Pipeline to Failure: Social Inequality and the False Promises of American Public Schooling

My experience as a New York City public school student was absolutely electrifying, though filled with many trials. While my mother would have preferred to put me in private school, having access to some of the world’s greatest institutions and resources offered unique opportunities and exposures. The performing arts provided me with an outlet to express myself and build skills and confidence. In particular, dance education kept me occupied and disciplined in a large city full of danger. Every so often, I witnessed hostile, or even violent exchanges between students, or students and staff. While some of my schoolmates became doctors and Olympic medalists, others were parents at the age of fifteen. Unfortunately, too many teachers lacked the passion or desire needed to ignite their students’ true potential. My long-time compassion for youth led me to a career as an educator and administrator. Through my work with several non-profit and educational organizations, I honed invaluable instructional and managerial skills; I learned to write and deliver engaging arts and academic curricula and manage contracts, programs and budgets. Over time, I began to discover the multifaceted issues that plague the urban education system. Despite my commitment to changing the American educational landscape, I often felt hopeless as I encountered endless obstacles. My desire to gain a deeper understanding of the social, cultural, political and economic factors that affect one’s educational pursuit led me on a journey to study at the Graduate Center, City University of New York. The research I have conducted has provided me with mounting evidence that public-schooling fails to ameliorate social inequalities; instead they play a major role in reproducing them. In Schooling in Capitalist America, economists and social theorists Bowles and Gintis eloquently explain: The perpetuation of the class structure requires that the hierarchical division of labor be reproduced in the consciousness of its participants. The educational system is one of the … reproduction mechanisms through which dominant elites seek to achieve this objective. By providing skills, legitimating inequalities in economic positions, and facilitating certain types of social intercourse among individuals, U.S. education patterns personal development around the requirements of alienated work. The educational system reproduces the capitalist social division of labor, in part, through a correspondence between its own internal social relationships and those of the workplace. (p. 147). Bowles and Gintis’ correspondence theory still holds true. Race and class are undeniably intertwined and serve as the backdrop, while a record-breaking number of lower-class students continue to be set on a trajectory of failure. When we begin to understand the world in which we live and how it has come to be, it is only then that we can make it a better place. I dedicate this research to our nation’s young and the marginalized communities that continue to be intentionally left out of the rat race

From risky places to safe spaces : Re-assembling spaces and places in Vancouver's downtown eastside : [infographic]

This infographic is based on the following scholarly article: Ivsins, A., Vancouver Area Network of Drug Users, Benoit, C., Kobayashi, K., & Boyd, S. (2019). From risky places to safe spaces: Re-assembling spaces and places in Vancouver's downtown eastside. Health & Place, 59: 102164. https://doi.org/10.1016/j.healthplace.2019.102164. This undergraduate student work is a product of a collaboration between the Making Research Accessible initiative (MRAi), researchers, Dr. Evan Mauro and the students of ASTU 100 at UBC. This student work has been reviewed by the lead author of the original item. Revisions provided by the lead author have been incorporated into the student work with support from the UBC Learning Exchange and members of the MRAi. The reader should bear in mind that this is a student research project/report and is not an official document of UBC.Arts, Faculty ofUnreviewedUndergraduat

Genome-wide CRISPR/Cas9 screen shows that loss of GET4 increases mitochondria-endoplasmic reticulum contact sites and is neuroprotective.

Acknowledgements: We thank the Cambridge Advanced Imaging Centre (CAIC) for EM sample preparation and sectioning. We also thank the Cambridge Institute for Medical Research (CIMR) Mass Spectrometry facility for conducting the mass spectrometry protocol and analysis. We thank the Vienna Drosophila RNAi Centre for fly stocks. We also wish to say thank you to Tom Smith for proofreading the paper and providing independent input.Funder: UK DRI Grant RRZA/175Funder: Medical Research Council UK (MC_UU_00028/5)Funder: UK Medical Research Council, intramural project MC_UU_00025/3 (RG94521)Organelles form membrane contact sites between each other, allowing for the transfer of molecules and signals. Mitochondria-endoplasmic reticulum (ER) contact sites (MERCS) are cellular subdomains characterized by close apposition of mitochondria and ER membranes. They have been implicated in many diseases, including neurodegenerative, metabolic, and cardiac diseases. Although MERCS have been extensively studied, much remains to be explored. To uncover novel regulators of MERCS, we conducted a genome-wide, flow cytometry-based screen using an engineered MERCS reporter cell line. We found 410 genes whose downregulation promotes MERCS and 230 genes whose downregulation decreases MERCS. From these, 29 genes were selected from each population for arrayed screening and 25 were validated from the high population and 13 from the low population. GET4 and BAG6 were highlighted as the top 2 genes that upon suppression increased MERCS from both the pooled and arrayed screens, and these were subjected to further investigation. Multiple microscopy analyses confirmed that loss of GET4 or BAG6 increased MERCS. GET4 and BAG6 were also observed to interact with the known MERCS proteins, inositol 1,4,5-trisphosphate receptors (IP3R) and glucose-regulated protein 75 (GRP75). In addition, we found that loss of GET4 increased mitochondrial calcium uptake upon ER-Ca2+ release and mitochondrial respiration. Finally, we show that loss of GET4 rescues motor ability, improves lifespan and prevents neurodegeneration in a Drosophila model of Alzheimer's disease (Aβ42Arc). Together, these results suggest that GET4 is involved in decreasing MERCS and that its loss is neuroprotective

Identification of 5‑(1-Methyl-5-(trifluoromethyl)‑1<i>H</i>‑pyrazol-3-yl)thiophene-2-Carboxamides as Novel and Selective Monoamine Oxidase B Inhibitors Used to Improve Memory and Cognition

Initial work in <i>Drosophila</i> and mice demonstrated that the transcription factor cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) is a master control gene for memory formation. The relationship between CREB and memory has also been found to be true in other species, including aplysia and rats. It is thus well-established that CREB activation plays a central role in memory enhancement and that CREB is activated during memory formation. On the basis of these findings, a phenotypic high-throughput screening campaign utilizing a CRE-luciferase (CRE-Luci) SK-N-MC cell line was performed to identify compounds that enhance transcriptional activation of the CRE promoter with a suboptimal dose of forskolin. A number of small-molecule hits of unknown mechanisms of action were identified in the screening campaign, including HT-0411. Follow-up studies suggested that the CREB activation by HT-0411 is attributed to its specific and selective inhibition of monoamine oxidase B (MAO-B). Further, HT-0411 was shown to improve 24 h memory in rodents in a contextual fear conditioning model. This report describes the lead optimization of a series of 5-(1-methyl-5-(trifluoromethyl)-1<i>H</i>-pyrazol-3-yl) thiophene-2-carboxamides that were identified as novel, potent, and selective inhibitors of MAO-B. Extensive SAR studies and in vivo behavioral evaluations of this and other related analogue series identified a number of potential clinical development candidates; ultimately, compound <b>8f</b> was identified as a candidate molecule with high selectivity toward MAO-B (29–56 nM) over MAO-A (19% inhibition at a screening concentration of 50 μM), an excellent profile against a panel of other enzymes and receptors, good pharmacokinetic properties in rodents and dogs, and efficacy in multiple rodent memory models