108 research outputs found

    Toward affective language arts teaching: the utilization of culturally relevant literature on urban african american high school students

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    ABSTRACT TOWARD AFFECTIVE LANGUAGE ARTS TEACHING: THE UTILIZATION OF CULTURALLY RELEVANT LITERATURE ON URBAN AFRICAN AMERICAN HIGH SCHOOL STUDENTS by BARBARA-BENITA CRAFT August 2012 Advisor: Dr. Monte Piliawsky Major: Curriculum and Instruction Degree: Doctor of Philosophy Data collected and analyzed from English Language Arts teachers in urban, metro-city, and suburban school districts related to the use and extent of use of culturally relevant pedagogy (Ladson-Billings, 1994a), culturally relevant literature (Ladson-Billings, 1994a), activities and strategies from African American familial culture (Hale-Benson, 1986), and cultural modeling (Lee, 1993), showed similarities and differences in the pedagogical practices and methodologies among the three teachers in the three school districts. Three teachers from each respective district, urban, metro-city, and suburban, were interviewed once, at the initiation of the study and again prior to exit, on their perspectives of teacher education, relationships with principals and Districts, teaching philosophies and styles, teaching pedagogies, curriculum and content, State and National Benchmarks and Standards, and their inclusion of culturally relevant elements in their lessons. The nine teachers, from the three school Districts were also observed in their classrooms during three separate observation periods. No students were observed or had data collected on them. Analysis of interview and observation content showed that of the nin

    Study on US wetland protection institution change

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    本文提出了分析湿地保护制度变迁的理论框架,使不同国家的湿地保护制度研究能在统一语境下比较。首先基于科学计量学和系统研究方法筛选出公众、科学、政府和法律为影响湿地保护制度变迁的四个关键要素,并依赖博弈论工具建立了分析美国湿地保护制度的理论架构。基于这一架构,本文对包括关键利益相关者、政策执行路径、政策工具和管理挑战等内容的美国湿地政策史进行了讨论。对美国湿地保护制度的演化进行了四阶断之划分:"西进运动"与全民开垦(1900年之前)、"水鸟保护"与公众参与(1900-1970年)、核心法律与科学研究(1971-1980年)和完善制度与新的挑战(1980年至今)。分析得出如下结论:在湿地保护制度中,公众是源头、科学是前提、有效的政府管治和将湿地保护的规则和与政策制度化是关键。通过借鉴美国湿地保护制度变迁研究,本文构建了湿地保护制度变迁的"竹节模式"经验性模型,揭示了各动因之间的作用机理。虽然美国湿地保护制度也面临着公众教育、科学定义和政府管辖权等挑战,但中国的湿地管理者与政策制定者仍可从美国湿地政策执行的历史背景中吸取经验。同时本文的理论分析结构也可为自然资源及管理策略的研究提供参考。The four key elements of public opinion,science,government and law were used to construct an empirical model built upon Game Theory. This theoretical framework,in which the wetland management policies of different countries can be compared,demonstrates the mechanism by which the four key elements interact to develop environmental policy and protect wetlands.Based on this empirical model,the history of wetland policies in the USA including key stakeholders,policy implementation approaches,policy instruments and management challenges were discussed. Evolution of the institution that protects American wetlands is broken down into four stages:Westward Movement and Reclamation(pre- 1900),Waterfowl Protection and Public Participation(1900- 1970),Core Laws and Scientific Research(1971- 1980)and Improved Institutions and New Challenges(1980- present). Wetland policies originate with public opinions and beliefs,scientific knowledge is a prerequisite for policy implementation and,lastly,effective governmental jurisdiction and institutionalization of wetland protection regulation and policy are critical. Although public education,scientific definition and governmental jurisdiction are challenging,Chinese wetland managers and policy makers can learn from the implementation of USA wetland policies. The analysis outlined in this paper is a template that other natural resource studies can follow when developing natural resource strategies.国家公派留学基金项目(2011-2013);; 康奈尔大学Jeffrey Sean Lehman基金项目(2012-2013

    Electrophysiological resting state brain network and episodic memory in healthy aging adults

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    Recent studies have emphasized the changes in large-scale brain networks related to healthy aging, with the ultimate purpose to aid in differentiating normal neurocognitive aging from neurodegenerative disorders that also arise with age. Emerging evidence from functional Magnetic Resonance Imaging (fMRI) indicates that connectivity patterns within specific brain networks, especially the Default Mode Network (DMN), distinguish those with Alzheimer's disease from healthy individuals. In addition, disruptive alterations in the large-scale brain systems that support high-level cognition are shown to accompany cognitive decline at the behavioral level, which is commonly observed in the aging populations, even in the absence of disease. Although fMRI is useful for assessing functional changes in brain networks, its high costs and limited accessibility discourage studies that need large populations. In this study, we investigated the aging-effect on large-scale networks of the human brain using high-density electroencephalography and electrophysiological source imaging, which is a less costly and more accessible alternative to fMRI. In particular, our study examined a group of healthy subjects in the age range from middle- to older-aged adults, which is an under-studied range in the literature. Employing a high-resolution computation model, our results revealed age associations in the connectivity pattern of DMN in a consistent manner with previous fMRI findings. Particularly, in combination with a standard battery of cognitive tests, our data showed that in the posterior cingulate / precuneus area of DMN higher brain connectivity was associated with lower performance on an episodic memory task. The findings demonstrate the feasibility of using electrophysiological imaging to characterize large-scale brain networks and suggest that changes in network connectivity are associated with normal aging.This study was supported by National Science Foundation RII Track-2 FEC 1539068, Oklahoma Center for the Advancement of Science & Technology HR16–057, and Institute for Biomedical Engineering, Science, and Technology at University of Oklahoma. Financial support was provided by the University of Oklahoma Libraries’ Open Access Fund.Ye

    Progesterone Receptor Activates Msx2 Expression by Downregulating TNAP/Akp2 and Activating the Bmp Pathway in EpH4 Mouse Mammary Epithelial Cells

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    Previously we demonstrated that EpH4 mouse mammary epithelial cells induced the homeobox transcription factor Msx2 either when transfected with the progesterone receptor (PR) or when treated with Bmp2/4. Msx2 upregulation was unaffected by Wnt inhibitors s-FRP or Dkk1, but was inhibited by the Bmp antagonist Noggin. We therefore hypothesized that PR signaling to Msx2 acts through the Bmp receptor pathway. Herein, we confirm that transcripts for Alk2/ActR1A, a non-canonical BmpR Type I, are upregulated in mammary epithelial cells overexpressing PR (EpH4-PR). Increased phosphorylation of Smads 1,5, 8, known substrates for Alk2 and other BmpR Type I proteins, was observed as was their translocation to the nucleus in EpH4-PR cells. Analysis also showed that Tissue Non-Specific Alkaline Phosphatase (TNAP/Akp2) was also found to be downregulated in EpH4-PR cells. When an Akp2 promoter-reporter construct containing a ½PRE site was transfected into EpH4-PR cells, its expression was downregulated. Moreover, siRNA mediated knockdown of Akp2 increased both Alk2 and Msx2 expression. Collectively these data suggest that PR inhibition of Akp2 results in increased Alk2 activity, increased phosphorylation of Smads 1,5,8, and ultimately upregulation of Msx2. These studies imply that re-activation of the Akp2 gene could be helpful in downregulating aberrant Msx2 expression in PR+ breast cancers

    Genetic effects on gene expression across human tissues

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    Characterization of the molecular function of the human genome and its variation across individuals is essential for identifying the cellular mechanisms that underlie human genetic traits and diseases. The Genotype-Tissue Expression (GTEx) project aims to characterize variation in gene expression levels across individuals and diverse tissues of the human body, many of which are not easily accessible. Here we describe genetic effects on gene expression levels across 44 human tissues. We find that local genetic variation affects gene expression levels for the majority of genes, and we further identify inter-chromosomal genetic effects for 93 genes and 112 loci. On the basis of the identified genetic effects, we characterize patterns of tissue specificity, compare local and distal effects, and evaluate the functional properties of the genetic effects. We also demonstrate that multi-tissue, multi-individual data can be used to identify genes and pathways affected by human disease-associated variation, enabling a mechanistic interpretation of gene regulation and the genetic basis of diseas

    Insights into the innate immunity of the Mediterranean mussel Mytilus galloprovincialis

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    <p>Abstract</p> <p>Background</p> <p>Sessile bivalves of the genus <it>Mytilus </it>are suspension feeders relatively tolerant to a wide range of environmental changes, used as sentinels in ecotoxicological investigations and marketed worldwide as seafood. Mortality events caused by infective agents and parasites apparently occur less in mussels than in other bivalves but the molecular basis of such evidence is unknown. The arrangement of Mytibase, interactive catalogue of 7,112 transcripts of <it>M. galloprovincialis</it>, offered us the opportunity to look for gene sequences relevant to the host defences, in particular the innate immunity related genes.</p> <p>Results</p> <p>We have explored and described the Mytibase sequence clusters and singletons having a putative role in recognition, intracellular signalling, and neutralization of potential pathogens in <it>M. galloprovincialis</it>. Automatically assisted searches of protein signatures and manually cured sequence analysis confirmed the molecular diversity of recognition/effector molecules such as the antimicrobial peptides and many carbohydrate binding proteins. Molecular motifs identifying complement C1q, C-type lectins and fibrinogen-like transcripts emerged as the most abundant in the Mytibase collection whereas, conversely, sequence motifs denoting the regulatory cytokine MIF and cytokine-related transcripts represent singular and unexpected findings. Using a cross-search strategy, 1,820 putatively immune-related sequences were selected to design oligonucleotide probes and define a species-specific Immunochip (DNA microarray). The Immunochip performance was tested with hemolymph RNAs from mussels injected with <it>Vibrio splendidus </it>at 3 and 48 hours post-treatment. A total of 143 and 262 differentially expressed genes exemplify the early and late hemocyte response of the <it>Vibrio</it>-challenged mussels, respectively, with AMP trends confirmed by qPCR and clear modulation of interrelated signalling pathways.</p> <p>Conclusions</p> <p>The Mytibase collection is rich in gene transcripts modulated in response to antigenic stimuli and represents an interesting window for looking at the mussel immunome (transcriptomes mediating the mussel response to non-self or abnormal antigens). On this basis, we have defined a new microarray platform, a mussel Immunochip, as a flexible tool for the experimental validation of immune-candidate sequences, and tested its performance on <it>Vibrio</it>-activated mussel hemocytes. The microarray platform and related expression data can be regarded as a step forward in the study of the adaptive response of the <it>Mytilus </it>species to an evolving microbial world.</p

    322. Evaluation of the BioFire® Bone and Joint Infection (BJI) Panel for the Detection of Microorganisms and Antimicrobial Resistance Genes in Synovial Fluid Specimens

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    Background Bone and Joint Infections (BJIs) present with non-specific symptoms that may include pain, swelling, and fever and are associated with high morbidity and significant risk of mortality. BJIs can be caused by a variety of bacteria and fungi, including anaerobes and microorganisms that can be challenging to culture or identify by traditional microbiological methods. Clinicians primarily rely on culture to identify the pathogen(s) responsible for infection. The BioFire® Bone and Joint Infection (BJI) Panel (BioFire Diagnostics, Salt Lake City, UT) is designed to detect 15 gram-positive bacteria (including seven anaerobes), 14 gram-negative bacteria (including one anaerobe), two yeast, and eight antimicrobial resistance (AMR) genes from synovial fluid specimens in about an hour. The objective of this study was to evaluate the performance of an Investigational Use Only (IUO) version of the BioFire BJI Panel compared to various reference methods. Methods Remnant synovial fluid specimens, which were collected for routine clinical care at 13 study sites in the US and Europe, underwent testing using an IUO version of the BioFire BJI Panel. Performance of this test was determined by comparison to Standard of Care (SoC) consisting of bacterial culture performed at each study site according to their routine procedures. Results A total of 1544 synovial fluid specimens were collected and tested with the BioFire BJI Panel. The majority of specimens were from knee joints (77.9%) and arthrocentesis (79.4%) was the most common collection method. Compared to SoC culture, overall sensitivity was 90.2% and specificity was 99.8%. The BioFire BJI Panel yielded a total of 268 Detected results, whereas SoC yielded a total of 215 positive results for on-panel analytes. Conclusion The BioFire BJI Panel is a sensitive, specific, and robust test for rapid detection of a wide range of analytes in synovial fluid specimens. The number of microorganisms and resistance genes included in the BioFire BJI Panel, together with a reduced time-to-result and increased diagnostic yield compared to culture, is expected to aid in the timely diagnosis and appropriate management of BJIs

    High-coverage whole-genome analysis of 1220 cancers reveals hundreds of genes deregulated by rearrangement-mediated cis-regulatory alterations.

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    The impact of somatic structural variants (SVs) on gene expression in cancer is largely unknown. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole-genome sequencing data and RNA sequencing from a common set of 1220 cancer cases, we report hundreds of genes for which the presence within 100 kb of an SV breakpoint associates with altered expression. For the majority of these genes, expression increases rather than decreases with corresponding breakpoint events. Up-regulated cancer-associated genes impacted by this phenomenon include TERT, MDM2, CDK4, ERBB2, CD274, PDCD1LG2, and IGF2. TERT-associated breakpoints involve ~3% of cases, most frequently in liver biliary, melanoma, sarcoma, stomach, and kidney cancers. SVs associated with up-regulation of PD1 and PDL1 genes involve ~1% of non-amplified cases. For many genes, SVs are significantly associated with increased numbers or greater proximity of enhancer regulatory elements near the gene. DNA methylation near the promoter is often increased with nearby SV breakpoint, which may involve inactivation of repressor elements

    An Economic Model for Bioprospecting Contracts

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    Genetic effects on gene expression across human tissues

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    Characterization of the molecular function of the human genome and its variation across individuals is essential for identifying the cellular mechanisms that underlie human genetic traits and diseases. The Genotype-Tissue Expression (GTEx) project aims to characterize variation in gene expression levels across individuals and diverse tissues of the human body, many of which are not easily accessible. Here we describe genetic effects on gene expression levels across 44 human tissues. We find that local genetic variation affects gene expression levels for the majority of genes, and we further identify inter-chromosomal genetic effects for 93 genes and 112 loci. On the basis of the identified genetic effects, we characterize patterns of tissue specificity, compare local and distal effects, and evaluate the functional properties of the genetic effects. We also demonstrate that multi-tissue, multi-individual data can be used to identify genes and pathways affected by human disease-associated variation, enabling a mechanistic interpretation of gene regulation and the genetic basis of disease
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