The Single State Dominance Hypothesis and the Two-Neutrino Double Beta Decay of Mo100

The hypothesis of the single state dominance (SSD) in the calculation of the two-neutrino double beta decay of Mo100 is tested by exact consideration of the energy denominators of the perturbation theory. Both transitions to the ground state as well as to the 0+ and 2+ excited states of the final nucleus Ru100 are considered. We demonstrate, that by experimental investigation of the single electron energy distribution and the angular correlation of the outgoing electrons, the SSD hypothesis can be confirmed or ruled out by a precise two-neutrino double beta decay measurement (e.g. by NEMO III collaboration).Comment: 13 pages, RevTex, 1 figur

Search for double beta decay of Zinc and Tungsten with the help of low-background ZnWO4 crystal scintillators

Double beta processes in 64-Zn, 70-Zn, 180-W, and 186-W have been searched for with the help of large volume (0.1-0.7 kg) low background ZnWO4 crystal scintillators at the Gran Sasso National Laboratories of the INFN. Total time of measurements exceeds 10 thousands hours. New improved half-life limits on double electron capture and electron capture with positron emission in 64-Zn have been set, in particular (all the limits are at 90% C.L.): T1/2(0nu2EC)> 1.1e20 yr, T1/2(2nuECbeta+)>7.0e20 yr, and T1/2(0nuECbeta+)>4.3e20 yr. The different modes of double beta processes in 70-Zn, 180-W, and 186-W have been restricted at the level of 1e17-1e20 yr.Comment: 20 p., submitted to Phys. Rev.

Neutrino statistics and big bang nucleosynthesis

Neutrinos may possibly violate the spin-statistics theorem, and hence obey Bose statistics or mixed statistics despite having spin half. We find the generalized equilibrium distribution function of neutrinos which depends on a single fermi-bose parameter, \kappa, and interpolates continuously between the bosonic and fermionic distributions when \kappa changes from -1 to +1. We consider modification of the Big Bang Nucleosynthesis (BBN) in the presence of bosonic or partly bosonic neutrinos. For pure bosonic neutrinos the abundances change (in comparison with the usual Fermi-Dirac case) by -3.2% for 4He (which is equivalent to a decrease of the effective number of neutrinos by \Delta N_\nu = - 0.6), +2.6% for 2H and -7% for 7Li. These changes provide a better fit to the BBN data. Future BBN studies will be able to constrain the fermi-bose parameter to \kappa > 0.5, if no deviation from fermionic nature of neutrinos is found. We also evaluate the sensitivity of future CMB and LSS observations to the fermi-bose parameter.Comment: 11 pages, 3 figures, matches version in JCAP, discussion and references extended slightl

Measurement of double beta decay of 100Mo to excited states in the NEMO 3 experiment

The double beta decay of 100Mo to the 0^+_1 and 2^+_1 excited states of 100Ru is studied using the NEMO 3 data. After the analysis of 8024 h of data the half-life for the two-neutrino double beta decay of 100Mo to the excited 0^+_1 state is measured to be T^(2nu)_1/2 = [5.7^{+1.3}_{-0.9}(stat)+/-0.8(syst)]x 10^20 y. The signal-to-background ratio is equal to 3. Information about energy and angular distributions of emitted electrons is also obtained. No evidence for neutrinoless double beta decay to the excited 0^+_1 state has been found. The corresponding half-life limit is T^(0nu)_1/2(0^+ --> 0^+_1) > 8.9 x 10^22 y (at 90% C.L.). The search for the double beta decay to the 2^+_1 excited state has allowed the determination of limits on the half-life for the two neutrino mode T^(2nu)_1/2(0^+ --> 2^+_1) > 1.1 x 10^21 y (at 90% C.L.) and for the neutrinoless mode T^(0nu)_1/2(0^+ --> 2^+_1) > 1.6 x 10^23 y (at 90% C.L.).Comment: 23 pages, 7 figures, 4 tables, submitted to Nucl. Phy

Limits on different Majoron decay modes of 100^{100}Mo and 82^{82}Se for neutrinoless double beta decays in the NEMO-3 experiment

The NEMO-3 tracking detector is located in the Fr\'ejus Underground Laboratory. It was designed to study double beta decay in a number of different isotopes. Presented here are the experimental half-life limits on the double beta decay process for the isotopes $^{100}$Mo and $^{82}$Se for different Majoron emission modes and limits on the effective neutrino-Majoron coupling constants. In particular, new limits on "ordinary" Majoron (spectral index 1) decay of $^{100}$Mo ($T_{1/2} > 2.7\cdot10^{22}$ y) and $^{82}$Se ($T_{1/2} > 1.5\cdot10^{22}$ y) have been obtained. Corresponding bounds on the Majoron-neutrino coupling constant are $< (0.4-1.9) \cdot 10^{-4}$ and $< (0.66-1.7) \cdot 10^{-4}$.Comment: 23 pages includind 4 figures, to be published in Nuclear Physics

Are motor inhibition and cognitive flexibility dead ends in ADHD?

Contains fulltext : 53518.pdf (publisher's version ) (Closed access)Executive dysfunction has been postulated as the core deficit in ADHD, although many deficits in lower order cognitive processes have also been identified. By obtaining an appropriate baseline of lower order cognitive functioning light may be shed on as to whether executive deficits result from problems in lower order and/or higher order cognitive processes. We examined motor inhibition and cognitive flexibility in relation to a baseline measure in 816 children from ADHD and control families. Multiple children in a family were tested in order to examine the familiality of the measures. No evidence was found for deficits in motor inhibition or cognitive flexibility in children with ADHD or their nonaffected siblings: Compared to their baseline speed and accuracy of responding, children with ADHD and their (non)affected siblings were not disproportionally slower or inaccurate when demands for motor inhibition or cognitive flexibility were added to the task. However, children with ADHD and their (non)affected siblings were overall less accurate than controls, which could not be attributed to differences in response speed. This suggests that inaccuracy of responding is characteristic of children having (a familial risk for) ADHD. Motor inhibition and cognitive flexibility as operationalized with mean reaction time were found to be familial. It is concluded that poorer performance on executive tasks in children with ADHD and their (non)affected siblings may result from deficiencies in lower order cognitive processes and not (only) from higher order cognitive processes/executive functions

Novel roles for class II Phosphoinositide 3-Kinase C2 beta in signalling pathways involved in prostate cancer cell invasion

Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions such as proliferation, growth, survival and migration. The eight PI3K isoforms are grouped into three classes and the three enzymes belonging to the class II subfamily (PI3K-C2a, ß and ?) are the least investigated amongst all PI3Ks. Interest on these isoforms has been recently fuelled by the identification of specific physiological roles for class II PI3Ks and by accumulating evidence indicating their involvement in human diseases. While it is now established that these isoforms can regulate distinct cellular functions compared to other PI3Ks, there is still a limited understanding of the signalling pathways that can be specifically regulated by class II PI3Ks. Here we show that PI3K-C2ß regulates mitogen-activated protein kinase kinase (MEK1/2) and extracellular signal-regulated kinase (ERK1/2) activation in prostate cancer (PCa) cells. We further demonstrate that MEK/ERK and PI3K-C2ß are required for PCa cell invasion but not proliferation. In addition we show that PI3K-C2ß but not MEK/ERK regulates PCa cell migration as well as expression of the transcription factor Slug. These data identify novel signalling pathways specifically regulated by PI3K-C2ß and they further identify this enzyme as a key regulator of PCa cell migration and invasion

Spatiotemporal scaling of North American continental interior wetlands: implications for shorebird conservation

Within interior North America, erratic weather patterns and heterogeneous wetland complexes cause wide spatio-temporal variation in the resources available to migrating shorebirds. Identifying the pattern-generating components of landscape-level resources and the scales at which shorebirds respond to these patterns will better facilitate conservation efforts for these species. We constructed descriptive models that identified weather variables associated with creating the spatio-temporal patterns of shorebird habitat in ten landscapes in north-central Oklahoma. We developed a metric capable of measuring the dynamic composition and configuration of shorebird habitat in the region and used field data to empirically estimate the spatial scale at which shorebirds respond to the amount and configuration of habitat. Precipitation, temperature, solar radiation and wind speed best explained the incidence of wetland habitat, but relationships varied among wetland types. Shorebird occurrence patterns were best explained by habitat density estimates at a 1.5 km scale. This model correctly classified 86 % of shorebird observations. At this scale, when habitat density was low, shorebirds occurred in 5 % of surveyed habitat patches but occurrence reached 60 % when habitat density was high. Our results suggest scale dependence in the habitat-use patterns of migratory shorebirds. We discuss potential implications of our results and how integrating this information into conservation efforts may improve conservation strategies and management practices

Topographical expression of class IA and class II phosphoinositide 3-kinase enzymes in normal human tissues is consistent with a role in differentiation

BACKGROUND: Growth factor, cytokine and chemokine-induced activation of PI3K enzymes constitutes the start of a complex signalling cascade, which ultimately mediates cellular activities such as proliferation, differentiation, chemotaxis, survival, trafficking, and glucose homeostasis. The PI3K enzyme family is divided into 3 classes; class I (subdivided into IA and IB), class II (PI3K-C2α, PI3K-C2β and PI3K-C2γ) and class III PI3K. Expression of these enzymes in human tissue has not been clearly defined. METHODS: In this study, we analysed the immunohistochemical topographical expression profile of class IA (anti-p85 adaptor) and class II PI3K (PI3K-C2α and PI3K-C2β) enzymes in 104 formalin-fixed, paraffin embedded normal adult human (age 33–71 years, median 44 years) tissue specimens including those from the gastrointestinal, genitourinary, hepatobiliary, endocrine, integument and lymphoid systems. Antibody specificity was verified by Western blotting of cell lysates and peptide blocking studies. Immunohistochemistry intensity was scored from undetectable to strong. RESULTS: PI3K enzymes were expressed in selected cell populations of epithelial or mesenchymal origin. Columnar epithelium and transitional epithelia were reactive but mucous secreting and stratified squamous epithelia were not. Mesenchymal elements (smooth muscle and endothelial cells) and glomerular epithelium were only expressed PI3K-C2α while ganglion cells expressed p85 and PI3K-C2β. All three enzymes were detected in macrophages, which served as an internal positive control. None of the three PI3K isozymes was detected in the stem cell/progenitor compartments or in B lymphocyte aggregates. CONCLUSIONS: Taken together, these data suggest that PI3K enzyme distribution is not ubiquitous but expressed selectively in fully differentiated, non-proliferating cells. Identification of the normal in vivo expression pattern of class IA and class II PI3K paves the way for further analyses which will clarify the role played by these enzymes in inflammatory, neoplastic and other human disease conditions

Cloning of a human phosphoinositide 3-kinase with a C2 domain that displays reduced sensitivity to the inhibitor wortmannin

The generation of phosphatidylinositide 3-phosphates has been observed in a variety of cellular responses. The enzymes that mediate synthesis are the phosphoinositide 3-kinases (PI3-Ks) that form a family of structurally diverse enzymes with distinct substrate specificities. In this paper, we describe the cloning of a novel human PI3-K, namely PI3-K-C2α, which contains a C-terminal C2 domain. This enzyme can be assigned to the class II PI3-Ks, which was defined by characterization of the Drosophila 68D enzyme and includes the recently described murine enzymes m-cpk and p170. Despite the overall similarity in the amino acid sequence of the murine and human enzymes, which suggests that they are encoded by closely related genes, these molecules show marked sequence heterogeneity at their N-termini. Biochemical analysis of recombinant PI3-K-C2α demonstrates a restricted lipid substrate specificity. As reported for other members of this class, the enzyme only phosphorylates PtdIns and PtdIns4P when the lipids are presented alone. However, when lipids were presented together with phosphatidylserine acting as a carrier, phosphorylation of PtdIns(4,5)P2 was also observed. The catalytic activity of PI3-K-C2α is refractory to concentrations of wortmannin and LY294002 which inhibit the PI3-K activity of other family members. The comparative insensitivity of PI3-K-C2α to these inhibitors suggests that their use should be re-evaluated in the study of PI3-Ks.</jats:p