Service, Sacrifice, and Citizenship: The Experiences of Muslims Serving in the U.S. Military

The events of 9/11 and the subsequent "War on Terror" activated long standing stereotypes in the United States that portrayed Muslims as fundamentally different from other Americans. In this project, I interview 15 Muslims who have served in the U.S. military since 9/11 to determine if and how the activation of this us/them boundary shaped their military experiences. I find that the us/them atmosphere that characterizes civilian discourse about Muslims is present in the military. However, most of my respondents felt that it had little practical effect on them. I discuss this in terms of the presence but irrelevance of this boundary. I connect this finding to the history of racial integration in the U.S. military, arguing that characteristics of the military, including an emphasis on policies of equal opportunity, the ability to compel certain behaviors, and the nature of military service, which promotes close contact among diverse individuals, can mitigate some of the negatives effects of being othered. While most of my respondents had positive experiences, in some units the us/them discourse was exacerbated, creating atmospheres of distrust and suspicion which led to negative outcomes including harassment, accusations, and decisions by Muslim service members to leave the military. A theme that emerged in exploring this dichotomy of experience among my respondents was the role of leadership. Leadership that saw value in diversity and was invested in supporting it, mitigated negative effects of othering, making this an irrelevant frame. However, leadership that repeated stereotypes or fears reinforced this tension, creating toxic environments in which Muslim service members felt excluded. I began this project with the expectation that citizenship would be a central narrative for Muslim service members, as it was for Japanese Americans in World War II. However, the respondents in my sample rarely use their military service to directly make claims on citizenship. They do however express institutional motivations to serve and engage in dialogue, bridge building, and other aspects of everyday citizenship

Book Review: Ancient Mediterranean Art

The genesis of this catalogue stemmed from the generous gift of William D. and Jane Walsh, who donated their sizeable collection of ancient Mediterranean art to Fordham University in 2006. Mr. Walsh’s life-long passion for antiquity dates to his undergraduate days when he studied classics at Fordham in the early 1950s. Though his career took a different path (i.e., law and business), Walsh never lost his love for the ancient past. In fact, over the past thirty years, he built a collection of primarily Greek, Etruscan and Roman antiquities

Identity of GD1C, GT1a and GQ1b synthase in Golgi vesicles from rat liver

AbstractCompetition experiments using GM1b, GD1a and GT1b as substrates, and as mutual inhibitors for ganglioside sialyltransferase activity in preparations of Golgi vesicles derived form rat liver, suggested that sialyl transfer to these three respective compounds, leading to gangliosides GD1C , GT1a and GQ1b, respectively, is catalyzed by one enzyme. These results are incorporated into a model for ganglioside biosynthesis and its regulation

Tuning Monte Carlo Generators: The Perugia Tunes

We present 9 new tunes of the pT-ordered shower and underlying-event model in PYTHIA 6.4. These "Perugia" tunes update and supersede the older "S0" family. The data sets used to constrain the models include hadronic Z0 decays at LEP, Tevatron minimum-bias data at 630, 1800, and 1960 GeV, Tevatron Drell-Yan data at 1800 and 1960 GeV, and SPS min-bias data at 200, 546, and 900 GeV. In addition to the central parameter set, called "Perugia 0", we introduce a set of 8 related "Perugia Variations" that attempt to systematically explore soft, hard, parton density, and colour structure variations in the theoretical parameters. Based on these variations, a best-guess prediction of the charged track multiplicity in inelastic, nondiffractive minimum-bias events at the LHC is made. Note that these tunes can only be used with PYTHIA 6, not with PYTHIA 8. Note: this report was updated in March 2011 with a new set of variations, collectively labeled "Perugia 2011", that are optimized for matching applications and which also take into account some lessons from the early LHC data. In order not to break the original text, these are described separately in Appendix B. Note 2: a subsequent "Perugia 2012" update is described in Appendix C.Comment: 46 page

Lysosomal degradation of membrane lipids

AbstractThe constitutive degradation of membrane components takes place in the acidic compartments of a cell, the endosomes and lysosomes. Sites of lipid degradation are intralysosomal membranes that are formed in endosomes, where the lipid composition is adjusted for degradation. Cholesterol is sorted out of the inner membranes, their content in bis(monoacylglycero)phosphate increases, and, most likely, sphingomyelin is degraded to ceramide. Together with endosomal and lysosomal lipid-binding proteins, the Niemann–Pick disease, type C2-protein, the GM2-activator, and the saposins sap-A, -B, -C, and -D, a suitable membrane lipid composition is required for degradation of complex lipids by hydrolytic enzymes

Accumulation of protein-bound epidermal glucosylceramides in β-glucocerebrosidase deficient type 2 Gaucher mice

AbstractThe epidermal permeability barrier for water is essentially maintained by extracellular lipid membranes within the interstices of the stratum corneum. Ceramides, the main components of these membranes, derive in large part from hydrolysis of glucosylceramides mediated by the lysosomal enzyme β-glucocerebrosidase. As analyzed in this work, the β-glucocerebrosidase deficiency in type 2 Gaucher mice (RecNci I) resulted in an accumulation of all epidermal glucosylceramide species accompanied with a decrease of the related ceramides. However, the levels of one ceramide subtype, which possesses an α-hydroxypalmitic acid, was not altered in RecNci I mice suggesting that the β-glucocerebrosidase pathway is not required for targeting of this lipid to interstices of the stratum corneum. Most importantly, ω-hydroxylated glucosylceramides which are protein-bound to the epidermal cornified cell envelope of the transgenic mice accumulated up to 35-fold whereas levels of related protein-bound ceramides and fatty acids were decreased to 10% of normal control. These data support the hypothesis that in wild-type epidermis ω-hydroxylated glucosylceramides are first transferred enzymatically from their linoleic esters to proteins of the epidermal cornified cell envelope and then catabolized to protein-bound ceramides and fatty acids, thus contributing at least in part to the formation of the lipid-bound envelope

From amaurotic idiocy to biochemically defined lipid storage diseases: the first identification of GM1-Gangliosidosis

On February 23rd 1936, a boy-child (“Kn”) died in an asylum near Munich after years of severe congenital dis-ease, which had profoundly impaired his development leading to inability to walk, talk and see as well as to severe epilepsy. While a diagnosis of “Little’s disease” was made during life, his postmortem brain investiga-tion at Munich neuropathology (“Deutsche Forschungsanstalt für Psychiatrie”) revealed the diagnosis of “amaurotic idiocy” (AI). AI, as exemplified by Tay-Sachs-Disease (TSD), back then was not yet understood as a specific inborn error of metabolism encompassing several disease entities. Many neuropathological studies were performed on AI, but the underlying processes could only be revealed by new scientific techniques such as biochemical analysis of nervous tissue, deciphering AI as nervous system lipid storage diseases, e.g. GM2-gangliosidosis. In 1963, Sandhoff & Jatzkewitz published an article on a “biochemically special form of AI” reporting striking differences when comparing their biochemical observations of hallmark features of TSD to tissue composition in a single case: the boy Kn. This was the first description of “GM1-Gangliosidosis”, later understood as resulting from genetically determined deficiency in beta-galactosidase. Here we present illus-trative materials from this historic patient, including selected diagnostic slides from the case “Kn” in virtual microscopy, original records and other illustrative material available. Finally, we present results from genetic analysis performed on archived tissue proving beta-galactosidase-gene mutation, verifying the 1963 interpre-tation as correct. This synopsis shall give a first-hand impression of this milestone finding in neuropathology