SOURCES 4C : a code for calculating ([alpha],n), spontaneous fission, and delayed neutron sources and spectra.

SOURCES 4C is a computer code that determines neutron production rates and spectra from ({alpha},n) reactions, spontaneous fission, and delayed neutron emission due to radionuclide decay. The code is capable of calculating ({alpha},n) source rates and spectra in four types of problems: homogeneous media (i.e., an intimate mixture of a-emitting source material and low-Z target material), two-region interface problems (i.e., a slab of {alpha}-emitting source material in contact with a slab of low-Z target material), three-region interface problems (i.e., a thin slab of low-Z target material sandwiched between {alpha}-emitting source material and low-Z target material), and ({alpha},n) reactions induced by a monoenergetic beam of {alpha}-particles incident on a slab of target material. Spontaneous fission spectra are calculated with evaluated half-life, spontaneous fission branching, and Watt spectrum parameters for 44 actinides. The ({alpha},n) spectra are calculated using an assumed isotropic angular distribution in the center-of-mass system with a library of 107 nuclide decay {alpha}-particle spectra, 24 sets of measured and/or evaluated ({alpha},n) cross sections and product nuclide level branching fractions, and functional {alpha}-particle stopping cross sections for Z < 106. The delayed neutron spectra are taken from an evaluated library of 105 precursors. The code provides the magnitude and spectra, if desired, of the resultant neutron source in addition to an analysis of the'contributions by each nuclide in the problem. LASTCALL, a graphical user interface, is included in the code package

HPRT Deficiency Coordinately Dysregulates Canonical Wnt and Presenilin-1 Signaling: A Neuro-Developmental Regulatory Role for a Housekeeping Gene?

We have used microarray-based methods of global gene expression together with quantitative PCR and Western blot analysis to identify dysregulation of genes and aberrant cellular processes in human fibroblasts and in SH-SY5Y neuroblastoma cells made HPRT-deficient by transduction with a retrovirus stably expressing an shRNA targeted against HPRT. Analysis of the microarray expression data by Gene ontology (GO) and Gene Set Enrichment Analysis (GSEA) as well as significant pathway analysis by GeneSpring GX10 and Panther Classification System reveal that HPRT deficiency is accompanied by aberrations in a variety of pathways known to regulate neurogenesis or to be implicated in neurodegenerative disease, including the canonical Wnt/β-catenin and the Alzheimer's disease/presenilin signaling pathways. Dysregulation of the Wnt/β-catenin pathway is confirmed by Western blot demonstration of cytosolic sequestration of β-catenin during in vitro differentiation of the SH-SY5Y cells toward the neuronal phenotype. We also demonstrate that two key transcription factor genes known to be regulated by Wnt signaling and to be vital for the generation and function of dopaminergic neurons; i.e., Lmx1a and Engrailed 1, are down-regulated in the HPRT knockdown SH-SY5Y cells. In addition to the Wnt signaling aberration, we found that expression of presenilin-1 shows severely aberrant expression in HPRT-deficient SH-SY5Y cells, reflected by marked deficiency of the 23 kDa C-terminal fragment of presenilin-1 in knockdown cells. Western blot analysis of primary fibroblast cultures from two LND patients also shows dysregulated presenilin-1 expression, including aberrant proteolytic processing of presenilin-1. These demonstrations of dysregulated Wnt signaling and presenilin-1 expression together with impaired expression of dopaminergic transcription factors reveal broad pleitropic neuro-regulatory defects played by HPRT expression and suggest new directions for investigating mechanisms of aberrant neurogenesis and neuropathology in LND and potential new targets for restoration of effective signaling in this neuro-developmental defect

Denial of long-term issues with agriculture on tropical peatlands will have devastating consequences

Non peer reviewe

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

A scoping review and thematic analysis of social and behavioural research among HIV-serodiscordant couples in high-income settings.

CAPRISA, 2015.Abstract available in pdf