The fluorine and manganese content of certain Missouri waters

Since early in 1931, considerable attention has been brought to bear upon the subject of fluorides in drinking water supplies, following the discovery of high fluoride concentrations in waters consumed by persons afflicted with the dental defect known as mottled enamel. Analyses have been made, in the course of this study, of a comparatively large number of Missouri waters. The waters analyzed have been collected and made available by the Missouri Geological Survey and Water Resources. They have been secured from diverse sources and include surface waters and underground waters from different geological formations, throughout the State of Missouri --Introduction, page 3

The combustion of phosphorus

Phosphorus first joined the ranks of large-tonnage industrial raw materials about ten years ago, with the development of the electric furnace method for its production from rock phosphate. For many years before the present era of large-scale production, phosphorus had been little more than a laboratory curiosity. Thereafter, it found extensive application in pyrotechnics, match tips, rat poisons, and other uses not requiring more than a few hundred of tons in a year. Phosphoric acids were generally produced by the reaction of sulfuric acid with rock phosphate. The development and growth of electro-thermal processes for the reduction of rock phosphate completely changed the method of producing phosphoric acids. Phosphorus, produced in electric furnaces, is now an industrial commodity that may be burned to the oxide, then hydrated to phosphoric acids, and finally converted into a great number of phosphate compounds. A brief catalogue of the significant events leading up to the present state of development of the electric-furnace process for the production of phosphorus is shown --Introduction, page 1

Dietary genistein influences function of mouse aorta

Abstract only availableCardiovascular disease is the leading cause of death for men and postmenopausal women in the United States. Estrogen is thought to be cardioprotective. An important action of estrogen is increasing endothelial-dependent vasodilation of coronary arteries. Because of their estrogen-like components and activities, phytoestrogens, especially isoflavones such as genistein found in high concentrations in soy products, are being studied as a potential means to prevent cardiovascular disease and as an alternative to estrogen replacement therapy. In the current study we examined the effects of high dietary genistein on vascular function of mice. Since genistein is considered estrogenic, we hypothesized that genistein also would enhance vasodilation. Mice were divided into three diet groups: standard fed (200 mg genistein), high genistein (600 mg), and genistein-free (0 mg). After being on their respective diets for at least one month, the mice were sacrificed, thoracic aortas were isolated, cleaned of surrounding fat and connective tissue, and then cut into rings to measure contractile capacity. Receptor independent contractility was measured by adding increasing doses of potassium chloride (KCl). Both males and females fed 600 mg genistein showed significantly greater force of contractions at all doses of KCl above 30mM compared to other groups. The 0 mg group exhibited the least amount of tension for all KCl doses. Receptor dependent contractility was measured following increasing concentrations of norepinephrine (NE) in the presence and absence of NG-nitro-L-arginine methyl esther (L-NAME), a nitric oxide synthase (NOS) inhibitor. In the absence of L-NAME contractile responses to NE followed the KCl pattern for diet groups except for the 600 mg male group which was similar to the standard fed males. Therefore, the NE curves were normalized to the maximal KCl force. Normalization of NE to KCl indicated NE responses were similar for all groups except 600 mg males. To evaluate whether endothelial vasodilators alter contractile force mediated by NE, data were collected in the presence of L-NAME. The NE contractile responses with L-NAME were significantly greater than contractility without L-NAME for all groups. NOS contribution to vasodilation was significantly less in males compared to females. In females the contribution of NOS appeared greatest in the 600 mg group compared to other groups. These results show that vasodilation capacity is increased with high genistein (600 mg) diets with females, but not males. Surprisingly genistein significantly increased contractile force to KCl. Possible mechanisms that may underlie genistein effects on KCl contractions include increased L-type calcium currents and/or smooth muscle hypertrophy/hyperplasia.Life Sciences Undergraduate Research Opportunity Progra

Distribution and abundance of Dungeness crab and crangon shrimp, and dredging-related mortality of invertebrates and fish in Grays Harbor, Washington

The impacts of widening and deepening the existing navigation channel in Grays Harbor on Dungeness crab, crangon shrimp and fish was investigated. The spatial and temporal distribution of these organisms was studied using an otter trawl and ring nets, and the uptake of organisms by dredges was estimated from samples collected on working hopper and pipeline dredges. ... Impacts of the dredging project on crabs, shrimp and fish could be associated with entrainment, food loss and toxicants released from sediments. Scenarios are presented that predict impacts. Suggestions for reducing impacts are given

Delayed maturation of an IL-12–producing dendritic cell subset explains the early Th2 bias in neonatal immunity

Primary neonatal T cell responses comprise both T helper (Th) cell subsets, but Th1 cells express high levels of interleukin 13 receptor α1 (IL-13Rα1), which heterodimerizes with IL-4Rα. During secondary antigen challenge, Th2-produced IL-4 triggers the apoptosis of Th1 cells via IL-4Rα/IL-13Rα1, thus explaining the Th2 bias in neonates. We show that neonates acquire the ability to overcome the Th2 bias and generate Th1 responses starting 6 d after birth. This transition was caused by the developmental maturation of CD8α+CD4− dendritic cells (DCs), which were minimal in number during the first few days of birth and produced low levels of IL-12. This lack of IL-12 sustained the expression of IL-13Rα1 on Th1 cells. By day 6 after birth, however, a significant number of CD8α+CD4− DCs accumulated in the spleen and produced IL-12, which triggered the down-regulation of IL-13Rα1 expression on Th1 cells, thus protecting them against IL-4–driven apoptosis

Innocuous IFNγ induced by adjuvant-free antigen restores normoglycemia in NOD mice through inhibition of IL-17 production

The role of Th17 cells in type I diabetes (TID) remains largely unknown. Glutamic acid decarboxylase (GAD) sequence 206–220 (designated GAD2) represents a late-stage epitope, but GAD2-specific T cell receptor transgenic T cells producing interferon γ (IFNγ) protect against passive TID. Because IFNγ is known to inhibit Th17 cells, effective presentation of GAD2 peptide under noninflammatory conditions may protect against TID at advanced disease stages. To test this premise, GAD2 was genetically incorporated into an immunoglobulin (Ig) molecule to magnify tolerance, and the resulting Ig-GAD2 was tested against TID at different stages of the disease. The findings indicated that Ig-GAD2 could not prevent TID at the preinsulitis phase, but delayed TID at the insulitis stage. More importantly, Ig-GAD2 sustained both clearance of pancreatic cell infiltration and β-cell division and restored normoglycemia when given to hyperglycemic mice at the prediabetic stage. This was dependent on the induction of splenic IFNγ that inhibited interleukin (IL)-17 production. In fact, neutralization of IFNγ led to a significant increase in the frequency of Th17 cells, and the treatment became nonprotective. Thus, IFNγ induced by an adjuvant free antigen, contrary to its usual inflammatory function, restores normoglycemia, most likely by localized bystander suppression of pathogenic IL-17–producing cells

The Dichotomous Pattern of IL-12R and IL-23R Expression Elucidates the Role of IL-12 and IL-23 in Inflammation

IL-12 and IL-23 cytokines respectively drive Th1 and Th17 type responses. Yet, little is known regarding the biology of these receptors. As the IL-12 and IL-23 receptors share a common subunit, it has been assumed that these receptors are co-expressed. Surprisingly, we find that the expression of each of these receptors is restricted to specific cell types, in both mouse and human. Indeed, although IL-12Rβ2 is expressed by NK cells and a subset of γδ T cells, the expression of IL-23R is restricted to specific T cell subsets, a small number of B cells and innate lymphoid cells. By exploiting an IL-12- and IL-23-dependent mouse model of innate inflammation, we demonstrate an intricate interplay between IL-12Rβ2 NK cells and IL-23R innate lymphoid cells with respectively dominant roles in the regulation of systemic versus local inflammatory responses. Together, these findings support an unforeseen lineage-specific dichotomy in the in vivo role of both the IL-12 and IL-23 pathways in pathological inflammatory states, which may allow more accurate dissection of the roles of these receptors in chronic inflammatory diseases in humans

Don't be such a baby! or the effects of the environment and T cells on neonatal immunity [abstract]

It is known that neonates are highly susceptible to microbial infections and allergic reactions. This susceptibility is due to a lack of Th1 cells and an excess of its Th2 counterparts. However, the mechanism underlying this Th1/Th2 imbalance has not been clearly elucidated. Although both Th1 and Th2 cells are present in the primary response, only Th1 cells up-regulate the IL- 13R[alpha]1 chain. Consequently IL-13R[alpha]1 can associate with IL-4R[alpha] to form a heteroreceptor through which IL-4 from Th2 cells can signal and cause the apoptosis of Th1 cells upon secondary re-challenge with antigen. Formation of this IL-13R[alpha]1/IL-4R[alpha] heteroreceptor is influenced by two factors: the neonatal environment and intrinsic T cell factors

Dendritic cells, IL-12Rbeta2, and IL-13Ralpha1 signaling: the battle for control of neonatal immunity

Title from PDF of title page (University of Missouri--Columbia, viewed on March 11, 2013).The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.Dissertation advisor: Dr. Habib ZaghouaniIncludes bibliographical references.Vita.Ph. D. University of Missouri-Columbia 2012."December 2012"[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Newborns are highly susceptible to microbial infections and allergic reactions. This susceptibility is due to a lack of Th1 cells and an excess of Th2 cells. However, the mechanism underlying this Th1/Th2 imbalance has not been clearly elucidated. Although Th1 cells are present in the primary response, they up-regulate the IL-13R[alpha]1 chain. Consequently, IL-13R[alpha]1 can bind with IL-4R[alpha] to form a heteroreceptor through which IL-4 from Th2 cells can signal and cause the death of Th1 cells. Formation of this death receptor is influenced by the neonatal environment and intrinsic T cell factors. Here we show that limited IL12 in the neonatal environment supports IL-13Ralpha1 up-regulation and Th1 cell death. This lack of IL-12 is due to a low frequency of CD8[alpha]+CD4- DCs, the main producer of IL-12. However, by day 6 after birth, this DC subset reaches a significant accumulation and produces sufficient IL-12 that can downregulate IL-13R[alpha]1 and restore Th1 responses. Interestingly, T cells also contribute to the Th2 bias of neonatal immunity as adult T cells do not up-regulate IL-13Ralpha1 when primed within the neonatal environment. In fact, by 8 days after birth T cells do not up-regulate IL-13R[alpha]1 after antigen stimulation as they express the IL-12R[beta]2 chain which serves as a compensation mechanism that prevents death. Finally, IL-4 induced death appears to be due to activation of the extrinsic and intrinsic apoptosis pathways as neonatal Th1 cells have increased FasL and Bim expression. Together these results could have direct impact on pediatric vaccine development.--From public.pdfIncludes bibliographical references