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

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

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.

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

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

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

Selective mGluR1 Antagonist EMQMCM Inhibits the Kainate-Induced Excitotoxicity in Primary Neuronal Cultures and in the Rat Hippocampus

Abundant evidence suggests that indirect inhibitory modulation of glutamatergic transmission, via metabotropic glutamatergic receptors (mGluR), may induce neuroprotection. The present study was designed to determine whether the selective antagonist of mGluR1 (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate (EMQMCM), showed neuroprotection against the kainate (KA)-induced excitotoxicity in vitro and in vivo. In in vitro studies on mouse primary cortical and hippocampal neuronal cultures, incubation with KA (150 μM) induced strong degeneration [measured as lactate dehydrogenase (LDH) efflux] and apoptosis (measured as caspase-3 activity). EMQMCM (0.1–100 μM) added 30 min to 6 h after KA, significantly attenuated the KA-induced LDH release and prevented the increase in caspase-3 activity in the cultures. Those effects were dose- and time-dependent. In in vivo studies KA (2.5 nmol/1 μl) was unilaterally injected into the rat dorsal CA1 hippocampal region. Degeneration was calculated by counting surviving neurons in the CA pyramidal layer using stereological methods. It was found that EMQMCM (5–10 nmol/1 μl) injected into the dorsal hippocampus 30 min, 1 h, or 3 h (the higher dose only) after KA significantly prevented the KA-induced neuronal degeneration. In vivo microdialysis studies in rat hippocampus showed that EMQMCM (100 μM) significantly increased γ-aminobutyric acid (GABA) and decreased glutamate release. When perfused simultaneously with KA, EMQMCM substantially increased GABA release and prevented the KA-induced glutamate release. The obtained results indicate that the mGluR1 antagonist, EMQMCM, may exert neuroprotection against excitotoxicity after delayed treatment (30 min to 6 h). The role of enhanced GABAergic transmission in the neuroprotection is postulated

Health Industries in the Twentieth Century. Introduction

This article is the introduction to the special issue' Health Industries in the Twentieth Century'. It offers a broad literature review of scholarly works about the history of health and medicine, and stresses the opportunities for business historians to tackle the field of healthcare

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

Connecting Biology and Mathematics: First Prepare the Teachers

Developing the connection between biology and mathematics is one of the most important ways to shift the paradigms of both established science disciplines. However, adding some mathematic content to biology or biology content to mathematics is not enough but must be accompanied by development of suitable pedagogical models. I propose a model of pedagogical mathematical biological content knowledge as a feasible starting point for connecting biology and mathematics in schools and universities. The process of connecting these disciplines should start as early as possible in the educational process, in order to produce prepared minds that will be able to combine both disciplines at graduate and postgraduate levels of study. Because teachers are a crucial factor in introducing innovations in education, the first step toward such a goal should be the education of prospective and practicing elementary and secondary school teachers