Framing Absence: Visuals of the Wall and the Vanishing Landscapes in Palestine

This dissertation explores peoples relationship to the landscapes of material, abstract, and visual borders in the context of Palestine-Israel. Since 2002, the construction of the Israeli separation Wall in the Occupied Palestinian Territories has significantly transformed the way locals, particularly on the Palestinian side of the Wall see and articulate their relation to the landscape. Already living in a state of military occupation through restriction of movement, limited access to land and urban expansion on occupied territory, the Wall has considerably shifted Palestinians relationships to the landscape. To them the landscape has become a visual field on which power dynamics and political structures are embodied and expressed. Moreover, for many Palestinians the Israeli construction of the Wall is visible evidence of the on-going process of destruction of the Palestinian landscape. But what is the view of Palestinians and Israelis living on the Israeli side of the Wall and those living in Palestine but in close proximity to the Wall? What is their engagement with the Wall? To answer these questions, this dissertation draws on more than 12 months of ethnographic research in Israel and Palestine that involved extended interviews with Palestinian and Israeli photographers and activists in Israel, as well as Palestinians whose lives were affected by the Walls construction in proximity to their homes and for whom the Wall route brought them into direct confrontation with the Israeli military. This research also examined representations of the Wall in different visual projects. From a theoretical perspective, this dissertation asks how do visual fields facilitate the structuring of national imaginaries and what sights and future visions are offered by different readings of the landscape? To answer these questions, I employ anthropological theories of violence, borders and the visual, and propose the concept of landscapocide, a violent visual process through which landscapes are framed, and made to be seen and unseen. Through landscapocide and other anthropologically grounded theories and concepts I offer a new reading of the ways in which people in bordered contexts give meaning to what they see

A Novel Conserved Isoform of the Ubiquitin Ligase UFD2a/UBE4B Is Expressed Exclusively in Mature Striated Muscle Cells

Yeast Ufd2p was the first identified E4 multiubiquitin chain assembly factor. Its vertebrate homologues later referred to as UFD2a, UBE4B or E4B were also shown to have E3 ubiquitin ligase activity. UFD2a function in the brain has been well established in vivo, and in vitro studies have shown that its activity is essential for proper condensation and segregation of chromosomes during mitosis. Here we show that 2 alternative splice forms of UFD2a, UFD2a-7 and -7/7a, are expressed sequentially during myoblast differentiation of C2C12 cell cultures and during cardiotoxin-induced regeneration of skeletal muscle in mice. UFD2a-7 contains an alternate exon 7, and UFD2a-7/7a, the larger of the 2 isoforms, contains an additional novel exon 7a. Analysis of protein or mRNA expression in mice and zebrafish revealed that a similar pattern of isoform switching occurs during developmental myogenesis of cardiac and skeletal muscle. In vertebrates (humans, rodents, zebrafish), UFD2a-7/7a is expressed only in mature striated muscle. This unique tissue specificity is further validated by the conserved presence of 2 muscle-specific splicing regulatory motifs located in the 3′ introns of exons 7 and 7a. UFD2a interacts with VCP/p97, an AAA-type ATPase implicated in processes whose functions appear to be regulated, in part, through their interaction with one or more of 15 previously identified cofactors. UFD2a-7/7a did not interact with VCP/p97 in yeast 2-hybrid experiments, which may allow the ATPase to bind cofactors that facilitate its muscle-specific functions. We conclude that the regulated expression of these UFD2a isoforms most likely imparts divergent functions that are important for myogenisis

MyoD and myogenin protein expression in skeletal muscles of senile rats

We analyzed the level of protein expression of two myogenic regulatory factors (MRFs), MyoD and myogenin, in senile skeletal muscles and determined the cellular source of their production in young adult (4 months old), old (24, 26, and 28 months old), and senile (32 months old) male rats. Immunoblotting demonstrated levels of myogenin ~3.2, ~4.0, and ~5.5 times higher in gastrocnemius muscles of 24-, 26-, and 32-month-old animals, respectively, than in those of young adult rats. Anti-MyoD antibody recognized two major areas of immunoreactivity in Western blots: a single MyoD-specific band (~43–45 kDa) and a double (or triple) MyoD-like band (~55–65 kDa). Whereas the level of MyoD-specific protein in the 43- to 45-kDa band remained relatively unchanged during aging compared with that of young adult rats, the total level of MyoD-like immunoreactivity within the 55- to 65-kDa bands was ~3.4, ~4.7, ~9.1, and ~11.7 times higher in muscles of 24-, 26-, 28-, and 32-month-old rats, respectively. The pattern of MRF protein expression in intact senile muscles was similar to that recorded in young adult denervated muscles. Ultrastructural analysis of extensor digitorum longus muscle from senile rats showed that, occasionally, the area of the nerve-muscle junction was partially or completely devoid of axons, and satellite cells with the features of activated cells were found on the surface of living fibers. Immunohistochemistry detected accumulated MyoD and myogenin proteins in the nuclei of both fibers and satellite cells in 32-month-old muscles. We suggest that the up-regulated production of MyoD and myogenin proteins in the nuclei of both fibers and satellite cells could account for the high level of MRF expression in muscles of senile rats.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42276/1/s00441-002-0686-9.pd

Blunted hypertrophic response in old mouse muscle is associated with a lower satellite cell density and is not alleviated by resveratrol

Background Sarcopenia contributes to the decreased quality of life in the older person. While resistance exercise is an effective measure to increase muscle mass and strength, the hypertrophic response may be blunted in old age. Objectives To determine 1) whether hypertrophy in the m. plantaris of old mice was blunted compared to adult and 2) whether this was related to a reduced satellite cell (SC) density and 3) how resveratrol affects hypertrophy in old mice. Methods In adult (7.5 months, n = 11), old (23.5 months, n = 10) and old-resveratrol-treated (n = 10) male C57BL/6J mice, hypertrophy of the left m. plantaris was induced by denervation of its synergists. The contralateral leg served as control. Results After six weeks, overload-induced myofiber hypertrophy and IIB–IIA shift in myofiber type composition were less pronounced in old than adult mice (P = 0.03), irrespective of resveratrol treatment. Muscles from old mice had a lower SC density than adult muscles (P = 0.002). Overload-induced SC proliferation (P < 0.05) resulted in an increased SC density in old, but not adult muscles (P = 0.02), while a decrease occurred after resveratrol supplementation (P = 0.044). Id2 and myogenin protein expression levels were higher in old than adult muscles (P < 0.05). Caspase-3 was expressed more in hypertrophied than control muscles and was reduced with resveratrol (P < 0.05). Conclusion The blunted hypertrophic response in old mice was associated with a lower SC density, but there was no evidence for a lower capacity for proliferation. Resveratrol did not rescue the hypertrophic response and even reduced, rather than increased, the number of SCs in hypertrophied muscles

Online Collaborative Discourse jako forma wsparcia uczniów z trudnościami w uczeniu się matematyki

The present research study was carried out in an online learning environment in a small group of eighth-grade students. The research proposes a learning framework that relies on collaborative mathematical discourse with the intention to promote the reasoning ability of students with difficulties in mathematics. The aim of mathematical discourse is the reciprocal building of the ability of the learner with difficulties to provide explanations during the discourse between the learner and his peers and between the learner and the teacher. This type of learning was found to be effective, and the communicational continuum between the learner and the material and between the learner and the group is preserved. The learning process built on authentic mathematical tasks strengthened the learners’ ability to create communication among themselves. The discourse encouraged the development of mathematical thinking abilities among the learners with difficulties, such as posing arguments and drawing conclusions while explaining and justifying these arguments. The mathematical discourse also encouraged students to choose and to monitor the form and processes of their thinking and increased their problem-solving ability

Multiple novel functions of lamina associated polypeptide 2α in striated muscle

Lamina-associated polypeptide 2α (LAP2α) is a nucleoplasmic protein that interacts with A-type lamins and the retinoblastoma protein (pRb) and affects pRb-mediated cell cycle regulation and chromatin organization. Mutations in lamin A/C and LAP2α cause late onset striated muscle diseases, but the molecular mechanisms are poorly understood. We have recently reported on the striated muscle phenotype of LAP2α-deficient mice, revealing new unexpected roles of LAP2α. Loss of LAP2α in skeletal muscle caused an upregulated stem cell-type gene expression in muscle satellite cell progeny and their delayed myogenic differentiation in vitro. In vivo, the myofiber-associated muscle stem cell pool was increased. In addition, absence of LAP2α promoted muscle remodeling towards fast myofiber types in the soleus muscle of old animals. In cardiac tissue, deletion of LAP2α caused systolic dysfunction in young mice with an increased susceptibility for fibrosis in old animals. The functional impairment in the heart was accompanied by a deregulation of major cardiac transcription factors, GATA4 and MEF2c and activation of compensatory pathways, including the downregulation of β-adrenergic receptor signaling