617 research outputs found

    Violence and Silence: The Prison Rape Elimination Act and Beyond

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    Connecting the #MeToo movement to sexual abuse in prisons, this paper analyzes the flaws of the Prison Rape Elimination Act of 2003. Examining the genesis behind PREA, the lack of enforcement and accountability, and the remaining unresolved issues, I argue that the law fails to meaningfully combat the pervasive and multifaceted problem of sexual abuse in US prisons. The racist, sexist, and homophobic ideologies that gave rise to PREA, as well as its focus on prison efficiency rather than prisoners’ lives, only serve to further entrench harmful biases within United States prisons and broader society

    Shifting Binaries: American War Fiction from Vietnam to Iraq

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    This project builds off historical and literary war theories about binaries to interrogate whether the nature of war writing has changed as war has changed. I analyze two Vietnam and two Iraq war novels for the ways they challenge or uphold the binaries of war, and how these binaries shift over time. I argue that the breakdown of a coherent ‘enemy’ due to the increase of a diffuse and decentralized insurgent force increasing from the Vietnam War to the Iraq War begins to collapse the binaries of ally versus enemy and combatant versus noncombatant in the countries in which the United States wages war. At the same time, the elimination of the American draft widens the gap between American soldiers and civilians as fewer and fewer Americans serve or know anyone who has served in the military

    Introduction to Tapestries Volume 7: Breaking the Shackles of Silence: Knowledge Production as Activism and Resistance

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    Introduction to volume 7 of Macalester College\u27s journal Tapestries: Interwoven voices of local and global identities

    Results from Six Years of Community-Based Volunteer Water Quality Monitoring By the Upper Oconee Watershed Network

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    Proceedings of the 2007 Georgia Water Resources Conference, March 27-29, 2007, Athens, Georgia.The Upper Oconee Watershed Network (UOWN), an Athens, GA-based non-profit volunteer organization, was organized in 2000 with the mission to improve water quality in the Upper Oconee River basin through community-based advocacy, monitoring, and education. Quarterly monitoring of both reference and impaired stream segments form the basis for achieving all three of UOWN’s mission objectives. UOWN has developed a model for engaging the public in quarterly monitoring and in the larger annual River Rendezvous events. Quarterly monitoring not only tracks long-term trends in targeted stream segments, but also has resulted in the discovery and remediation of acute incidences of pollution. Six years of data collection revealed high levels of contamination in urban streams as evidenced by high conductivity and bacterial numbers, and potential limitations when using quarterly water quality monitoring to assess the health of Piedmont streams.Sponsored and Organized by: U.S. Geological Survey, Georgia Department of Natural Resources, Natural Resources Conservation Service, The University of Georgia, Georgia State University, Georgia Institute of TechnologyThis book was published by the Institute of Ecology, The University of Georgia, Athens, Georgia 30602-2202. The views and statements advanced in this publication are solely those of the authors and do not represent official views or policies of The University of Georgia, the U.S. Geological Survey, the Georgia Water Research Institute as authorized by the Water Resources Research Act of 1990 (P.L. 101-397) or the other conference sponsors

    The Genome and Methylome of a Beetle with Complex Social Behavior,Nicrophorus vespilloides(Coleoptera: Silphidae)

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    Testing for conserved and novelmechanisms underlying phenotypic evolution requires a diversity of genomes available for comparisonspanning multiple independent lineages. For example, complex social behavior in insects has been investigated primarily witheusocial lineages, nearly all of which are Hymenoptera. If conserved genomic influences on sociality do exist, we need data from awider range of taxa that also vary in their levels of sociality. Here,we present the assembled and annotated genome of the subsocialbeetle Nicrophorus vespilloides, a species long used to investigate evolutionary questions of complex social behavior. We used thisgenome to address two questions. First, do aspects of life history, such as using a carcass to breed, predict overlap in gene modelsmore strongly than phylogeny? We found that the overlap in gene models was similar between N. vespilloides and all other insectgroups regardless of life history. Second, like other insects with highly developed social behavior but unlike other beetles, doesN. vespilloides have DNA methylation?We found strong evidence for an active DNA methylation system. The distribution of methylationwassimilar to other insects with exons having themostmethylatedCpGs. Methylation status appears highly conserved; 85%of themethylated genes in N. vespilloides are alsomethylated in the hymentopteran Nasonia vitripennis. The addition of this genomeadds a coleopteran resource to answer questions about the evolution and mechanistic basis of sociality and to address questionsabout the potential role of methylation in social behavior

    The First European Interdisciplinary Ewing Sarcoma Research Summit

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    The European Network for Cancer Research in Children and Adolescents (ENCCA) provides an interaction platform for stakeholders in research and care of children with cancer. Among ENCCA objectives is the establishment of biology-based prioritization mechanisms for the selection of innovative targets, drugs, and prognostic markers for validation in clinical trials. Specifically for sarcomas, there is a burning need for novel treatment options, since current chemotherapeutic treatment protocols have met their limits. This is most obvious for metastatic Ewing sarcoma (ES), where long term survival rates are still below 20%. Despite significant progress in our understanding of ES biology, clinical translation of promising laboratory results has not yet taken place due to fragmentation of research and lack of an institutionalized discussion forum. To fill this gap, ENCCA assembled 30 European expert scientists and five North American opinion leaders in December 2011 to exchange thoughts and discuss the state of the art in ES research and latest results from the bench, and to propose biological studies and novel promising therapeutics for the upcoming European EWING2008 and EWING2012 clinical trials

    Mutations in ALK signaling pathways conferring resistance to ALK inhibitor treatment lead to collateral vulnerabilities in neuroblastoma cells

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    Background: Development of resistance to targeted therapies has tempered initial optimism that precision oncology would improve poor outcomes for cancer patients. Resistance mechanisms, however, can also confer new resistance-specific vulnerabilities, termed collateral sensitivities. Here we investigated anaplastic lymphoma kinase (ALK) inhibitor resistance in neuroblastoma, a childhood cancer frequently affected by activating ALK alterations. Methods: Genome-wide forward genetic CRISPR-Cas9 based screens were performed to identify genes associated with ALK inhibitor resistance in neuroblastoma cell lines. Furthermore, the neuroblastoma cell line NBLW-R was rendered resistant by continuous exposure to ALK inhibitors. Genes identified to be associated with ALK inhibitor resistance were further investigated by generating suitable cell line models. In addition, tumor and liquid biopsy samples of four patients with ALK-mutated neuroblastomas before ALK inhibitor treatment and during tumor progression under treatment were genomically profiled. Results: Both genome-wide CRISPR-Cas9-based screens and preclinical spontaneous ALKi resistance models identified NF1 loss and activating NRASQ61K mutations to confer resistance to chemically diverse ALKi. Moreover, human neuroblastomas recurrently developed de novo loss of NF1 and activating RAS mutations after ALKi treatment, leading to therapy resistance. Pathway-specific perturbations confirmed that NF1 loss and activating RAS mutations lead to RAS-MAPK signaling even in the presence of ALKi. Intriguingly, NF1 loss rendered neuroblastoma cells hypersensitive to MEK inhibition. Conclusions: Our results provide a clinically relevant mechanistic model of ALKi resistance in neuroblastoma and highlight new clinically actionable collateral sensitivities in resistant cells

    Accelerating drug development for neuroblastoma - New Drug Development Strategy: an Innovative Therapies for Children with Cancer, European Network for Cancer Research in Children and Adolescents and International Society of Paediatric Oncology Europe Neuroblastoma project

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    Introduction: Neuroblastoma, the commonest paediatric extra-cranial tumour, remains a leading cause of death from cancer in children. There is an urgent need to develop new drugs to improve cure rates and reduce long-term toxicity and to incorporate molecularly targeted therapies into treatment. Many potential drugs are becoming available, but have to be prioritised for clinical trials due to the relatively small numbers of patients. Areas covered: The current drug development model has been slow, associated with significant attrition, and few new drugs have been developed for neuroblastoma. The Neuroblastoma New Drug Development Strategy (NDDS) has: 1) established a group with expertise in drug development; 2) prioritised targets and drugs according to tumour biology (target expression, dependency, pre-clinical data; potential combinations; biomarkers), identifying as priority targets ALK, MEK, CDK4/6, MDM2, MYCN (druggable by BET bromodomain, aurora kinase, mTORC1/2) BIRC5 and checkpoint kinase 1; 3) promoted clinical trials with target-prioritised drugs. Drugs showing activity can be rapidly transitioned via parallel randomised trials into front-line studies. Expert opinion: The Neuroblastoma NDDS is based on the premise that optimal drug development is reliant on knowledge of tumour biology and prioritisation. This approach will accelerate neuroblastoma drug development and other poor prognosis childhood malignancies
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