The hydrogenation of metals upon interaction with water

Hydrogen evolution at 600 deg and 5 x 10 to the 7th power - 10 to the 6th power torr from AVOOO Al samples, which were pickled in 10 percent NaOH, is discussed. An H evolution kinetic equation is derived for samples of equal vol. and different surfaces (5 and 20 sq cm). The values of the H evolution coefficient K indicated an agreement with considered H diffusion mechanism through an oxide layer. The activation energy for the H evolution process, obtained from the K-temp. relation, was 13,000 2000 cal/g-atom

The detection of patients at risk of gastrointestinal toxicity during pelvic radiotherapy by electronic nose and FAIMS : a pilot study

It is well known that the electronic nose can be used to identify differences between human health and disease for a range of disorders. We present a pilot study to investigate if the electronic nose and a newer technology, FAIMS (Field Asymmetric Ion Mobility Spectrometry), can be used to identify and help inform the treatment pathway for patients receiving pelvic radiotherapy, which frequently causes gastrointestinal side-effects, severe in some. From a larger group, 23 radiotherapy patients were selected where half had the highest levels of toxicity and the others the lowest. Stool samples were obtained before and four weeks after radiotherapy and the volatiles and gases emitted analysed by both methods; these chemicals are products of fermentation caused by gut microflora. Principal component analysis of the electronic nose data and wavelet transform followed by Fisher discriminant analysis of FAIMS data indicated that it was possible to separate patients after treatment by their toxicity levels. More interestingly, differences were also identified in their pre-treatment samples. We believe these patterns arise from differences in gut microflora where some combinations of bacteria result to give this olfactory signature. In the future our approach may result in a technique that will help identify patients at “high risk” even before radiation treatment is started

Structural evolution in Pt isotopes with the Interacting Boson Model Hamiltonian derived from the Gogny Energy Density Functional

Spectroscopic calculations are carried out, for the description of the shape/phase transition in Pt nuclei in terms of the Interacting Boson Model (IBM) Hamiltonian derived from (constrained) Hartree-Fock-Bogoliubov (HFB) calculations with the finite range and density dependent Gogny-D1S Energy Density Functional. Assuming that the many-nucleon driven dynamics of nuclear surface deformation can be simulated by effective bosonic degrees of freedom, the Gogny-D1S potential energy surface (PES) with quadrupole degrees of freedom is mapped onto the corresponding PES of the IBM. Using this mapping procedure, the parameters of the IBM Hamiltonian, relevant to the low-lying quadrupole collective states, are derived as functions of the number of valence nucleons. Merits of both Gogny-HFB and IBM approaches are utilized so that the spectra and the wave functions in the laboratory system are calculated precisely. The experimental low-lying spectra of both ground-state and side-band levels are well reproduced. From the systematics of the calculated spectra and the reduced E2 transition probabilities $B$(E2), the prolate-to-oblate shape/phase transition is shown to take place quite smoothly as a function of neutron number $N$ in the considered Pt isotopic chain, for which the $\gamma$-softness plays an essential role. All these spectroscopic observables behave consistently with the relevant PESs and the derived parameters of the IBM Hamiltonian as functions of $N$. Spectroscopic predictions are also made for those nuclei which do not have enough experimental E2 data.Comment: 11 pages, 5 figure

Abrupt changes in alpha decay systematics as a manifestation of collective nuclear modes

An abrupt change in $\alpha$ decay systematics around the N=126 neutron shell closure is discussed. It is explained as a sudden hindrance of the clustering of the nucleons that eventually form the $\alpha$ particle. This is because the clustering induced by the pairing mode acting upon the four nucleons is inhibited if the configuration space does not allow a proper manifestation of the pairing collectivity.Comment: 6 pages, 3 figures, submitted to Phys. Rev. C, a few new references adde

On the Validity of the Geiger-Nuttall Alpha-Decay Law and its Microscopic Basis

The Geiger-Nuttall (GN) law relates the partial $\alpha$-decay half-life with the energy of the escaping $\alpha$ particle and contains for every isotopic chain two experimentally determined coefficients. The expression is supported by several phenomenological approaches, however its coefficients lack a fully microscopic basis. In this paper we will show that: 1) the empirical coefficients that appear in the GN law have a deep physical meaning and 2) the GN law is successful within the restricted experimental data sets available so far, but is not valid in general. We will show that, when the dependence of logarithm values of the $\alpha$ formation probability on the neutron number is not linear or constant, the GN law is broken. For the $\alpha$ decay of neutron-deficient nucleus $^{186}$Po, the difference between the experimental half-life and that predicted by the GN Law is as large as one order of magnitude.Comment: 4 pages, 5 figures, to appear in Phys. Lett.

Simulations of a micro-PET System based on Liquid Xenon

The imaging performance of a high-resolution preclinical microPET system employing liquid xenon as the gamma ray detection medium was simulated. The arrangement comprises a ring of detectors consisting of trapezoidal LXe time projection ionization chambers and two arrays of large area avalanche photodiodes for the measurement of ionization charge and scintillation light. A key feature of the LXePET system is the ability to identify individual photon interactions with high energy resolution and high spatial resolution in 3 dimensions and determine the correct interaction sequence using Compton reconstruction algorithms. The simulated LXePET imaging performance was evaluated by computing the noise equivalent count rate, the sensitivity and point spread function for a point source, and by examining the image quality using a micro-Derenzo phantom according to the NEMA-NU4 standard. Results of these simulation studies included NECR peaking at 1326 kcps at 188 MBq (705 kcps at 184 MBq) for an energy window of 450 - 600 keV and a coincidence window of 1 ns for mouse (rat) phantoms. The absolute sensitivity at the center of the field of view was 12.6%. Radial, tangential, and axial resolutions of 22Na point sources reconstructed with a list-mode maximum likelihood expectation maximization algorithm were <= 0.8 mm (FWHM) throughout the field of view. Hot-rod inserts of < 0.8 mm diameter were resolvable in the transaxial image of a micro-Derenzo phantom. The simulations show that a liquid xenon system would provide new capabilities for significantly enhancing PET images

Inhibition of the mitochondrial pyruvate carrier protects from excitotoxic neuronal death.

Glutamate is the dominant excitatory neurotransmitter in the brain, but under conditions of metabolic stress it can accumulate to excitotoxic levels. Although pharmacologic modulation of excitatory amino acid receptors is well studied, minimal consideration has been given to targeting mitochondrial glutamate metabolism to control neurotransmitter levels. Here we demonstrate that chemical inhibition of the mitochondrial pyruvate carrier (MPC) protects primary cortical neurons from excitotoxic death. Reductions in mitochondrial pyruvate uptake do not compromise cellular energy metabolism, suggesting neuronal metabolic flexibility. Rather, MPC inhibition rewires mitochondrial substrate metabolism to preferentially increase reliance on glutamate to fuel energetics and anaplerosis. Mobilizing the neuronal glutamate pool for oxidation decreases the quantity of glutamate released upon depolarization and, in turn, limits the positive-feedback cascade of excitotoxic neuronal injury. The finding links mitochondrial pyruvate metabolism to glutamatergic neurotransmission and establishes the MPC as a therapeutic target to treat neurodegenerative diseases characterized by excitotoxicity

Shape of primary proton spectrum in multi-TeV region from data on vertical muon flux

It is shown, that primary proton spectrum, reconstructed from sea-level and underground data on muon spectrum with the use of QGSJET 01, QGSJET II, NEXUS 3.97 and SIBYLL 2.1 interaction models, demonstrates not only model-dependent intensity, but also model-dependent form. For correct reproduction of muon spectrum shape primary proton flux should have non-constant power index for all considered models, except SIBYLL 2.1, with break at energies around 10-15 TeV and value of exponent before break close to that obtained in ATIC-2 experiment. To validate presence of this break understanding of inclusive spectra behavior in fragmentation region in p-air collisions should be improved, but we show, that it is impossible to do on the basis of the existing experimental data on primary nuclei, atmospheric muon and hadron fluxes.Comment: Submitted to Phys. Rev.

Wolfram Syndrome protein, Miner1, regulates sulphydryl redox status, the unfolded protein response, and Ca2+ homeostasis.

Miner1 is a redox-active 2Fe2S cluster protein. Mutations in Miner1 result in Wolfram Syndrome, a metabolic disease associated with diabetes, blindness, deafness, and a shortened lifespan. Embryonic fibroblasts from Miner1(-/-) mice displayed ER stress and showed hallmarks of the unfolded protein response. In addition, loss of Miner1 caused a depletion of ER Ca(2+) stores, a dramatic increase in mitochondrial Ca(2+) load, increased reactive oxygen and nitrogen species, an increase in the GSSG/GSH and NAD(+)/NADH ratios, and an increase in the ADP/ATP ratio consistent with enhanced ATP utilization. Furthermore, mitochondria in fibroblasts lacking Miner1 displayed ultrastructural alterations, such as increased cristae density and punctate morphology, and an increase in O2 consumption. Treatment with the sulphydryl anti-oxidant N-acetylcysteine reversed the abnormalities in the Miner1 deficient cells, suggesting that sulphydryl reducing agents should be explored as a treatment for this rare genetic disease