Some Flexure Formulas and Diagrams for Reinforced Concrete Beams

A thesis submitted to the Department of Civil Engineering and the Faculty of the Graduate School in partial fulfillment of the Requirements for the Master's Degree

Petting Fetishes

Petting Fetishes: Fetishes and Gender Oppression in M. Butterfly and For Whom the Bell Tolls M. Butterfly by Henry Hwang and For Whom the Bell Tolls by Ernest Hemingway both portray ideas of masculinity in countries experiencing political turmoil. Both pieces express ideas of masculinity from the perspective of Western foreigners in newly developing political settings post World War (Hwang’s post WWII China and Hemmingway’s post WWI, pre WWII Spain). Hwang’s play depicts Gallimard’s personal and national perception through the lens of Orientalist masculinity. Hemmingway’s novel depicts hyper-nationalism and narcissism through Robert Jordan’s expressed ideas of self and masculinity. Although both pieces have been celebrated as acclaimed literary works, the rhetoric of fetishes and gender oppression have not been closely examined. My paper examines how the main characters in the two pieces express dehumanizing fetishized ideas and gender oppression in their rhetorical choices, especially the use of the terms of endearment. My essay explores ideas of masculinity, femininity, gender oppression, fetishes, and Western domination in these works and their ideological impact on readers

Letter to Sonora Dodd from Luther S. Beard, May 23, 1911

Letter to Sonora Dodd, from Luther S. Beard, News Editor for The North American.https://digitalcommons.whitworth.edu/fathers-day-correspondence/1011/thumbnail.jp

Palmitoyl Acyltransferase DHHC21 Mediates Endothelial Dysfunction in Systemic Inflammatory Response Syndrome

Endothelial dysfunction is a hallmark of systemic inflammatory response underlying multiple organ failure. Here we report a novel function of DHHC-containing palmitoyl acyltransferases (PATs) in mediating endothelial inflammation. Pharmacological inhibition of PATs attenuates barrier leakage and leucocyte adhesion induced by endothelial junction hyperpermeability and ICAM-1 expression during inflammation. Among 11 DHHCs detected in vascular endothelium, DHHC21 is required for barrier response. Mice with DHHC21 function deficiency (Zdhhc21dep/dep) exhibit marked resistance to injury, characterized by reduced plasma leakage, decreased leucocyte adhesion and ameliorated lung pathology, culminating in improved survival. Endothelial cells from Zdhhc21dep/dep display blunted barrier dysfunction and leucocyte adhesion, whereas leucocytes from these mice did not show altered adhesiveness. Furthermore, inflammation enhances PLCb1 palmitoylation and signalling activity, effects significantly reduced in Zdhhc21dep/dep and rescued by DHHC21 overexpression. Likewise, overexpression of wild-type, not mutant, PLCb1 augments barrier dysfunction. Altogether, these data suggest the involvement of DHHC21-mediated PLCb1 palmitoylation in endothelial inflammation

REE Zoning in Allanite Related to Changing Partition Coefficients During Crystallization: Implications for REE Behaviour in an Epidote-Bearing Tonalite

Allanite is present in most samples of the tonalitic Bell Island Pluton, with an average mode near 0.05 wt.%. Allanite occurs as cores in igneous epidote-clinozoisite and exhibits characteristic and consistent zoning patterns. REE-rich cores (All40–70) grade out towards epidote-clinozoisite with REE below electron microprobe detection limits. La, Ce and Pr contents are highest in the REE-rich cores of zoned crystals. Nd and Sm contents both initially increase as total REE decreases and are highest in intermediate zones. Y contents are generally low throughout, but tend to be highest in analyses with All5–20. The zoning behaviour exhibited by the allanite, specifically the rimward increases in Nd, Sm, and Y, cannot be accounted for by simple fractionation and are best explained by increases in allanite/melt partition coefficients (Kd values) for these elements during crystallization. We propose that the variation in Kd values reflects modification of the allanite structure with changing REE content. These modifications are manifested by changes in colour, extinction, and pleochroism within the zoned crystals and include changes in unit-cell volume and dimensions. The changes in Kd values are large enough to result in crossing REE patterns within single allanite crystals. Fractional crystallization of zoned allanite can have noticeable effects on LREE contents and La/Sm (and almost certainly La/Lu) in magmas. In the Bell Island pluton, 80% of La, but \u3c3% of Y is contained in allanite. Although some of the variation in the LREE chemistry of the pluton is attributable to statistical sampling error, much of it appears to reflect petrogenetic processes that controlled LREE abundance and, ultimately, allanite mode. One sample of Bell Island tonalite is depleted in LREE and has low La/Lu and La/Sm. These chemical features can be modelled by fractionation of zoned allanite

Focal Adhesion Kinase and Src Mediate Microvascular Hyperpermeability Caused by Fibrinogen- γC- Terminal Fragments

Objectives We previously reported microvascular leakage resulting from fibrinogen-γ chain C-terminal products (γC) occurred via a RhoA-dependent mechanism. The objective of this study was to further elucidate the signaling mechanism by which γC induces endothelial hyperpermeability. Since it is known that γC binds and activates endothelial αvβ3, a transmembrane integrin receptor involved in intracellular signaling mediated by the tyrosine kinases FAK and Src, we hypothesized that γC alters endothelial barrier function by activating the FAK-Src pathway leading to junction dissociation and RhoA driven cytoskeletal stress-fiber formation. Methods and results Using intravital microscopy of rat mesenteric microvessels, we show increased extravasation of plasma protein (albumin) resulting from γC administration. In addition, capillary fluid filtration coefficient (Kfc) indicated γC-induced elevated lung vascular permeability. Furthermore, γC decreased transendothelial barrier resistance in a time-dependent and dose-related fashion in cultured rat lung microvascular endothelial cells (RLMVECs), accompanied by increased FAK/Src phosphorylation detection by western blot. Experiments with pharmacological inhibition or gene silencing of FAK showed significantly reduced γC-induced albumin and fluid leakage across microvessels, stress-fiber formation, VE-cadherin tyrosine phosphorylation, and improved γC-induced endothelial barrier dysfunction, indicating the involvement of FAK in γC mediated hyperpermeability. Comparable results were found when Src was targeted in a similar manner, however inhibition of FAK prevented Src activation, suggesting that FAK is upstream of Src in γC-mediated hyperpermeability. In addition, γC-induced cytoskeletal stress-fiber formation was attenuated during inhibition or silencing of these tyrosine kinases, concomitantly with RhoA inhibition. Conclusion The FAK-Src pathway contributes to γC-induced microvascular barrier dysfunction, junction protein phosphorylation and disorganization in a manner that involves RhoA and stress-fiber formation

Stochastic Projections for Water Resources Planning

U.S. Department of the InteriorCenter for Water and the Environmen