A structural evaluation of the tungsten isotopes via thermal neutron capture

Total radiative thermal neutron-capture $\gamma$-ray cross sections for the $^{182,183,184,186}$W isotopes were measured using guided neutron beams from the Budapest Research Reactor to induce prompt and delayed $\gamma$ rays from elemental and isotopically-enriched tungsten targets. These cross sections were determined from the sum of measured $\gamma$-ray cross sections feeding the ground state from low-lying levels below a cutoff energy, E$_{\rm crit}$, where the level scheme is completely known, and continuum $\gamma$ rays from levels above E$_{\rm crit}$, calculated using the Monte Carlo statistical-decay code DICEBOX. The new cross sections determined in this work for the tungsten nuclides are: $\sigma_{0}(^{182}{\rm W}) = 20.5(14)$ b and $\sigma_{11/2^{+}}(^{183}{\rm W}^{m}, 5.2 {\rm s}) = 0.177(18)$ b; $\sigma_{0}(^{183}{\rm W}) = 9.37(38)$ b and $\sigma_{5^{-}}(^{184}{\rm W}^{m}, 8.33 \mu{\rm s}) = 0.0247(55)$ b; $\sigma_{0}(^{184}{\rm W}) = 1.43(10)$ b and $\sigma_{11/2^{+}}(^{185}{\rm W}^{m}, 1.67 {\rm min}) = 0.0062(16)$ b; and, $\sigma_{0}(^{186}{\rm W}) = 33.33(62)$ b and $\sigma_{9/2^{+}}(^{187}{\rm W}^{m}, 1.38 \mu{\rm s}) = 0.400(16)$ b. These results are consistent with earlier measurements in the literature. The $^{186}$W cross section was also independently confirmed from an activation measurement, following the decay of $^{187}$W, yielding values for $\sigma_{0}(^{186}{\rm W})$ that are consistent with our prompt $\gamma$-ray measurement. The cross-section measurements were found to be insensitive to choice of level density or photon strength model, and only weakly dependent on E$_{\rm crit}$. Total radiative-capture widths calculated with DICEBOX showed much greater model dependence, however, the recommended values could be reproduced with selected model choices. The decay schemes for all tungsten isotopes were improved in these analyses.Comment: 25 pages, 15 figures, 15 table

New neutron cross section and fission yield data for SNManalysis

Neutron cross-section data are fundamental for the design ofnuclear interrogation systems, the maintenance of nuclear materials andwaste, and the understanding the consequences of nuclear catastrophe.Although a large body of nuclear data exists, it is often old,unreliable, or poorly determined. For several years we have collaborated,as part of an IAEA Coordinated Research Project, to precisely measure thepartial thermal neutron gamma ray cross sections for all elements fromhydrogen to uranium at the Budapest Reactor. These data will replace theunreliable tables of Lone et al [1], still widely in use, and will bepublished as an IAEA TECDOC

Investigation of \u3csup\u3e186\u3c/sup\u3eRe via radiative thermal-neutron capture on \u3csup\u3e185\u3c/sup\u3eRe

Partial -ray production cross sections and the total radiative thermal-neutron capture cross section for the 185Re(n,)186Re reaction were measured using the Prompt Gamma Activation Analysis facility at the Budapest Research Reactor with an enriched 185Re target. The 186Re cross sections were standardized using well-known 35Cl(n,)36Cl cross sections from irradiation of a stoichiometric natReCl3 target. The resulting cross sections for transitions feeding the 186Re ground state from low-lying levels below a cutoff energy of Ec=746keV were combined with a modeled probability of ground-state feeding from levels above Ec to arrive at a total cross section of σ0=111(6)b for radiative thermal-neutron capture on 185Re. A comparison of modeled discrete-level populations with measured transition intensities led to proposed revisions for seven tentative spin-parity assignments in the adopted level scheme for 186Re. Additionally, 102 primary rays were measured, including 50 previously unknown. A neutron-separation energy of Sn=6179.59(5)keV was determined from a global least-squares fit of the measured -ray energies to the known 186Re decay scheme. The total capture cross section and separation energy results are comparable to earlier measurements of these values

Developments in Capture- γ Libraries for Nonproliferation Applications

The neutron-capture reaction is fundamental for identifying and analyzing the γ-ray spectrum from an unknown assembly because it provides unambiguous information on the neutron-absorbing isotopes. Nondestructive-assay applications may exploit this phenomenon passively, for example, in the presence of spontaneous-fission neutrons, or actively where an external neutron source is used as a probe. There are known gaps in the Evaluated Nuclear Data File libraries corresponding to neutron-capture γ-ray data that otherwise limit transport-modeling applications. In this work, we describe how new thermal neutron-capture data are being used to improve information in the neutron-data libraries for isotopes relevant to nonproliferation applications. We address this problem by providing new experimentally-deduced partial and total neutron-capture reaction cross sections and then evaluate these data by comparison with statistical-model calculations

A Large Expansion of the HSFY Gene Family in Cattle Shows Dispersion across Yq and Testis-Specific Expression

Heat shock transcription factor, Y-linked (HSFY) is a member of the heat shock transcriptional factor (HSF) family that is found in multiple copies on the Y chromosome and conserved in a number of species. Its function still remains unknown but in humans it is thought to play a role in spermatogenesis. Through real time polymerase chain reaction (PCR) analyses we determined that the HSFY family is largely expanded in cattle (∼70 copies) compared with human (2 functional copies, 4 HSFY-similar copies). Unexpectedly, we found that it does not vary among individual bulls as a copy number variant (CNV). Using fluorescence in situ hybridization (FISH) we found that the copies are dispersed along the long arm of the Y chromosome (Yq). HSFY expression in cattle appears restricted to the testis and its mRNA correlates positively with mRNA markers of spermatogonial and spermatocyte cells (UCHL1 and TRPC2, respectively) which suggests that HSFY is expressed (at least in part) in early germ cells

Barrel pattern formation requires serotonin uptake by thalamocortical afferents, and not vesicular monoamine release

Thalamocortical neurons innervating the barrel cortex in neonatal rodents transiently store serotonin (5-HT) in synaptic vesicles by expressing the plasma membrane serotonin transporter (5-HTT) and the vesicular monoamine transporter (VMAT2). 5-HTT knock-out (ko) mice reveal a nearly complete absence of 5-HT in the cerebral cortex by immunohistochemistry, and of barrels, both at P7 and adulthood. Quantitative electron microscopy reveals that 5-HTT ko affects neither the density of synapses nor the length of synaptic contacts in layer IV. VMAT2 ko mice, completely lacking activity-dependent vesicular release of monoamines including 5-HT, also show a complete lack of 5-HT in the cortex but display largely normal barrel fields, despite sometimes markedly reduced postnatal growth. Transient 5-HTT expression is thus required for barrel pattern formation, whereas activity-dependent vesicular 5-HT release is not

New catalog of neutron capture gamma rays for prompt gamma activation analysis

Thermal neutron capture gamma rays were measured for all stable elements at the guided neutron beam facility in Budapest. Energies, relative intensities, and partial production cross-sections were determined with high precision for about 14,000 gamma rays of 82 elements. The new experimental data were supplemented with isotopic data from ENSDF and the original papers and were evaluated. The resulting accurate new levels and decay schemes comprise 35,000 gamma-ray transitions. The new database is practically complete for light nuclei, hence capture cross sections could be inferred from the measured partial gamma-ray production cross-sections. Precise neutron separation energies were also deduced from fits to the level schemes. The new elemental datasets will be the basic input to an IAEA database for prompt gamma activation analysis, a chemical method of elemental analysis. The new isotopic sets will be provided for updating the thermal neutron capture datasets of ENSDF

H ? control of anaerobic digester for winery industry wastewater treatment

Genetic sex in mammals is determined by the sex chromosomal composition of the zygote. The X and Y chromosomes are responsible for numerous factors that must work in close concert for the proper development of a healthy sexual phenotype. The role of androgens in case of XY chromosomal constitution is crucial for normal male sex differentiation. The intracellular androgenic action is mediated by the androgen receptor (AR), and its impaired function leads to a myriad of syndromes with severe clinical consequences, most notably androgen insensitivity syndrome and prostate cancer. In this paper, we investigated the possibility that an alteration of the equine AR gene explains a recently described familial XY, SRY + disorder of sex development. We uncovered a transition in the first nucleotide of the AR start codon (c.1A>G). To our knowledge, this represents the first causative AR mutation described in domestic animals. It is also a rarely observed mutation in eukaryotes and is unique among the >750 entries of the human androgen receptor mutation database. In addition, we found another quiet mis- sense mutation in exon 1 (c.322C>T). Transcription of AR was confirmed by RT-PCR amplification of several exons. Translation of the full-length AR protein from the initiating GTG start codon was confirmed by Western blot using N- and C-terminal- specific antibodies. Two smaller peptides (25 and 14 amino acids long) were identified from the middle of exon 1 and across exons 5 and 6 by mass spectrometry. Based upon our experimental data and the supporting literature, it appears that the AR is expressed as a full-length protein and in a functional form, and the observed phenotype is the result of reduced AR protein expression levels. Copyright " 2011 S. Karger AG, Basel.",,,,,,"10.1159/000334049",,,"http://hdl.handle.net/20.500.12104/41813","http://www.scopus.com/inward/record.url?eid=2-s2.0-84857365898&partnerID=40&md5=6001c7ff3814f57e07b0f2916c1bfde0",,,,,,"01-mar",,"Sexual Development",,"10

GTG mutation in the start codon of the androgen receptor gene in a family of horses with 64,XY disorder of sex development

Genetic sex in mammals is determined by the sex chromosomal composition of the zygote. The X and Y chromosomes are responsible for numerous factors that must work in close concert for the proper development of a healthy sexual phenotype. The role of androgens in case of XY chromosomal constitution is crucial for normal male sex differentiation. The intracellular androgenic action is mediated by the androgen receptor (AR), and its impaired function leads to a myriad of syndromes with severe clinical consequences, most notably androgen insensitivity syndrome and prostate cancer. In this paper, we investigated the possibility that an alteration of the equine AR gene explains a recently described familial XY, SRY + disorder of sex development. We uncovered a transition in the first nucleotide of the AR start codon (c.1A>G). To our knowledge, this represents the first causative AR mutation described in domestic animals. It is also a rarely observed mutation in eukaryotes and is unique among the >750 entries of the human androgen receptor mutation database. In addition, we found another quiet mis- sense mutation in exon 1 (c.322C>T). Transcription of AR was confirmed by RT-PCR amplification of several exons. Translation of the full-length AR protein from the initiating GTG start codon was confirmed by Western blot using N- and C-terminal- specific antibodies. Two smaller peptides (25 and 14 amino acids long) were identified from the middle of exon 1 and across exons 5 and 6 by mass spectrometry. Based upon our experimental data and the supporting literature, it appears that the AR is expressed as a full-length protein and in a functional form, and the observed phenotype is the result of reduced AR protein expression levels. Copyright © 2011 S. Karger AG, Basel