1,602 research outputs found

    Northern Eurasian large lakes history: sediment records obtained in the frame of Russian-German research project PLOT

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    Russian-German project PLOT (Paleolimnological Transect) aims at investigating the regional responses of the quaternary climate and environment on external forcing and feedback mechanisms along a more than 6000 km long longitudinal transect crossing Northern Eurasia. The well-dated record from Lake El´gygytgyn used as reference site for comparison the local climatic and environmental histories. Seismic surveys and sediment coring up to 54 m below lake floor performed in the frame of the project on Ladoga Lake (North-West of Russia; 2013), Lake Bolshoye Shchuchye (Polar Ural; 2016), Lake Levinson-Lessing and Lake Taymyr (Taymyr Peninsula; 2016-2017), Lake Emanda (Verkhoyansk Range; 2017). Fieldwork at Polar Ural and Taymyr Peninsula was conducted in collaboration with the Russian-Norwegian CHASE (Climate History along the Arctic Seaboard of Eurasia) project. Here, we present the major results of the project obtained so far

    Bose-Einstein Correlations of Three Charged Pions in Hadronic Z^0 Decays

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    Bose-Einstein Correlations (BEC) of three identical charged pions were studied in 4 x 10^6 hadronic Z^0 decays recorded with the OPAL detector at LEP. The genuine three-pion correlations, corrected for the Coulomb effect, were separated from the known two-pion correlations by a new subtraction procedure. A significant genuine three-pion BEC enhancement near threshold was observed having an emitter source radius of r_3 = 0.580 +/- 0.004 (stat.) +/- 0.029 (syst.) fm and a strength of \lambda_3 = 0.504 +/- 0.010 (stat.) +/- 0.041 (syst.). The Coulomb correction was found to increase the \lambda_3 value by \~9% and to reduce r_3 by ~6%. The measured \lambda_3 corresponds to a value of 0.707 +/- 0.014 (stat.) +/- 0.078 (syst.) when one takes into account the three-pion sample purity. A relation between the two-pion and the three-pion source parameters is discussed.Comment: 19 pages, LaTeX, 5 eps figures included, accepted by Eur. Phys. J.

    Mouse nuclear myosin I knock-out shows interchangeability and redundancy of myosin isoforms in the cell nucleus.

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    Nuclear myosin I (NM1) is a nuclear isoform of the well-known "cytoplasmic" Myosin 1c protein (Myo1c). Located on the 11(th) chromosome in mice, NM1 results from an alternative start of transcription of the Myo1c gene adding an extra 16 amino acids at the N-terminus. Previous studies revealed its roles in RNA Polymerase I and RNA Polymerase II transcription, chromatin remodeling, and chromosomal movements. Its nuclear localization signal is localized in the middle of the molecule and therefore directs both Myosin 1c isoforms to the nucleus. In order to trace specific functions of the NM1 isoform, we generated mice lacking the NM1 start codon without affecting the cytoplasmic Myo1c protein. Mutant mice were analyzed in a comprehensive phenotypic screen in cooperation with the German Mouse Clinic. Strikingly, no obvious phenotype related to previously described functions has been observed. However, we found minor changes in bone mineral density and the number and size of red blood cells in knock-out mice, which are most probably not related to previously described functions of NM1 in the nucleus. In Myo1c/NM1 depleted U2OS cells, the level of Pol I transcription was restored by overexpression of shRNA-resistant mouse Myo1c. Moreover, we found Myo1c interacting with Pol II. The ratio between Myo1c and NM1 proteins were similar in the nucleus and deletion of NM1 did not cause any compensatory overexpression of Myo1c protein. We observed that Myo1c can replace NM1 in its nuclear functions. Amount of both proteins is nearly equal and NM1 knock-out does not cause any compensatory overexpression of Myo1c. We therefore suggest that both isoforms can substitute each other in nuclear processes

    Lidar-Radiometer Inversion Code (LIRIC) for the retrieval of vertical aerosol properties from combined lidar/radiometer data: development and distribution in EARLINET

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    The financial support by the European Union's Horizon 2020 research and innovation programme (ACTRIS-2, grant agreement no. 654109) is gratefully acknowledged. The background of LIRIC algorithm and software was developed under the ACTRIS Research Infrastructure project, grant agreement no. 262254, within the European Union Seventh Framework Programme, which financial support is gratefully acknowledged.r I. Binietoglou received funding from the European Union's Seventh Framework Programme for research, technological development and demonstration under the grant agreement no. 289923 - ITARS.This paper presents a detailed description of LIRIC (LIdar-Radiometer Inversion Code) algorithm for simultaneous processing of coincident lidar and radiometric (sun photometric) observations for the retrieval of the aerosol concentration vertical profiles. As the lidar/radiometric input data we use measurements from European Aerosol Research Lidar Network (EARLINET) lidars and collocated sun-photometers of Aerosol Robotic Network (AERONET). The LIRIC data processing provides sequential inversion of the combined lidar and radiometric data. The algorithm starts with the estimations of column-integrated aerosol parameters from radiometric measurements followed by the retrieval of height dependent concentrations of fine and coarse aerosols from lidar signals using integrated column characteristics of aerosol layer as a priori constraints. The use of polarized lidar observations allows us to discriminate between spherical and non-spherical particles of the coarse aerosol mode. The LIRIC software package was implemented and tested at a number of EARLINET stations. Intercomparison of the LIRIC-based aerosol retrievals was performed for the observations by seven EARLINET lidars in Leipzig, Germany on 25 May 2009. We found close agreement between the aerosol parameters derived from different lidars that supports high robustness of the LIRIC algorithm. The sensitivity of the retrieval results to the possible reduction of the available observation data is also discussed.European Union (EU) 654109ACTRIS Research Infrastructure project within the European Union 262254European Union (EU) 289923 - ITAR

    Early decrements in bone density after completion of neoadjuvant chemotherapy in pediatric bone sarcoma patients

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    <p>Abstract</p> <p>Background</p> <p>Bone mineral density (BMD) accrual during childhood and adolescence is important for attaining peak bone mass. BMD decrements have been reported in survivors of childhood bone sarcomas. However, little is known about the onset and development of bone loss during cancer treatment. The objective of this cross-sectional study was to evaluate BMD in newly diagnosed Ewing's and osteosarcoma patients by means of dual-energy x-ray absorptiometry (DXA) after completion of neoadjuvant chemotherapy.</p> <p>Methods</p> <p>DXA measurements of the lumbar spine (L2-4), both femora and calcanei were performed perioperatively in 46 children and adolescents (mean age: 14.3 years, range: 8.6-21.5 years). Mean <it>Z</it>-scores, areal BMD (g/cm<sup>2</sup>), calculated volumetric BMD (g/cm<sup>3</sup>) and bone mineral content (BMC, g) were determined.</p> <p>Results</p> <p>Lumbar spine mean Z-score was -0.14 (95% CI: -0.46 to 0.18), areal BMD was 1.016 g/cm<sup>2 </sup>(95% CI: 0.950 to 1.082) and volumetric BMD was 0.330 g/cm<sup>3 </sup>(95% CI: 0.314 to 0.347) which is comparable to healthy peers. For patients with a lower extremity tumor (n = 36), the difference between the affected and non-affected femoral neck was 12.1% (95% CI: -16.3 to -7.9) in areal BMD. The reduction of BMD was more pronounced in the calcaneus with a difference between the affected and contralateral side of 21.7% (95% CI: -29.3 to -14.0) for areal BMD. Furthermore, significant correlations for femoral and calcaneal DXA measurements were found with Spearman-rho coefficients ranging from ρ = 0.55 to ρ = 0.80.</p> <p>Conclusions</p> <p>The tumor disease located in the lower extremity in combination with offloading recommendations induced diminished BMD values, indicating local osteopenia conditions. However, the results revealed no significant decrements of lumbar spine BMD in pediatric sarcoma patients after completion of neoadjuvant chemotherapy. Nevertheless, it has to be taken into account that bone tumor patients may experience BMD decrements or secondary osteoporosis in later life. Furthermore, the peripheral assessment of BMD in the calcaneus via DXA is a feasible approach to quantify bone loss in the lower extremity in bone sarcoma patients and may serve as an alternative procedure, when the established assessment of femoral BMD is not practicable due to endoprosthetic replacements.</p

    Systematic Identification of Novel, Essential Host Genes Affecting Bromovirus RNA Replication

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    Positive-strand RNA virus replication involves viral proteins and cellular proteins at nearly every replication step. Brome mosaic virus (BMV) is a well-established model for dissecting virus-host interactions and is one of very few viruses whose RNA replication, gene expression and encapsidation have been reproduced in the yeast Saccharomyces cerevisiae. Previously, our laboratory identified ∼100 non-essential host genes whose loss inhibited or enhanced BMV replication at least 3-fold. However, our isolation of additional BMV-modulating host genes by classical genetics and other results underscore that genes essential for cell growth also contribute to BMV RNA replication at a frequency that may be greater than that of non-essential genes. To systematically identify novel, essential host genes affecting BMV RNA replication, we tested a collection of ∼900 yeast strains, each with a single essential gene promoter replaced by a doxycycline-repressible promoter, allowing repression of gene expression by adding doxycycline to the growth medium. Using this strain array of ∼81% of essential yeast genes, we identified 24 essential host genes whose depleted expression reproducibly inhibited or enhanced BMV RNA replication. Relevant host genes are involved in ribosome biosynthesis, cell cycle regulation and protein homeostasis, among other cellular processes. BMV 2aPol levels were significantly increased in strains depleted for a heat shock protein (HSF1) or proteasome components (PRE1 and RPT6), suggesting these genes may affect BMV RNA replication by directly or indirectly modulating 2aPol localization, post-translational modification or interacting partners. Investigating the diverse functions of these newly identified essential host genes should advance our understanding of BMV-host interactions and normal cellular pathways, and suggest new modes of virus control

    Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo

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    Deep vein thrombosis (DVT) is a major cause of cardiovascular death. The sequence of events that promote DVT remains obscure, largely as a result of the lack of an appropriate rodent model. We describe a novel mouse model of DVT which reproduces a frequent trigger and resembles the time course, histological features, and clinical presentation of DVT in humans. We demonstrate by intravital two-photon and epifluorescence microscopy that blood monocytes and neutrophils crawling along and adhering to the venous endothelium provide the initiating stimulus for DVT development. Using conditional mutants and bone marrow chimeras, we show that intravascular activation of the extrinsic pathway of coagulation via tissue factor (TF) derived from myeloid leukocytes causes the extensive intraluminal fibrin formation characteristic of DVT. We demonstrate that thrombus-resident neutrophils are indispensable for subsequent DVT propagation by binding factor XII (FXII) and by supporting its activation through the release of neutrophil extracellular traps (NETs). Correspondingly, neutropenia, genetic ablation of FXII, or disintegration of NETs each confers protection against DVT amplification. Platelets associate with innate immune cells via glycoprotein Ibα and contribute to DVT progression by promoting leukocyte recruitment and stimulating neutrophil-dependent coagulation. Hence, we identified a cross talk between monocytes, neutrophils, and platelets responsible for the initiation and amplification of DVT and for inducing its unique clinical features
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