A new cross section measurement of reactions induced by 3He-particles on a carbon target

International audienceThe production of intense beams of light radioactive nuclei can be achieved at the SPIRAL2 facility using intense stable beams accelerated by the driver accelerator and impinging on light targets. The isotope 14O is identied to be of high interest for future experiments. The excitation function of the production reaction 12C(3He, n)14O was measured between 7 and 35 MeV. Results are compared with literature data. As an additional result, we report the rst cross-section measurement for the 12C(3He, +n)10C reaction. Based on this new result, the potential in-target 14O yield at SPIRAL2 was estimated: 2.4x1011 pps, for 1 mA of 3He at 35 MeV. This is a factor 140 higher than the in-target yield at SPIRAL1

New astrophysical S factor for the (15)N(p,gamma)(16)O reaction via the asymptotic normalization coefficient (ANC) method

Journals published by the American Physical Society can be found at http://publish.aps.org/The (15)N(p,gamma)(16)O reaction provides a path from the CN cycle to the CNO bi-cycle and CNO tri-cycle. The measured astrophysical factor for this reaction is dominated by resonant capture through two strong J(pi) = 1(-) resonances at E(R) = 312 and 962 keV and direct capture to the ground state. Asymptotic normalization coefficients (ANCs) for the ground and seven excited states in (16)O were extracted from the comparison of experimental differential cross sections for the (15)N((3)He,d)(16)O reaction with distorted-wave Born approximation calculations. Using these ANCs and proton and alpha resonance widths determined from an R-matrix fit to the data from the (15)N(p,alpha)(12)C reaction, we carried out an R-matrix calculation to obtain the astrophysical factor for the (15)N(p,gamma)(16)O reaction. The results indicate that the direct capture contribution was previously overestimated. We find the astrophysical factor to be S(0) = 36.0 +/- 6.0 keV b, which is about a factor of 2 lower than the presently accepted value. We conclude that for every 2200 +/- 300 cycles of the main CN cycle one CN catalyst is lost due to this reaction

Comparative Developmental Expression Profiling of Two C. elegans Isolates

Gene expression is known to change during development and to vary among genetically diverse strains. Previous studies of temporal patterns of gene expression during C. elegans development were incomplete, and little is known about how these patterns change as a function of genetic background. We used microarrays that comprehensively cover known and predicted worm genes to compare the landscape of genetic variation over developmental time between two isolates of C. elegans. We show that most genes vary in expression during development from egg to young adult, many genes vary in expression between the two isolates, and a subset of these genes exhibit isolate-specific changes during some developmental stages. This subset is strongly enriched for genes with roles in innate immunity. We identify several novel motifs that appear to play a role in regulating gene expression during development, and we propose functional annotations for many previously unannotated genes. These results improve our understanding of gene expression and function during worm development and lay the foundation for linkage studies of the genetic basis of developmental variation in gene expression in this important model organism

The role of the myosin ATPase activity in adaptive thermogenesis by skeletal muscle

Resting skeletal muscle is a major contributor to adaptive thermogenesis, i.e., the thermogenesis that changes in response to exposure to cold or to overfeeding. The identification of the “furnace” that is responsible for increased heat generation in resting muscle has been the subject of a number of investigations. A new state of myosin, the super relaxed state (SRX), with a very slow ATP turnover rate has recently been observed in skeletal muscle (Stewart et al. in Proc Natl Acad Sci USA 107:430–435, 2010). Inhibition of the myosin ATPase activity in the SRX was suggested to be caused by binding of the myosin head to the core of the thick filament in a structural motif identified earlier by electron microscopy. To be compatible with the basal metabolic rate observed in vivo for resting muscle, most myosin heads would have to be in the SRX. Modulation of the population of this state, relative to the normal relaxed state, was proposed to be a major contributor to adaptive thermogenesis in resting muscle. Transfer of only 20% of myosin heads from the SRX into the normal relaxed state would cause muscle thermogenesis to double. Phosphorylation of the myosin regulatory light chain was shown to transfer myosin heads from the SRX into the relaxed state, which would increase thermogenesis. In particular, thermogenesis by myosin has been proposed to play a role in the dissipation of calories during overfeeding. Up-regulation of muscle thermogenesis by pharmaceuticals that target the SRX would provide new approaches to the treatment of obesity or high blood sugar levels

The response of single crystal diamond detectors to 17–34 MeV neutrons

The first measurements of the response of diamond detectors to neutrons in the energy range 17–34MeV are presented. The diamond detectors were irradiated with quasi-monoenergetic neutrons generatedthrough the 7Li(p,n)7Be reaction. The measured pulse-height spectra show specific peaks associated to neutroninduced reactions in carbon. The peak of the 12C(n,0)9Be was clearly separated from the rest of thespectra. The 12C(n,d0)11B and 12C(n,p0)12B peaks were clearly identified on a continuum originating fromthe breakup 12C(n,3) reaction, which dominates the low-energy part of the pulse-height spectra. The 12C(n,0)9Be, 12C(n,d0)11B and 12C(n,p0)12B cross sections that have never been measured in this high-energy rangebefore were determined. The measured data are compared with the European Activation File EAF-2010 libraryevaluated values.JRC.G.2-Standards for Nuclear Safety, Security and Safeguard

In vitro toxicity profiling of ultrapure non-dioxin-like polychlorinated biphenyl (NDL-PCB) congeners and their relative toxic contribution to PCB-mixtures in humans

The toxic equivalency concept used for the risk assessment of polychlorinated biphenyls (PCBs) is based on the aryl hydrocarbon receptor (AhR)-mediated toxicity of coplanar dioxin-like (DL) PCBs. Most PCBs in the environment, however, are non-dioxin-like (NDL) PCBs that cannot adopt a coplanar structure required for AhR activation. For NDL-PCBs, no generally accepted risk concept is available because their toxicity is insufficiently characterized. Here,we systematically determined in vitro toxicity profiles for 24 PCBs regarding 10 different mechanisms of action. Prior to testing, NDL-PCB standards were purified to remove traces of DL compounds. All NDL-PCBs antagonized androgen receptor activation and inhibited gap junctional intercellular communication (GJIC). Lower chlorinated NDL-PCBswereweak estrogen receptor (ER) agonists,whereas higher chlorinated NDL-PCBs were weak ER antagonists. Several NDL-PCBs inhibited estradiol-sulfotransferase activity and bound to transthyretin (TTR) but with much weaker potencies than reported for hydroxylated PCB metabolites. AhR-mediated expression of uridine-glucuronyl transferase isozyme UGT1A6 was induced by DL-PCBs only. Hierarchical cluster analysis of the toxicity profiles yielded three separate clusters of NDL-PCBs and a fourth cluster of reference DL-PCBs. Due to small differences in relative potency among congeners, the highly abundant indicator PCBs 28, 52, 101, 118, 138, 153, and 180 also contributed most to the antiandrogenic, (anti)estrogenic, antithyroidal, tumorpromoting, and neurotoxic potencies calculated for PCB mixtures reported in human samples, whereas the most potent AhRactivating DL-PCB-126 contributed at maximum 0.2% to any of these calculated potencies. PCB-168 is recommended as an additional indicator congener, given its relatively high abundance and antiandrogenic, TTR-binding, and GJIC-inhibiting potencies. © The Author 2011. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved