Study of the 2-d CP(N-1) models at \theta=0 and \pi

We present numerical results for 2-d CP(N-1) models at \theta=0 and \pi obtained in the D-theory formulation. In this formulation we construct an efficient cluster algorithm and we show numerical evidence for a first order transition for CP(N-1\geq 2) models at \theta = \pi. By a finite size scaling analysis, we also discuss the equivalence in the continuum limit of the D-theory formulation of the 2-d CP(N-1) models and the usual lattice definition.Comment: 3 pages, 2 figures. Talk presented at Lattice2004(spin), Fermilab, June 21-26, 200

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

From Spin Ladders to the 2-d O(3) Model at Non-Zero Density

The numerical simulation of various field theories at non-zero chemical potential suffers from severe complex action problems. In particular, QCD at non-zero quark density can presently not be simulated for that reason. A similar complex action problem arises in the 2-d O(3) model -- a toy model for QCD. Here we construct the 2-d O(3) model at non-zero density via dimensional reduction of an antiferromagnetic quantum spin ladder in a magnetic field. The complex action problem of the 2-d O(3) model manifests itself as a sign problem of the ladder system. This sign problem is solved completely with a meron-cluster algorithm.Comment: Based on a talk by U.-J. Wiese, 6 pages, 12 figures, to be published in computer physics communication

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

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