Hyperfine Structure of Indium Fluoride

The radiofrequency spectrum of the indium fluoride molecule, 115In19F, has been measured with a high resolution molecular beam electric resonance spectrometer. We determined the hyperfine structure in the J=1 and the J=2 rotational states of several vibrational levels under conditions of very weak external electric and magnetic fields. The ∼700 MHz electric quadrupole interaction constant of the indium nucleus changes by 0.010(1) MHz between adjacent rotational states. We looked for, but did not find, an electric hexadecapole interaction of the indium nucleus; the upper limit for the (hexadecapole) interaction constant is 2 kHz.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/70971/2/JCPSA6-57-10-4068-1.pd

Hyperfine Structure of Thallium Chloride

The radio‐frequency spectra of TlCl at very weak electric and magnetic fields have been measured with a molecular beam electric resonance spectrometer. From these spectra the hyperfine interaction constants for the four isotopic species of the molecule were calculated. The constants for 205Tl35Cl in the J  =  2,υ  =  0J=2,υ=0 state are: eqQ  =  − 15793.32(50)kHz,cCl  =  1.38(10)kHz,cTl  =  76.35(10)kHz,c3  =  − 0.13(10)kHz,c4  =  − 1.54(10)kHz.eqQ=−15793.32(50)kHz,cCl=1.38(10)kHz,cTl=76.35(10)kHz,c3=−0.13(10)kHz,c4=−1.54(10)kHz. A test was made for the polarization of the chlorine nucleus in the electric field of the molecule by comparing the ratio of the quadrupole interaction constants for 205Tl35Cl and 205Tl37Cl to the ratio of the quadrupole interaction constants for the free chlorine atoms. The agreement of the two ratios is within their uncertainties, thus providing no evidence for a polarization effect. In addition, the dependence of the spin–rotation and spin–spin interaction constants on isotope was found to show good agreement with theory.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/69724/2/JCPSA6-50-5-2086-1.pd

Redshift and Shear Calibration: Impact on Cosmic Shear Studies and Survey Design

The cosmological interpretation of weak lensing by large-scale structures requires knowledge of the redshift distribution of the source galaxies. Current lensing surveys are often calibrated using external redshift samples which span a significantly smaller sky area in comparison to the lensing survey, and are thus subject to sample variance. Some future lensing surveys are expected to be calibrated in the same way, in particular the fainter galaxy populations where the entire color coverage, and hence photometric redshift estimate, could be challenging to obtain. Using N-body simulations, we study the impact of this sample variance on cosmic shear analysis and show that, to first approximation, it behaves like a shear calibration error 1+/-epsilon. Using the Hubble Deep Field as a redshift calibration survey could therefore be a problem for current lensing surveys. We discuss the impact of the redshift distribution sampling error and a shear calibration error on the design of future lensing surveys, and find that a lensing survey of area Theta square degrees and limiting magnitude m_lim}, has a minimum shear and redshift calibration accuracy requirements given by epsilon = epsilon_0 10^{beta(m_lim-24.5)} / sqrt(Theta/ 200). Above that limit, lensing surveys would not reach their full potential. Using the galaxy number counts from the Hubble Ultra-Deep Field, we find (epsilon_0,beta)=(0.015,-0.18) and (epsilon_0,beta)=(0.011,-0.23) for ground and space based surveys respectively. Lensing surveys with no or limited redshift information and/or poor shear calibration accuracy will loose their potential to analyse the cosmic shear signal in the sub-degree angular scales, and therefore complete photometric redshift coverage should be a top priority for future lensing surveys.Comment: Accepted version to Astroparticle Physic

Ageing is associated with molecular signatures of inflammation and type 2 diabetes in rat pancreatic islets.

AIMS/HYPOTHESIS: Ageing is a major risk factor for development of metabolic diseases such as type 2 diabetes. Identification of the mechanisms underlying this association could help to elucidate the relationship between age-associated progressive loss of metabolic health and development of type 2 diabetes. We aimed to determine molecular signatures during ageing in the endocrine pancreas. METHODS: Global gene transcription was measured in pancreatic islets isolated from young and old rats by Ilumina BeadChip arrays. Promoter DNA methylation was measured by Sequenom MassArray in 46 genes that showed differential expression with age, and correlations with expression were established. Alterations in morphological and cellular processes with age were determined by immunohistochemical methods. RESULTS: Age-related changes in gene expression were found at 623 loci (>1.5-fold, false discovery rate [FDR] <5%), with a significant (FDR < 0.05) enrichment in genes previously implicated in islet-cell function (Enpp1, Abcc8), type 2 diabetes (Tspan8, Kcnq1), inflammatory processes (Cxcl9, Il33) and extracellular matrix organisation (Col3a1, Dpt). Age-associated transcriptional differences negatively correlated with promoter DNA methylation at several loci related to inflammation, glucose homeostasis, cell proliferation and cell-matrix interactions (Il33, Cxcl9, Gpr119, Fbp2, Col3a1, Dpt, Spp1). CONCLUSIONS/INTERPRETATION: Our findings suggest that a significant proportion of pancreatic islets develop a low-grade 'chronic' inflammatory status with ageing and this may trigger altered functional plasticity. Furthermore, we identified changes in expression of genes previously linked to type 2 diabetes and associated changes in DNA methylation that could explain their age-associated dysregulation. These findings provide new insights into key (epi)genetic signatures of the ageing process in islets.Biotechnology and Biological Sciences Research Council (Grant ID: BB/H003312/1), British Heart Foundation, FP6 Epigenome Network of Excellence programme, GlaxoSmithKline, Nuffield Foundation, Royal Society, Medical Research Council (Grant ID: MRC_MC_UU_12012/4)This is the final version of the article. It first appeared from Springer via http://dx.doi.org/10.1007/s00125-015-3837-

The Rewiring of Ubiquitination Targets in a Pathogenic Yeast Promotes Metabolic Flexibility, Host Colonization and Virulence

Funding: This work was funded by the European Research Council [http://erc.europa.eu/], AJPB (STRIFE Advanced Grant; C-2009-AdG-249793). The work was also supported by: the Wellcome Trust [www.wellcome.ac.uk], AJPB (080088, 097377); the UK Biotechnology and Biological Research Council [www.bbsrc.ac.uk], AJPB (BB/F00513X/1, BB/K017365/1); the CNPq-Brazil [http://cnpq.br], GMA (Science without Borders fellowship 202976/2014-9); and the National Centre for the Replacement, Refinement and Reduction of Animals in Research [www.nc3rs.org.uk], DMM (NC/K000306/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Acknowledgments We thank Dr. Elizabeth Johnson (Mycology Reference Laboratory, Bristol) for providing strains, and the Aberdeen Proteomics facility for the biotyping of S. cerevisiae clinical isolates, and to Euroscarf for providing S. cerevisiae strains and plasmids. We are grateful to our Microscopy Facility in the Institute of Medical Sciences for their expert help with the electron microscopy, and to our friends in the Aberdeen Fungal Group for insightful discussions.Peer reviewedPublisher PD

Разработка автоматизированной системы блока эжектора установки комплексной подготовки газа

Описание технологического процесса. Выбор структуры АСУ. Подбор датчиков, контроллерного оборудования, исполнительных устройств. Раработка алгоритмов управления для блока подготовки газа УКПГDescription of the technological process. Selection of the structure of automatic control system. Selection of sensors, control equipment, executive devices. Development of control algorithms for gas preparation unit of installation of complex gas preparation

Mesenchyme-derived IGF2 is a major paracrine regulator of pancreatic growth and function

The genetic mechanisms that determine the size of the adult pancreas are poorly understood. Imprinted genes, which are expressed in a parent-of-origin-specific manner, are known to have important roles in development, growth and metabolism. However, our knowledge regarding their roles in the control of pancreatic growth and function remains limited. Here we show that many imprinted genes are highly expressed in pancreatic mesenchyme-derived cells and explore the role of the paternally-expressed insulin-like growth factor 2 (Igf2) gene in mesenchymal and epithelial pancreatic lineages using a newly developed conditional Igf2 mouse model. Mesenchyme-specific Igf2 deletion results in acinar and beta-cell hypoplasia, postnatal whole-body growth restriction and maternal glucose intolerance during pregnancy, suggesting that the mesenchyme is a developmental reservoir of IGF2 used for paracrine signalling. The unique actions of mesenchymal IGF2 are demonstrated by the absence of any discernible growth or functional phenotypes upon Igf2 deletion in the developing pancreatic epithelium. Additionally, increased IGF2 levels specifically in the mesenchyme, through conditional Igf2 loss-of-imprinting or Igf2r deletion, leads to pancreatic acinar overgrowth. Furthermore, ex-vivo exposure of primary acinar cells to exogenous IGF2 activates AKT, a key signalling node, and increases their number and amylase production. Based on these findings, we propose that mesenchymal Igf2, and perhaps other imprinted genes, are key developmental regulators of adult pancreas size and function