United States Suicide Analysis: 1999-2016

The purpose of this thesis is to create information visualizations surrounding suicide trends from 1999-2016 in the United States. The original data was obtained from the Centers for Disease Control and Prevention’s Compressed Mortality Database. This database permits users to download several fields of information regarding deaths for the years given. Using this information, many graphs below show trends and patterns for suicide. One notable trend includes the higher proportion of male to female suicides for all categories explored including: age group, race, and metro/nonmetro status. The goal is to bring awareness and understanding surrounding the suicide epidemic in the United States

Evaluation of linkages between climate change and sedimentary biogeochemistry in the glacial/interglacial North Atlantic

Over the past 125,000 years, global climate has varied in lock step with the growth and decay of large continental ice sheets. Concomitant with these large-scale glacial/interglacial climate shifts are marked changes in deep-sea sedimentation in the North Atlantic basin. Warm interglacial climates are generally associated with more CaCO3-rich deep-sea sediments, while cold glacial intervals are typically manifest as more clay-rich intervals. This study examines the impact of these glacial/interglacial sedimentologic changes on benthic (ocean bottom) biogeochemistry, and also investigates potential feedbacks between benthic processes and climate. In addition to documenting the glacial/interglacial response of marine sedimentation in the North Atlantic, with respect to select major, minor and trace elements that can be used to reconstruct changes in lithogenous, biogenic and authigenic processes, this work addresses a number of key biogeochemical interactions that centrally involve iron, which is plentiful in the clay-rich glacial sediments, but scarce in the interglacial sediments

Influence of pH on Bile Salt Deconjugation and Removal of Cholesterol from Media by Lactobacillus Casei and Lacto Bacillus Acidophilus During Growth

Food Scienc

Influence of Harvest Time on Stability of Cells of Lactobacillus Acidophilus During Frozen and Subsequent Refrigerated Storage

Food Scienc

Embryonic Lethality in Mice Homozygous for a Targeted Disruption of the N-myc Gene

The N-myc gene encodes a putative transcription factor that is thought to function in the regulation of gene expression during cell differentiation and/or growth. To examine the role of N-myc during development, we have used targeted mutagenesis in embryonic stem cells to produce a mouse line that carries an N-myc null allele. Mice homozygous for the mutation died between 10.5 and 12.5 days of gestation. Histological analysis of mutant embryos revealed that organs and tissues expected at these stages of development were present. However, multiple defects were observed, primarily in tissues and organs that normally express N-myc. In particular, mutant hearts were underdeveloped, often retaining the S-shape more typical of 9-day-old embryos. In addition, cranial and spinal ganglia were reduced in size and/or cellularity. Most of the noted defects were more consistent with a role of N-myc in proliferation of precursor populations than with a block in differentiation per se, at least at these early stages. These results demonstrate that N-myc plays an essential role during development and clearly confirm that N-myc has a physiological function that is distinct from that of the other myc-family genes

Homeostatic MyD88-dependent signals cause lethal inflamMation in the absence of A20

Toll-like receptors (TLRs) on host cells are chronically engaged by microbial ligands during homeostatic conditions. These signals do not cause inflammatory immune responses in unperturbed mice, even though they drive innate and adaptive immune responses when combating microbial infections. A20 is a ubiquitin-modifying enzyme that restricts exogenous TLR-induced signals. We show that MyD88-dependent TLR signals drive the spontaneous T cell and myeloid cell activation, cachexia, and premature lethality seen in A20-deficient mice. We have used broad spectrum antibiotics to demonstrate that these constitutive TLR signals are driven by commensal intestinal flora. A20 restricts TLR signals by restricting ubiquitylation of the E3 ligase tumor necrosis factor receptor–associated factor 6. These results reveal both the severe proinflammatory pathophysiology that can arise from homeostatic TLR signals as well as the critical role of A20 in restricting these signals in vivo. In addition, A20 restricts MyD88-independent TLR signals by inhibiting Toll/interleukin 1 receptor domain–containing adaptor inducing interferon (IFN) β–dependent nuclear factor κB signals but not IFN response factor 3 signaling. These findings provide novel insights into how physiological TLR signals are regulated

Convergence of cMyc and β-catenin on Tcf7l1 enables endoderm specification.

The molecular machinery that directs formation of definitive endoderm from pluripotent stem cells is not well understood. Wnt/β-catenin and Nodal signalling have been implicated, but the requirements for lineage specification remain incompletely defined. Here, we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm production. We find that downstream of GSK3 inhibition, elevated cMyc and β-catenin act in parallel to reduce transcription and DNA binding, respectively, of the transcriptional repressor Tcf7l1. Tcf7l1 represses FoxA2, a pioneer factor for endoderm specification. Deletion of Tcf7l1 is sufficient to allow upregulation of FoxA2 in the presence of Activin. In wild-type cells, cMyc contributes by reducing Tcf7l1 mRNA, while β-catenin acts on Tcf7l1 protein. GSK3 inhibition is further required for consolidation of endodermal fate via upregulation of Sox17, highlighting sequential roles for Wnt signalling. The identification of a cMyc/β-catenin-Tcf7l1-FoxA2 axis reveals a de-repression mechanism underlying endoderm induction that may be recapitulated in other developmental and patho-logical contexts.This study was funded by the Juvenile Diabetes Research Foundation International, the European Commission FP7 project BetaCellTherapy (agreement No. 241883), a core support grant from the Wellcome Trust and MRC to the Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute, and a University of Edinburgh Chancellor’s Fellowship awarded to GM. GM was a JDRF advanced postdoctoral fellow. AS is a Medical Research Council Professor.This is the final version of the article. It was first available from Wiley via http://dx.doi.org/10.15252/embj.20159211