99 research outputs found

    Sustainability Education in Textile and Apparel: A Web-Based Content Analysis

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    Sustainability is a composite view of diverse and interwoven themes related to human welfare, economic growth, and the natural environment. Inclusion of education for sustainable development is a crucial paradigmatic shift within higher education. This study examines how sustainability is integrated in the T&A curriculum. 69 educational institutions were selected from the 2015 U.S. rankings of the top 50 fashion merchandising and top 50 fashion design schools and colleges by www.fashion-schools.org. Web-published curriculum of each department/school was analyzed through content analysis. Results show sustainability is being integrated within the curricula of T&A programs in the U.S. Over half offer at least one sustainability embedded course in their curricula. Institutions with graduate programs show stronger adoption of sustainability indicative of faculty expertise and research interests

    DEFINITION OF THE LANDSCAPE OF CHROMATIN STRUCTURE AT THE FRATAXIN GENE IN FRIEDREICHā€™S ATAXIA

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    Friedreichā€™s ataxia (FRDA) is caused by the transcriptional silencing of the frataxin (FXN) gene. FRDA patients have expansion of GAA repeats in intron 1 of the FXN gene in both alleles. A number of studies demonstrated that specific histone deacetylase inhibitors (HDACi) affect either histone modifications at the FXN gene or FXN expression in FRDA cells, indicating that the hyperexpanded GAA repeat may facilitate heterochromatin formation. However, the correlation between chromatin structure and transcription at the FXN gene is currently limited due to a lack of more detailed analysis. Therefore, I analyzed the effects of the hyperexpanded GAA repeats on transcription status and chromatin structure using lymphoid cell lines derived from FRDA patients. Using chromatin immunoprecipitation and quantitative PCR, I observed significant changes in the landscape of histone modifications in the vicinity of the GAA tract in FRDA cells relative to control cells. Similar epigenetic changes were observed in GFP reporter construct containing 560 GAA repeats. Further, I detected similar levels of FXN pre-mRNA at a region upstream of hyperexpanded GAA repeats in FRDA and control cells, indicating similar efficiency of transcription initiation in FRDA cells. I also showed that histone modifications associated with hyperexpanded GAA repeats are independent of transcription progression using the GFP reporter system. My data strongly support evidence that FXN deficiency in FRDA patients is consequence of defective transition from initiation to elongation of FXN transcription due to heterochromatin-like structures formed in the proximity of the hyperexpanded GAAs

    Utilizing University-based Enterprise to Foster Industry-Academia Collaboration in the Field of Product Development

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    University-based enterprise (UBE) system has been adopted and implemented in diverse fields focusing on practice-based learning. The aim of the presentation is to introduce the UBE system integrated into product development course and active collaborations with regional government and other companies to enhance studentsā€™ practical abilities. Presented are the UBE system and two cases utilizing the system for product development education

    eIF2A, an initiator tRNA carrier refractory to eIF2 kinases, functions synergistically with eIF5B

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    The initiator tRNA (Met-tRNA(i)(Met)) at the P site of the small ribosomal subunit plays an important role in the recognition of an mRNA start codon. In bacteria, the initiator tRNA carrier, IF2, facilitates the positioning of Met-tRNAiMet on the small ribosomal subunit. Eukarya contain the Met-tRNAiMet carrier, eIF2 (unrelated to IF2), whose carrier activity is inhibited under stress conditions by the phosphorylation of its -subunit by stress-activated eIF2 kinases. The stress-resistant initiator tRNA carrier, eIF2A, was recently uncovered and shown to load Met-tRNAiMet on the 40S ribosomal subunit associated with a stress-resistant mRNA under stress conditions. Here, we report that eIF2A interacts and functionally cooperates with eIF5B (a homolog of IF2), and we describe the functional domains of eIF2A that are required for its binding of Met-tRNAiMet, eIF5B, and a stress-resistant mRNA. The results indicate that the eukaryotic eIF5B-eIF2A complex functionally mimics the bacterial IF2 containing ribosome-, GTP-, and initiator tRNA-binding domains in a single polypeptide.112Ysciescopu

    The Combination of TRAIL Treatment and Cancer Cell Selective Expression of TRAIL-Death Receptor DR4 Induces Cell Death in TRAIL-Resistant Cancer Cells

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    The human telomerase reverse transcriptase (hTERT) promoter can be used for the tumor-specific expression of transgenes in order to induce selective cancer cell death. The hTERT core promoter is active in cancer cells but not in normal cells. To examine whether the combination of TNF-related apoptosis inducing ligand (TRAIL) treatment and cancer cell-selective expression of the TRAIL-death receptor could induce cell death in TRAIL-resistant cancer cells, we generated a death receptor-4 (DR4)-expressing adenovirus (Ad-hTERT-DR4), in which the expression of DR4 is driven by the hTERT promoter. Upon infection, DR4 expression was slightly increased in cancer cell lines, and cell death was observed in TRAIL-resistant cancer cell lines but not in normal human cells when DR4 infection was combined with TRAIL treatment. We also generated an adenovirus that expresses a secretable isoleucine zipper (ILZ)-fused, extracellular portion of TRAIL (Ad-ILZ-TRAIL). In cells infected with Ad-ILZ-TRAIL, TRAIL was expressed, secreted, oligomerized and biologically active in the induction of apoptosis in TRAIL-sensitive cancer cells. When Ad-hTERT-DR4 infected TRAIL-resistant HCE4 cells and Ad-ILZ-TRAIL infected TRAIL-resistant HCE7 cells were co-cultured, cell deaths were evident 24 h after co-culture. Taken together, our results reveal that the combination of TRAIL and cancer cell-specific expression of DR4 has the potential to overcome the resistance of cancer cells to TRAIL without inducing significant cell death in normal cells
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