. This study includes EM pictures of diatoms observed in Ramsar, Iran

    RC3H1 post-transcriptionally regulates A20 mRNA and modulates the activity of the IKK/NF-kappa B pathway

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    The RNA-binding protein RC3H1 (also known as ROQUIN) promotes TNF alpha mRNA decay via a 3'UTR constitutive decay element (CDE). Here we applied PAR-CLIP to human RC3H1 to identify similar to 3, 800 mRNA targets with 416, 000 binding sites. A large number of sites are distinct from the consensus CDE and revealed a structure-sequence motif with U-rich sequences embedded in hairpins. RC3H1 binds preferentially short-lived and DNA damage-induced mRNAs, indicating a role of this RNA-binding protein in the post-transcriptional regulation of the DNA damage response. Intriguingly, RC3H1 affects expression of the NF-kappa B pathway regulators such as I kappa B alpha and A20. RC3H1 uses ROQ and Zn-finger domains to contact a binding site in the A20 30UTR, demonstrating a not yet recognized mode of RC3H1 binding. Knockdown of RC3H1 resulted in increased A20 protein expression, thereby interfering with I kappa B kinase and NF-kappa B activities, demonstrating that RC3H1 can modulate the activity of the IKK/NF-kappa B pathway

    Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA): a molecularly distinct brain tumor type with recurrent NTRK gene fusions

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    Glioneuronal tumors are a heterogenous group of CNS neoplasms that can be challenging to accurately diagnose. Molecular methods are highly useful in classifying these tumors-distinguishing precise classes from their histological mimics and identifying previously unrecognized types of tumors. Using an unsupervised visualization approach of DNA methylation data, we identified a novel group of tumors (n = 20) that formed a cluster separate from all established CNS tumor types. Molecular analyses revealed ATRX alterations (in 16/16 cases by DNA sequencing and/or immunohistochemistry) as well as potentially targetable gene fusions involving receptor tyrosine-kinases (RTK; mostly NTRK1-3) in all of these tumors (16/16; 100%). In addition, copy number profiling showed homozygous deletions of CDKN2A/B in 55% of cases. Histological and immunohistochemical investigations revealed glioneuronal tumors with isomorphic, round and often condensed nuclei, perinuclear clearing, high mitotic activity and microvascular proliferation. Tumors were mainly located supratentorially (84%) and occurred in patients with a median age of 19 years. Survival data were limited (n = 18) but point towards a more aggressive biology as compared to other glioneuronal tumors (median progression-free survival 12.5 months). Given their molecular characteristics in addition to anaplastic features, we suggest the term glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) to describe these tumors. In summary, our findings highlight a novel type of glioneuronal tumor driven by different RTK fusions accompanied by recurrent alterations in ATRX and homozygous deletions of CDKN2A/B. Targeted approaches such as NTRK inhibition might represent a therapeutic option for patients suffering from these tumors

    Oligosarcomas, IDH‑mutant are distinct and aggressive

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    Oligodendrogliomas are defined at the molecular level by the presence of an IDH mutation and codeletion of chromosomal arms 1p and 19q. In the past, case reports and small studies described gliomas with sarcomatous features arising from oligodendrogliomas, so called oligosarcomas. Here, we report a series of 24 IDH-mutant oligosarcomas from 23 patients forming a distinct methylation class. The tumors were recurrences from prior oligodendrogliomas or developed de novo. Precursor tumors of 12 oligosarcomas were histologically and molecularly indistinguishable from conventional oligodendrogliomas. Oligosarcoma tumor cells were embedded in a dense network of reticulin fibers, frequently showing p53 accumulation, positivity for SMA and CALD1, loss of OLIG2 and gain of H3K27 trimethylation (H3K27me3) as compared to primary lesions. In 5 oligosarcomas no 1p/19q codeletion was detectable, although it was present in the primary lesions. Copy number neutral LOH was determined as underlying mechanism. Oligosarcomas harbored an increased chromosomal copy number variation load with frequent CDKN2A/B deletions. Proteomic profiling demonstrated oligosarcomas to be highly distinct from conventional CNS WHO grade 3 oligodendrogliomas with consistent evidence for a smooth muscle differentiation. Expression of several tumor suppressors was reduced with NF1 being lost frequently. In contrast, oncogenic YAP1 was aberrantly overexpressed in oligosarcomas. Panel sequencing revealed mutations in NF1 and TP53 along with IDH1/2 and TERT promoter mutations. Survival of patients was significantly poorer for oligosarcomas as first recurrence than for grade 3 oligodendrogliomas as first recurrence. These results establish oligosarcomas as a distinct group of IDH-mutant gliomas differing from conventional oligodendrogliomas on the histologic, epigenetic, proteomic, molecular and clinical level. The diagnosis can be based on the combined presence of (a) sarcomatous histology, (b) IDH-mutation and (c) TERT promoter mutation and/or 1p/19q codeletion, or, in unresolved cases, on its characteristic DNA methylation profile

    Analysis methods for the first KATRIN neutrino-mass measurement

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    We report on the dataset, data handling, and detailed analysis techniques of the first neutrino-mass measurement by the Karlsruhe Tritium Neutrino (KATRIN) experiment, which probes the absolute neutrino-mass scale via the ÎČ-decay kinematics of molecular tritium. The source is highly pure, cryogenic T2 gas. The ÎČ electrons are guided along magnetic field lines toward a high-resolution, integrating spectrometer for energy analysis. A silicon detector counts ÎČ electrons above the energy threshold of the spectrometer, so that a scan of the thresholds produces a precise measurement of the high-energy spectral tail. After detailed theoretical studies, simulations, and commissioning measurements, extending from the molecular final-state distribution to inelastic scattering in the source to subtleties of the electromagnetic fields, our independent, blind analyses allow us to set an upper limit of 1.1 eV on the neutrino-mass scale at a 90% confidence level. This first result, based on a few weeks of running at a reduced source intensity and dominated by statistical uncertainty, improves on prior limits by nearly a factor of two. This result establishes an analysis framework for future KATRIN measurements, and provides important input to both particle theory and cosmology

    Precision measurement of the electron energy-loss function in tritium and deuterium gas for the KATRIN experiment

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    The KATRIN experiment is designed for a direct and model-independent determination of the effective electron anti-neutrino mass via a high-precision measurement of the tritium ÎČ\beta-decay endpoint region with a sensitivity on mÎœm_\nu of 0.2 \,eV/c2^2 (90% CL). For this purpose, the ÎČ\beta-electrons from a high-luminosity windowless gaseous tritium source traversing an electrostatic retarding spectrometer are counted to obtain an integral spectrum around the endpoint energy of 18.6 \,keV. A dominant systematic effect of the response of the experimental setup is the energy loss of ÎČ\beta-electrons from elastic and inelastic scattering off tritium molecules within the source. We determined the \linebreak energy-loss function in-situ with a pulsed angular-selective and monoenergetic photoelectron source at various tritium-source densities. The data was recorded in integral and differential modes; the latter was achieved by using a novel time-of-flight technique. We developed a semi-empirical parametrization for the energy-loss function for the scattering of 18.6-keV electrons from hydrogen isotopologs. This model was fit to measurement data with a 95% T2_2 gas mixture at 30 \,K, as used in the first KATRIN neutrino mass analyses, as well as a D2_2 gas mixture of 96% purity used in KATRIN commissioning runs. The achieved precision on the energy-loss function has abated the corresponding uncertainty of σ(mÎœ2)<10−2 eV2\sigma(m_\nu^2)<10^{-2}\,\mathrm{eV}^2 [arXiv:2101.05253] in the KATRIN neutrino-mass measurement to a subdominant level.Comment: 12 figures, 18 pages; to be submitted to EPJ
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