684 research outputs found

    Marin overvåking i Ryfylke, 2012

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    Det har blitt utført marin overvåking i Ryfylke i 2012 med hensikt å få informasjon om den økologiske tilstanden. De aktuelle fjordområdene er Idsefjorden, Fisterfjorden, Erfjorden, Årdalsfjorden og Jøsenfjorden. Undersøkelsene omfattet bløtbunn, vannmasser og makroalger, hvor bløtbunn var hovedprioritet. Den foreliggende undersøkelsen er begrenset, og gir ikke grunnlag for en fullstendig klassifisering av vannforekomster i henhold til Vannforskriftens krav, men det er foretatt en tentativ klassifisering. Med unntak av Årdalsfjorden med svært dårlig tilstand på bløtbunn, var tilstanden generelt «svært god» eller «god». De undersøkte vannforekomstene i Ryfylke anses ikke å være sterkt preget av forstyrrelse i dag.Fylkesmannen i Rogalan

    Measurement of the Gluino Mass via Cascade Decays for SPS 1a

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    If R-parity conserving supersymmetry is realised with masses below the TeV scale, sparticles will be produced and decay in cascades at the LHC. In the case of a neutral LSP, which will not be detected, decay chains cannot be fully reconstructed, complicating the mass determination of the new particles. In this paper we extend the method of obtaining masses from kinematical endpoints to include a gluino at the head of a five-sparticle decay chain. This represents a non-trivial extension of the corresponding method for the squark decay chain. We calculate the endpoints of the new distributions and assess their applicability by examining the theoretical distributions for a variety of mass scenarios. The precision with which the gluino mass can be determined by this method is investigated for the mSUGRA point SPS 1a. Finally we estimate the improvement obtained from adding a Linear Collider measurement of the LSP mass.Comment: 40 pages; extended discussion of error

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

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    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

    Synapsins Differentially Control Dopamine and Serotonin Release

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    Synapsins are a family of synaptic vesicle proteins that are important for neurotransmitter release. Here we have used triple knockout (TKO) mice lacking all three synapsin genes to determine the roles of synapsins in the release of two monoamine neurotransmitters, dopamine and serotonin. Serotonin release evoked by electrical stimulation was identical in substantia nigra pars reticulata slices prepared from TKO and wild-type mice. In contrast, release of dopamine in response to electrical stimulation was approximately doubled in striatum of TKO mice, both in vivo and in striatal slices, in comparison to wild-type controls. This was due to loss of synapsin III, because deletion of synapsin III alone was sufficient to increase dopamine release. Deletion of synapsins also increased the sensitivity of dopamine release to extracellular calcium ions. Although cocaine did not affect the release of serotonin from nigral tissue, this drug did enhance dopamine release. Cocaine-induced facilitation of dopamine release was a function of external calcium, an effect that was reduced in TKO mice. We conclude that synapsins play different roles in the control of release of dopamine and serotonin, with release of dopamine being negatively regulated by synapsins, specifically synapsin III, while serotonin release appears to be relatively independent of synapsins. These results provide further support for the concept that synapsin function in presynaptic terminals varies according to the neurotransmitter being released

    Prenatal arsenic exposure and DNA methylation in maternal and umbilical cord blood leukocytes

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    Background: Arsenic is an epigenetic toxicant and could influence fetal developmental programming.Objectives: We evaluated the association between arsenic exposure and DNA methylation in maternal and umbilical cord leukocytes.Methods: Drinking-water and urine samples were collected when women were at 64 28 weeks gestation; the samples were analyzed for arsenic using inductively coupled plasma mass spectrometry. DNA methylation at CpG sites in p16 (n = 7) and p53 (n = 4), and in LINE-1 and Alu repetitive elements (3 CpG sites in each), was quantified using pyrosequencing in 113 pairs of maternal and umbilical blood samples. We used general linear models to evaluate the relationship between DNA methylation and tertiles of arsenic exposure.Results: Mean (\ub1 SD) drinking-water arsenic concentration was 14.8 \ub1 36.2 \u3bcg/L (range: < 1-230 \u3bcg/L). Methylation in LINE-1 increased by 1.36% [95% confidence interval (CI): 0.52, 2.21%] and 1.08% (95% CI: 0.07, 2.10%) in umbilical cord and maternal leukocytes, respectively, in association with the highest versus lowest tertile of total urinary arsenic per gram creatinine. Arsenic exposure was also associated with higher methylation of some of the tested CpG sites in the promoter region of p16 in umbilical cord and maternal leukocytes. No associations were observed for Alu or p53 methylation.Conclusions: Exposure to higher levels of arsenic was positively associated with DNA methylation in LINE-1 repeated elements, and to a lesser degree at CpG sites within the promoter region of the tumor suppressor gene p16. Associations were observed in both maternal and fetal leukocytes. Future research is needed to confirm these results and determine if these small increases in methylation are associated with any health effect

    Search for the glueball candidates f0(1500) and fJ(1710) in gamma gamma collisions

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    Data taken with the ALEPH detector at LEP1 have been used to search for gamma gamma production of the glueball candidates f0(1500) and fJ(1710) via their decay to pi+pi-. No signal is observed and upper limits to the product of gamma gamma width and pi+pi- branching ratio of the f0(1500) and the fJ(1710) have been measured to be Gamma_(gamma gamma -> f0(1500)). BR(f0(1500)->pi+pi-) < 0.31 keV and Gamma_(gamma gamma -> fJ(1710)). BR(fJ(1710)->pi+pi-) < 0.55 keV at 95% confidence level.Comment: 10 pages, 3 figure
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