Effects of Thermal Spiking on Graphite-Epoxy Composites

Tests were performed evaluating the effects of thermal spikes on the moisture absorption characteristics, the ultimate tensile strength, and the buckling modulus of Thornel 300/Fiberite 1034 composites. Measurements were made on unidirectional and π/4 laminates, using different types of thermal spikes. A survey was also made of the existing data. This survey, together with the present data indicate how thermal spikes affect the mois ture absorption and the mechanical properties of different graphite-epoxy composites.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66923/2/10.1177_002199837901300102.pd

Rotational excitation of methylidynium (CH+) by a helium atom at high temperature

We aim to obtain accurate rate coefficients for the collisional excitation of CH+ by He for high gas temperatures. The ab initio coupled-cluster [CCSD(T)] approximation was used to compute the interaction potential energy. Cross sections are then derived in the close coupling (CC) approach and rate coefficients inferred by averaging these cross sections over a Maxwell-Boltzmann distribution of kinetic energies. Cross sections are calculated up to 10'000 cm^-1 for J ranging from 0 to 10. Rate coefficients are obtained at high temperatures up to 2000 K.Comment: 4 pages, 3 figures, table with rate coefficients, accepted for publication by A&

Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2

Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-α expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the β-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17β-estradiol (E2) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E2 was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E2 suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E2 inhibition. E2 increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E2 was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GH/JAK/STAT pathway, in which SOCS-2 plays a central mechanistic role

Exact, Born–Oppenheimer, and quantum-chemistry-like calculations in helium clusters doped with light molecules: The He2N2(X) system

9 pages, 2 figures, 4 tables.-- PACS nrs.: 34.20.-b; 31.50.-x; 31.15.A-; 33.15.Mt; 33.20.Vq; 36.40.-c.Helium clusters doped with diatomic molecules, He(N)–BC, have been recently studied by means of a quantum-chemistry-like approach. The model treats He atoms as “electrons” and dopants as “nuclei” in standard electronic structure calculations. Due to the large mass difference between He atoms and electrons, and to the replacement of Coulomb interactions by intermolecular potentials, it is worth assessing up to what extent are the approximations involved in this model, i.e., decoupling of the BC rotation from the He-atom orbital angular momenta and Born–Oppenheimer separation of the BC stretch versus the He motions, accurate enough. These issues have been previously tackled elsewhere for the 4He2–Br2(X) system, which contains a heavy dopant [Roncero et al., Int. J. Quantum Chem. 107, 2756 (2007)]. Here, we consider a similar cluster but with a much lighter dopant such as N2(X). Although the model does not provide the correct energy levels for the cluster, positions and intensities of the main detectable lines of the vibrotational Raman spectrum at low temperature are accurately reproduced.This work has been partially supported by the DGICYT Spanish Grant Nos. FIS2007-62006 and CTQ2004-02415/BQU. M.P.de L.-C. acknowledges the support of a MEC-CSIC Spanish Grant No. 2007501004. The calculations presented here were performed at Centro de Cálculo of IMAFF (CSIC).Peer reviewe

Genome-Wide Assessment of AU-Rich Elements by the AREScore Algorithm

In mammalian cells, AU-rich elements (AREs) are well known regulatory sequences located in the 3′ untranslated region (UTR) of many short-lived mRNAs. AREs cause mRNAs to be degraded rapidly and thereby suppress gene expression at the posttranscriptional level. Based on the number of AUUUA pentamers, their proximity, and surrounding AU-rich regions, we generated an algorithm termed AREScore that identifies AREs and provides a numerical assessment of their strength. By analyzing the AREScore distribution in the transcriptomes of 14 metazoan species, we provide evidence that AREs were selected for in several vertebrates and Drosophila melanogaster. We then measured mRNA expression levels genome-wide to address the importance of AREs in SL2 cells derived from D. melanogaster hemocytes. Tis11, a zinc finger RNA–binding protein homologous to mammalian tristetraprolin, was found to target ARE–containing reporter mRNAs for rapid degradation in SL2 cells. Drosophila mRNAs whose expression is elevated upon knock down of Tis11 were found to have higher AREScores. Moreover high AREScores correlate with reduced mRNA expression levels on a genome-wide scale. The precise measurement of degradation rates for 26 Drosophila mRNAs revealed that the AREScore is a very good predictor of short-lived mRNAs. Taken together, this study introduces AREScore as a simple tool to identify ARE–containing mRNAs and provides compelling evidence that AREs are widespread regulatory elements in Drosophila

AU-Rich Element-Mediated mRNA Decay Can Occur Independently of the miRNA Machinery in Mouse Embryonic Fibroblasts and Drosophila S2-Cells

AU-rich elements (AREs) are regulatory sequences located in the 3′ untranslated region of many short-lived mRNAs. AREs are recognized by ARE-binding proteins and cause rapid mRNA degradation. Recent reports claimed that the function of AREs may be – at least in part – relayed through the miRNA pathway. We have revisited this hypothesis using dicer knock-out mouse embryonic fibroblasts and cultured Drosophila cells. In contrast to the published results, we find no evidence for a general requirement of the miRNA pathway in the function of AREs. Endogenous ier3 mRNA, which is known to contain a functional ARE, was degraded rapidly at indistinguishable rates in wild type and dicer knock-out mouse embryonic fibroblasts. In cultured Drosophila cells, both ARE-containing GFP reporter mRNAs and the endogenous cecA1 mRNA were resistant to depletion of the mi/siRNA factors dcr-1, dcr-2, ago1 and ago2. Furthermore, the Drosophila miRNA originally proposed to recognize AU-rich elements, miR-289, is not detectably expressed in flies or cultured S2 cells. Even our attempts to overexpress this miRNA from its genomic hairpin sequence failed. Thus, this sequence cannot serve as link between the miRNA and the AU-rich element mediated silencing pathways. Taken together, our studies in mammalian and Drosophila cells strongly argue that AREs can function independently of miRNAs

ZFP36L1 negatively regulates plasmacytoid differentiation of BCL1 cells by targeting BLIMP1 mRNA

The ZFP36/Tis11 family of zinc-finger proteins regulate cellular processes by binding to adenine uridine rich elements in the 3′ untranslated regions of various mRNAs and promoting their degradation. We show here that ZFP36L1 expression is largely extinguished during the transition from B cells to plasma cells, in a reciprocal pattern to that of ZFP36 and the plasma cell transcription factor, BLIMP1. Enforced expression of ZFP36L1 in the mouse BCL1 cell line blocked cytokine-induced differentiation while shRNA-mediated knock-down enhanced differentiation. Reconstruction of regulatory networks from microarray gene expression data using the ARACNe algorithm identified candidate mRNA targets for ZFP36L1 including BLIMP1. Genes that displayed down-regulation in plasma cells were significantly over-represented (P = <0.0001) in a set of previously validated ZFP36 targets suggesting that ZFP36L1 and ZFP36 target distinct sets of mRNAs during plasmacytoid differentiation. ShRNA-mediated knock-down of ZFP36L1 in BCL1 cells led to an increase in levels of BLIMP1 mRNA and protein, but not for mRNAs of other transcription factors that regulate plasmacytoid differentiation (xbp1, irf4, bcl6). Finally, ZFP36L1 significantly reduced the activity of a BLIMP1 3′ untranslated region-driven luciferase reporter. Taken together, these findings suggest that ZFP36L1 negatively regulates plasmacytoid differentiation, at least in part, by targeting the expression of BLIMP1

Dual RNA processing roles of Pat1b via cytoplasmic Lsm1-7 and nuclear Lsm2-8 complexes

Pat1 RNA-binding proteins, enriched in P-bodies, are key players in cytoplasmic 5’ to 3’ mRNA decay, activating decapping of mRNA in complex with the Lsm1-7 heptamer. Using co-immunoprecipitation and immunofluorescence approaches coupled with RNAi, we provide evidence for a nuclear complex of Pat1b with the Lsm2-8 heptamer, which binds to the spliceosomal U6 snRNA. Furthermore, we establish the set of interactions connecting Pat1b/Lsm2-8/U6 snRNA/SART3 and additional U4/U6.U5 tri-snRNP components, in Cajal bodies, the site of snRNP biogenesis. RNAseq following Pat1b depletion revealed the preferential up-regulation of mRNAs normally found in P-bodies and enriched in 3’ UTR AU-rich elements. Changes in >180 alternative splicing events were also observed, characterized by skipping of regulated exons with weak donor sites. Our data demonstrate the unsuspected dual role of a decapping enhancer in pre-mRNA processing as well as in mRNA decay via distinct nuclear and cytoplasmic Lsm complexes.This work was funded by a fellowship to CV from the Fondation Wiener – Anspach, BBSRC (BB/J00779X/1) and the Newton Trust (University of Cambridge) to NS, and CNRS PICS and ANR (14- CE09-0013-01ANR) to DW. The CMMI is supported by the European Regional Development Fund and the Walloon Region

Dual RNA processing roles of Pat1b via cytoplasmic Lsm1-7 and nuclear Lsm2-8 complexes

Pat1 RNA-binding proteins, enriched in P-bodies, are key players in cytoplasmic 5’ to 3’ mRNA decay, activating decapping of mRNA in complex with the Lsm1-7 heptamer. Using co-immunoprecipitation and immunofluorescence approaches coupled with RNAi, we provide evidence for a nuclear complex of Pat1b with the Lsm2-8 heptamer, which binds to the spliceosomal U6 snRNA. Furthermore, we establish the set of interactions connecting Pat1b/Lsm2-8/U6 snRNA/SART3 and additional U4/U6.U5 tri-snRNP components, in Cajal bodies, the site of snRNP biogenesis. RNAseq following Pat1b depletion revealed the preferential up-regulation of mRNAs normally found in P-bodies and enriched in 3’ UTR AU-rich elements. Changes in >180 alternative splicing events were also observed, characterized by skipping of regulated exons with weak donor sites. Our data demonstrate the unsuspected dual role of a decapping enhancer in pre-mRNA processing as well as in mRNA decay via distinct nuclear and cytoplasmic Lsm complexes.This work was funded by a fellowship to CV from the Fondation Wiener – Anspach, BBSRC (BB/J00779X/1) and the Newton Trust (University of Cambridge) to NS, and CNRS PICS and ANR (14- CE09-0013-01ANR) to DW. The CMMI is supported by the European Regional Development Fund and the Walloon Region

Molecular excitation in the Interstellar Medium: recent advances in collisional, radiative and chemical processes

We review the different excitation processes in the interstellar mediumComment: Accepted in Chem. Re