Political activists or violent fans? Understanding the Moroccan Ultras perspective through social media discourse analysis

This paper examines the origins, traditions, reasons behind rapid numbers expansion, and violent tendencies of organized groups of young football fans called Ultras. It also sheds the light on Al Raja Ultra groups, the first Moroccan Ultras groups and the most violent who started emerging in Casablanca in 2005, and since then thrived and diversified, not only in Casablanca but in Morocco as a whole. It’s unknown where the culture was derived from due to lack of literature on this matter but speculated to be a mimicking of neighboring countries such as Spain, and Tunisia where this phenomenon has been more prevalent. Ultras groups are the most loyal fans to Moroccan football clubs that created an entire culture surrounding teams of allegiance, and soccer in general. This paper was initially proposed to evaluate the Ultras activism against a ban that has been instituted against them. Yet, the research uncovered an unsolved problem of Ultras rioting even after the ban was lifted, indicating urgency to understand The Moroccan Ultras culture. Therefore, the research has been repurposed to tend to the violence problem. The back and forth battles amongst Ultra factions, and between Ultras and security forces has been leaving a trail of loses between lives and public-private properties. Through discourse analysis, this paper is going to attempt to present the Ultras perspective of rioting events and identify key themes to their involvement of such actions. It concludes with; if the Moroccan regulating bodies and security forces keep the lazy politics top down approach and do not take an inclusive approach to try and solve the issue of rioting, they’re risking further radicalization of the Ultras that might evolve into a much larger problem

Ella Fitzgerald: The Music, The Woman, The Voice of America!

Ella Fitzgerald, American jazz vocalist, had an extreme impact on the world of musicians and singers during her lifetime. Her influence is still felt today, as her recordings live on as a tribute to her lifelong commitment to her art. Most jazz vocalists have been inspired by Fitzgerald because of her versatility as a performer, her presentation of material, her scat singing, and her vocal musicianship. This thesis explores three aspects of Fitzgerald and her art. The first gives background on jazz history which makes it possible to place Ella Fitzgerald into the development of jazz. The second explores Fitzgerald\u27s experiences as a jazz musician. The third identifies the elements of Fitzgerald\u27s musical style that make her distinctive and shows how these elements insure her immortality in jazz history

GenerationY interns experiences with, and perceptions of, collaboration in educational settings

Using a phenomenological approach, the purpose of this study was to relate select Generation Y interns’ experiences with, and perceptions of, collaboration as a result of their internships. The theoretical framework of this study reviewed three distinct areas of literature: Generation Y and their role in the professional workforce, the induction and retention of new teachers, and the role of professional learning communities in schools. Both transcendental and hermeneutical approaches to phenomenology were employed in the analysis of interview data. The data for this study were obtained from in-depth interviews with five post-internship students at the University of Saskatchewan. The findings of this study revealed that the cultural characteristics of Generation Y teachers play a role in the desire of interns to engage in professional collaboration and have an impact on the profession as they see it. The implications of this paper outline that more research is needed to examine the effect of professional learning communities on the development of interns’ pedagogical skill and on the impact that Generation Y teachers will have on the way education is delivered in the future. Furthermore, when considering the nature of Generation Y interns and teachers, collaboration must be nurtured and emphasized as part of teacher education and induction programs, including the internship

A sequence-length sensitive approach to learning biological grammars using inductive logic programming.

This thesis aims to investigate if the ideas behind compression principles, such as the Minimum Description Length, can help us to improve the process of learning biological grammars from protein sequences using Inductive Logic Programming (ILP). Contrary to most traditional ILP learning problems, biological sequences often have a high variation in their length. This variation in length is an important feature of biological sequences which should not be ignored by ILP systems. However we have identified that some ILP systems do not take into account the length of examples when evaluating their proposed hypotheses. During the learning process, many ILP systems use clause evaluation functions to assign a score to induced hypotheses, estimating their quality and effectively influencing the search. Traditionally, clause evaluation functions do not take into account the length of the examples which are covered by the clause. We propose L-modification, a way of modifying existing clause evaluation functions so that they take into account the length of the examples which they learn from. An empirical study was undertaken to investigate if significant improvements can be achieved by applying L-modification to a standard clause evaluation function. Furthermore, we generally investigated how ILP systems cope with the length of examples in training data. We show that our L-modified clause evaluation function outperforms our benchmark function in every experiment we conducted and thus we prove that L-modification is a useful concept. We also show that the length of the examples in the training data used by ILP systems does have an undeniable impact on the results

Approximations for the Random Minimal Spanning Tree With Application to Network Provisioning

This paper considers the problem of determining the mean and distribution of the length of a minimal spanning tree (MST) on an undirected graph whose arc lengths are independently distributed random variables. We obtain bounds and approximations for the MST length and show that our upper bound is much tighter than the naive bound obtained by computing the MST length of the deterministic graph with the respective means as arc lengths. We analyze the asymptotic properties of our approximations and establish conditions under which our bounds are asymptotically optimal. We apply these results to a network provisioning problem and show that the relative error induced by using our approximations tends to zero as the graph grows large

LABOR STRIKES AND THE PRICE OF LETTUCE

This paper examines the economic impact of the 1979 labor strike against lettuce producer-shippers in the Imperial Valley of California. The theory presented suggests that formidable problems are encountered by agricultural labor unions in obtaining higher wages for farm workers. During the 1979 strike, ironically the returns to many of the lettuce producers in the Imperial Valley increased substantially.Demand and Price Analysis, Labor and Human Capital,

Discovering angiogenic cell signaling landscapes: Quantitative mapping through experiment and computation

Angiogenesis is a key regulator in over 70 diseases, and it is typically characterized via uni-family ligand-receptor interactions—primarily via VEGF-A:VEGFR2 binding. But targeting the VEGF family alone has not achieved the promise of stable vascular control, because angiogenesis involves other signaling axes, such as the PDGFs. In cancer, for example, anti- angiogenic therapeutics primarily target the VEGF signaling family, but their success is limited by the development of drug resistance. These challenges in VEGF targeting, and recent discoveries of VEGF-A:PDGFR binding and signaling, presents a compelling need to shift away from a uni-family (e.g., VEGF-alone) towards a multi- and cross-family (e.g., VEGF + PDGF, etc.) understanding of angiogenesis. VEGFs and PDGFs share significant structural and binding motifs, which could explain the new VEGF-A: PDGFR interaction and suggests that additional cross-family VEGF/PDGF cross-family binding may occur. To identify and measure new ligand:receptor binding pairs, I utilized a surface plasmon resonance-biosensor based kinetics assay. Here, I present my discovery of novel PDGF:VEGFR2 interactions, with: PDGF-AA:R2 KD = 530 nM, PDGF- AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM. For the first time, I measured the kinetic constants for VEGF-A:PDGFRβ and the canonical PDGF:PDGFR interactions. I then construct a model of VEGF-A: and PDGF:VEGFR2 interactions in endothelial cells (ECs),and predict that PDGF:VEGFR binding could contribute up to 96% of VEGFR2 ligation in healthy conditions and in cancer. Because VEGFR2-mediated signaling drives angiogenic responses, I investigated whether PDGF-binding could activate VEGFR2-mediated signaling, and ultimately stimulate EC proliferation and migration—steps key in angiogenesis. I found that PDGFs induce significant VEGFR2 phosphorylation at tyrosines 951, 1054/59, and 1175. Further, PDGFs activate the downstream signaling effectors FAK, PI3K, PLCγ and Src. Remarkably, PDGF-AA promoted a 1.2-fold larger increase in Y1054/59 phosphorylation than did the canonical VEGF-A. PDGF- BB stimulates a ~1.3-fold larger increase in FAK phosphorylation than VEGF-A. Furthermore, I show the PDGFs stimulate increased EC proliferation, and that only PDGF-AA, -BB, and -CC stimulated significant EC migration. Taken together, these findings that PDGFs can stimulate VEGFR2 signaling and downstream angiogenic cell responses will break new ground towards modulating angiogenesis in health and disease, offering new hypotheses for why angiogenesis- targeting therapies have proven unsuccessful. VEGF-A165 and its binding to VEGFRs is an important angiogenesis regulator. But several additional splice variants play prominent roles in regulating angiogenesis in health and in vascular disease, including VEGF-A121 and an anti-angiogenic variant VEGF-A165b. Despite their significance to physiological, therapeutic, and pathological angiogenesis, little is known about differences in their binding. I measured the binding kinetics for VEGF-A165, -A165b, and -A121 with VEGFR1 and –R2 using (SPR). I find that the VEGF-A variants differentially bind VEGFRs. VEGFR1 binds variants at strengths: VEGF-A165a > -A165b > -A121; and VEGFR2 binds variants at strengths: VEGF-A165b > -A165a > -A121. Interestingly, my findings suggest that the anti-angiogenic VEGF-A165a would preferentially bind VEGFR2, out-competing the pro- angiogenic isoform. My results suggest VEGF-A splice variants may play an important modulatory role in VEGFR-mediated angiogenesis, stressing the need to differentiate VEGF-A splice variants in future studies. Overall, my results demonstrate that that VEGFR-mediated angiogenesis involves a more complex network of ligand:receptor interactions than previously known. Computational approaches can provide key insight to detangle these signaling pathways but are limited by the sparse knowledge of cross-family interactions. Here, I present a framework for studying known and potential non-canonical interactions. I construct generalized models of RTK ligation and dimerization for systems of two, three, and four receptor types, and different degrees of cross- family ligation. Across each model, I develop parameter-space maps that fully determine relative receptor activation for any set of ligand:receptor binding kinetics, ligand concentrations, and receptor concentrations. My generalized models serve as a powerful reference tool for predicting dimerization for known ligand:receptor axes. They also can predict how unknown interactions could alter signaling dimerization patterns. Accordingly, they will drive exploration of cross- family interactions, and help guide therapeutic developments across processes like cancer and cardiovascular diseases that depend on RTK-mediated signaling

TGFβ signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke

<p>Abstract</p> <p>Background</p> <p>TGFβ is both neuroprotective and a key immune system modulator and is likely to be an important target for future stroke therapy. The precise function of increased TGF-β1 after stroke is unknown and its pleiotropic nature means that it may convey a neuroprotective signal, orchestrate glial scarring or function as an important immune system regulator. We therefore investigated the time course and cell-specificity of TGFβ signaling after stroke, and whether its signaling pattern is altered by gender and aging.</p> <p>Methods</p> <p>We performed distal middle cerebral artery occlusion strokes on 5 and 18 month old TGFβ reporter mice to get a readout of TGFβ responses after stroke in real time. To determine which cell type is the source of increased TGFβ production after stroke, brain sections were stained with an anti-TGFβ antibody, colocalized with markers for reactive astrocytes, neurons, and activated microglia. To determine which cells are responding to TGFβ after stroke, brain sections were double-labelled with anti-pSmad2, a marker of TGFβ signaling, and markers of neurons, oligodendrocytes, endothelial cells, astrocytes and microglia.</p> <p>Results</p> <p>TGFβ signaling increased 2 fold after stroke, beginning on day 1 and peaking on day 7. This pattern of increase was preserved in old animals and absolute TGFβ signaling in the brain increased with age. Activated microglia and macrophages were the predominant source of increased TGFβ after stroke and astrocytes and activated microglia and macrophages demonstrated dramatic upregulation of TGFβ signaling after stroke. TGFβ signaling in neurons and oligodendrocytes did not undergo marked changes.</p> <p>Conclusions</p> <p>We found that TGFβ signaling increases with age and that astrocytes and activated microglia and macrophages are the main cell types that undergo increased TGFβ signaling in response to post-stroke increases in TGFβ. Therefore increased TGFβ after stroke likely regulates glial scar formation and the immune response to stroke.</p