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      • The Butterfly Curriculum: Learning to help heal the community of all beings

        Shorb, Terril L Prescott College 2009 해외공개박사

        RANK : 247375

        This study describes effects of the Sustainable Community Development Program Butterfly Curriculum, first of its kind in the U.S., on students in the Adult Degree Program at Prescott College. The research methodology is a case study involving interviews with eleven graduates. Results are presented in rich description of graduates' experiences of the four realms of the Butterfly Curriculum. These four focal categories include right relationship with the natural world, shrinking the human footprint, restoring social bonds, and enhancing opportunities for learning and celebration of human-to-human and human to-nature connections across the community. This study of a working program in sustainability education provides a detailed reference point and model of an integral approach to authentic sustainable community development and learning.

      • Population control through the use of immigration law

        Ebarb, Henry Anthony Prescott College 2009 해외공개박사

        RANK : 247375

        As the United States population reached 300 million in 2006, mostly through immigration, scholars and politicians began to debate whether our continued rate of population growth is desirable. Many employers and some economists project a continuing need for younger low wage workers to support business and fund the Social Security System to provide benefits for an aging population. Many environmentalists believe the U.S. has reached its sustainable carrying capacity and warn that unless we stabilize our growth at the current level we will not leave a viable environment for posterity. Advocates from both extremes of this debate, and those with more centrist views, seek answers to the following question: What do opinions and beliefs of elected officials at the local level (as determined by surveys and interviews) reveal about how federal immigration law might be implemented and enforced in the Quad-Cities Area (Prescott, Prescott Valley, Chino Valley, and Dewey/Humboldt) of Yavapai County, Arizona. Answers to this question may prove useful in considerations regarding future immigration law.

      • The Contributions of Histones H3 and H4 to Gene Regulation in Saccharomyces cerevisiae: A Closer Look at Sum1 Repression and Sum1-1 Silencing

        Prescott, Eugenia Christine Tsamis Duke University 2011 해외박사(DDOD)

        RANK : 247343

        Chromatin is composed of DNA, histones, and other proteins and contributes to DNA packaging, controlling gene expression and DNA replication. This work focuses on the contributions of histones H3 and H4 to gene regulation in the yeast Saccharomyces cerevisiae. I identified a region of the nucleosome that is critical for three types of long-range transcriptional silencing but not for local repression mediated by some of the same proteins. In S. cerevisiae, the Sir complex performs long-range silencing of the mating type loci, while the promoter-specific Sum1 complex represses mid-sporulation genes. Interestingly, the SUM1-1 mutation changes the Sum1 repression complex into a silencing complex capable of long-range spreading. Sum1-1 provides a good model to distinguish between properties of nucleosomes important for long-range silencing (common to Sum1-1 and Sir silencing), and specific interactions nucleosomes might make with the Sum1 complex (common to Sum1 and Sum1-1 complexes). Interactions between nucleosomes and silencing proteins are critical to Sir silencing, and the spreading ability of Sum1-1p suggests that a component of the Sum1-1 complex may also interact with nucleosomes. Since the Sum1-1 and Sum1 complex components are shared, histone contacts may also contribute to wild type Sum1 repression. I investigated the contributions of histones H3 and H4 to Sum1-1 silencing and Sum1 repression using a genetic screen. Interestingly, I found histone mutations that disrupt Sum1-1 silencing and cluster in the H3 core/H4 region of the nucleosome, which was previously identified to disrupt silencing at the mating type loci, telomeres, and rDNA. Therefore, this region of the nucleosome is important to silencing mediated by three distinct complexes- Sir, RENT, and Sum1-1. The Sir3p bromo-adjacent homology (BAH) domain binds this region of the nucleosome to facilitate Sir spreading and silencing, and I tested Orc1p, a paralog of Sir3p, to determine if it makes similar contributions to Sum1-1 silencing. Using reporter mating assays and chromatin immunoprecipitation, I found that mutations and deletion of the BAH domain of Orc1p disrupt Sum1-1 silencing. These results suggest that Orc1p may interact with this region of the nucleosome and contribute to Sum1-1 silencing outside of recruitment. Surprisingly, Sum1 repression was not disrupted by histone mutations. I conducted in vitro binding assays to identify a region in Sum1p that may interact with histones and account for the spreading ability of Sum1-1p. Consistent with results that histones do not contribute to Sum1 repression, I did not find evidence of Sum1p binding to histone peptides. Therefore, interactions with histones H3 and H4 are important to Sir and Sum1-1 silencing and not Sum1 repression. These interactions with histones may facilitate the formation of higher-order chromatin structures necessary for long-range silencing complexes. I also identified mutations in the H3 tail that disrupt Sum1-1 silencing. Surprisingly, these mutations did not disrupt the enrichment of Sum1-1p. Similar observations have been made for Sir proteins in the absence of the H3 tail, and the H3 tail may contribute to chromatin compaction and silencing after the assembly of silencing proteins. Therefore, the Sir and Sum1-1 complexes may share several features that facilitate silencing. The use of the LRS/H4 region of the nucleosome may be a common interaction surface with silencing proteins, and the H3 tail may assist in the formation of a specialized chromatin structure. These interactions may also be utilized in the formation of heterochromatin in higher eukaryotes.

      • A molecular mechanism for thermal hypersensitivity

        Prescott, Elizabeth D University of California, San Francisco 2003 해외박사(DDOD)

        RANK : 247343

        Tissue injury generates endogenous factors that heighten our sense of pain by increasing the response of sensory nerve endings to noxious stimuli. Bradykinin and nerve growth factor (NGF) are two such pro-algesic agents that activate G protein-coupled (BK2) and tyrosine kinase (TrkA) receptors, respectively, to stimulate phospholipase C signaling pathways in primary afferent neurons. How these actions produce sensitization to physical or chemical stimuli has not been elucidated at the molecular level. Here we show that bradykinin- or NGF-mediated potentiation of thermal sensitivity in vivo requires expression of TRPV1, a heat-activated ion channel on sensory neurons. Diminution of plasma membrane PIP2 levels through antibody sequestration or PLC-mediated hydrolysis mimics the potentiating effects of bradykinin or NGF at the cellular level. Moreover, recruitment of phospholipase C-gamma to TrkA is essential for NGF-mediated potentiation of channel activity, and biochemical studies suggest that TRPV1 associates with this complex. Finally, we identify a site within the carboxy-terminal cytoplasmic domain of TRPV1 that is required for PIP2-mediated inhibition of channel gating. Mutations that weaken PIP2-TRPV1 interaction result in markedly decreased thresholds for chemical or thermal stimuli. TRPV1 channels in which this region has been replaced with a lipid binding domain from PIP2-activated potassium channels remain PIP2 inhibited, indicating that the directionality of modulation is determined not by the PIP2 binding site, per se, but by other aspects of channel structure. Our results identify a modular PIP2 interaction domain on TRPV1 that serves as a critical determinant of thermal threshold and dynamic sensitivity range, tuning the channel (and thus the sensory neuron) to appropriately detect heat under normal or pathophysiological conditions.

      • JP1 is a novel c-Myc target gene involved in anchorage independent growth

        Prescott, Julia Elizabeth The Johns Hopkins University 2000 해외박사(DDOD)

        RANK : 247343

        The c-Myc oncogenic transcription factor contributes to the development of numerous human malignancies, however the exact role that it plays remains to be elucidated. In order to delineate the various functions of <italic> c-myc,</italic> our lab carried out a representational difference analysis (RDA) screen to identify putative c-Myc targets. This screen identified JP1, which was subsequently cloned and shown to be directly regulated by c-Myc. In particular, JP1 expression is induced by serum in wild-type fibroblasts, but is not induced in fibroblasts nullizygous for <italic>c-myc.</italic> Furthermore, the JP1 transcript is induced in Rat1a-MycER cells treated with 4-OH-tamoxifen in the presence of the protein synthesis inhibitor cycloheximide. JP1 mRNA is most highly expressed in the small intestine and thymus, whereas expression is virtually absent in spleen, bone marrow, and peripheral leukocyte. JP1 is a 47 kDa nuclear protein with no significant homologies to any known proteins. In order to determine the role that JP1 plays in c-Myc mediated cellular phenotypes, stable JP1 over-expressing cell lines were created. JP1 transforms Rat1 a cells by inducing anchorage-independent growth, as does c-Myc. Furthermore, JP1 over-expression in CB33 B lymphoblast cells also induces anchorage independent growth in methylcellulose. Intriguingly, over-expression of JP1 does not induce apoptosis or tumorigenesis of Rat1a cells. Our observations define a novel c-Myc target gene that participates in selected c-Myc mediated phenotypes, providing an emerging concept that c-Myc target genes constitute nodal points in a network of pathways that lead from c-Myc to its various related phenotypes.

      • Providers for the household and nation: The localized production and migration of Filipino nurses

        Prescott, Megan The University of Arizona 2016 해외박사(DDOD)

        RANK : 247343

        In the context of increasing nursing labor shortages around the world, the Philippines has become a major producer and exporter of nurses, with 85 percent of employed Filipino nurses working outside of the Philippines. Based on 12 months of ethnographic research in a provincial center for nursing education and healthcare in Northern Luzon, Philippines, I utilize a global nurse care chain (Yeates 2004a, 2009a) framework to explore transnational nurse migration out of the Philippines through the experiences of nurses, nursing students, their families and other stakeholders in nurse production and migration. As a more local GNCC analysis, the present study traces the production and provision of nursing care labor through the family and local and transnational household, to formal training and nursing experiences in educational and health institutions, and through other encounters with state, private, and international agencies that facilitate and shape the experiences and subjectivities of migrant nurses. Chapter 2 traces the relationship between the production and migration industries and between these industries and the state, exploring the ways that both the healthcare landscape and experiences of new nursing graduates (as consumers and laborers) has been shaped by migration booms and busts. Chapters 3 and 4 examine the household as a site of nurse production and the role of the household's moral economy and structures of feeling (Williams 1977). In Chapter 3, I examine nursing students' narratives of choice in the decision to study nursing and argue that obligation to family and reciprocal financial and emotional relationships underlie nurse production. In Chapter 4, I explore the ways that nurses and students imagine their future lives and identities as migrant nurses, illustrating how subjectivities are shaped by a legacy of transnational migration, imagination, and family moral economy. In Chapter 5, I use the narrative of a returned migrant nurse to illustrate the long-term impacts of past and temporary migration, and the ways that returned migrants may construct their identities through remembering. The final chapter explores the nurse migration industry through recruitment agents and nurses navigating this privatized industry as they pursue migration opportunities. Beyond an ethnography of nursing students', nurses' and their families' experiences of nurse training and migration processes, this dissertation focuses the roles of the state, private industry, and family in the mobilization of gendered and filial subjectivities to stimulate nurse production and migration, and explores the complex effects of unregulated nurse migration industries on students, nurses, and families as consumers and laborers.

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