73 research outputs found

    Pembuatan Alat Peraga Lemari Pendingin Sebagai Media Pembelajaran Mata Kuliah Teknik Pendingin Di Universitas Negeri Semarang

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    — Media pembelajaran merupakan segala fisik yang menyajikan pesan serta perangsang peserta didik untuk belajar, sehingga keberadaan media pembelajaran penting untuk membantu dalam proses belajar mengajar. Alat peraga adalah salah satu media pembelajaran, dengan memanfaatkan alat peraga proses pembelajaran akan dapat mempermudah dalam memahami materi yang dipelajari oleh mahasiswa, karena ditampilkan dalam bentuk nyata. Teknik Pendingin adalah salah satu mata kuliah yang ada pada Prodi Pendidikan Teknik Elektro. Permasalahannya apakah alat peraga lemari pendingin layak sebagai media pembelajaran pada mata kuliah Teknik Pendingin jurusan Teknik Elektro Universitas Negeri Semarang. Untuk itu perlu diadakan penelitian untuk mengetahui apakah alat peraga lemari pendingin ini layak untuk dignakan sebagai media pembelajaran. Data dikumpulkan dengan metode angket tertutup maupun terbuka. Alat peraga lemari pendingin ini diujicoba oleh dosen ahli materi teknik pendingin. Metode analisis yang digunakan adalah metode analisis statistik deskriptif. Menurut hasil penelitian dari responden secara keseluruhan, alat peraga lemari pendingin pada mata kuliah Teknik Pendingin ini layak digunakan sebagai media pembelajaran. Dosen ahli materi mengemukakan alat peraga ini layak dijadikan alat peraga setelah adanya revisi alat. Berdasarkan dari hasil penelitian dan pembahasan, dapat disimpulkan bahwa menurut mahasiswa media pembelajaran yang berupa alat peraga lemari pendingin pada mata kuliah Teknik Pendingin diwujudkan dengan menyusun prosedur kerja dengan langkah-langkah sebagai berikut: perencanaan alat peraga, penyediaan alat dan bahan, pembuatan alat peraga, validasi alat peraga, uji coba alat peraga, dan evaluasi. Dari hasil penelitian yang telah dilakukan kepada mahasiswa dengan beberapa aspek, alat peraga lemari pendingin ini termasuk dalam kategori layak, sehingga alat peraga ini dapat digunakan sebagai media pembelajaran. Namun masih terdapat kekurangan pada bahan penutup yang dugunakan seharusnya tidak menggunakan kaca agar tidah mudah pecah, dan jika menggunakan kaca suhu yang ada di dalam lemari pendingin masih dapat terpengaruh oleh suhu udara luar. Kata kunci— Media Pembelajaran, teknik pendingin, universitas negeri semarang, alat peraga, lemari pendingi

    Genome-Wide H3K4me3 Analysis in Angus Cattle with Divergent Tenderness

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    <div><p>Tenderness is one of the most important properties of meat quality, which is influenced by genetic and environmental factors. As an intensively studied epigenetic marker, histone methylation, occurring on arginine and lysine residues, has pivotal regulatory functions on gene expression. To examine whether histone methylation involves in beef tenderness variation, we analyzed the transcriptome and H3K4me3 enrichment profiles of muscle strips obtained from the <i>longissimus dorsi</i> (LD) of Angus steers previously classify to the tender or tough group. We first plotted a global bovine H3K4me3 map on chromosomes and called peak-enriched regions and genes. We found that majorities of H3K4me3 on genes were occupying the first intron and intergenic regions and its maps displayed similar patterns in tender and tough groups, with high H3K4me3 enrichment surrounding the transcription start site (TSS). We also explored the relationship of H3K4me3 and gene expression. The results showed that H3K4me3 enrichment is highly positively correlated with gene expression across the whole genome. Cluster analysis results confirmed the relationship of H3K4me3 enrichment and gene expression. By using a pathway-based approach in genes with H3K4me3 enrichment in promoter regions from the tender cluster, we revealed that those genes involved in the development of different tissues–connective tissue, skeletal and muscular system and functional tissues–; while in tough group those genes engaged in cell death, lipid metabolism and small molecule biochemistry. The results from this study provide a deep insight into understanding of the mechanisms of epigenetic regulations in meat quality and beef tenderness.</p></div

    <i>Jmjd</i>3 ablation affects global histone methylation in lung tissues and methylation status of the promoter regions of target genes.

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    <p>(<b>A</b>) Global gene methylation analysis of <i>Jmjd3</i><sup>+/+</sup> and <i>Jmjd3</i><sup>−/−</sup> lung tissues at E17.5 by ChIP-Seq. ↑, methylation increased; ↓, methylation decreased. (<b>B</b>) ChIP-Seq analysis of H3K27me3 and H3K4me3 levels in the promoter and gene body regions of the <i>SP-B</i> gene in <i>Jmjd3</i><sup>+/+</sup> and <i>Jmjd3</i><sup>−/−</sup> lung tissues at E17.5. Data shown are representative of three independent experiments. (<b>C</b>) Jmjd3 binding to the SP-B promoter in lung tissues was determined by ChIP-PCR. Chromatin was immunoprecipitated from the lung tissues of E17.5 <i>Jmjd3</i><sup>+/+</sup> and <i>Jmjd3</i><sup>−/−</sup> embryos. Primer design for the ChIP-PCR assay of mouse <i>SP-B</i> promoter regions (<i>top panel</i>). The primers sets cover the following regions: A, −2347–−2142; B, −2065–−1835; C, −1451–−1334; D, −1001–−878; E, −516–−383; F, −218–+14. ChIP-PCR assay showing Jmjd3 binding around 2 kb upstream of the TSS of the <i>SP-B</i> promoter region (<i>bottom panel</i>). (<b>D</b>) ChIP-qPCR analysis of histone methylation levels in the <i>SP-B</i> promoter region in the lung tissues of E17.5 <i>Jmjd3</i><sup>+/+</sup> and <i>Jmjd3</i><sup>−/−</sup> embryos. (<b>E</b>) Locus-specific demethylation analysis of Jmjd3 by ChIP-Seq. ChIP-Seq was done to determine the H3K27 and H3K4 methylation level of genes located in the region (∼280 kb) containing <i>SP-B</i> on chromosome 6 and the region (∼160 kb) containing <i>AQP-5</i> on chromosome 15. Arrows indicate the gene expression direction.</p

    Genomic coordinates of the 3 kb human putative PRE regions and sequences of specific primers used in ChIP experiments for each of these regions (sequence information is based on the UCSC hg18 assembly).

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    <p>Genomic coordinates of the 3 kb human putative PRE regions and sequences of specific primers used in ChIP experiments for each of these regions (sequence information is based on the UCSC hg18 assembly).</p

    The relationship between H3K4me3 enrichment pattern and gene expression.

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    <p>(A) K-means clustering of different H3K4me3 enrichment pattern in promoters. (B) Box-plot for gene expression of different H3K4me3 enrichment pattern in LD.</p

    Stage-Dependent and Locus-Specific Role of Histone Demethylase Jumonji D3 (JMJD3) in the Embryonic Stages of Lung Development

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    <div><p>Histone demethylases have emerged as important players in developmental processes. Jumonji domain containing-3 (Jmjd3) has been identified as a key histone demethylase that plays a critical role in the regulation of gene expression; however, the <i>in vivo</i> function of Jmjd3 in embryonic development remains largely unknown. To this end, we generated <i>Jmjd3</i> global and conditional knockout mice. Global deletion of <i>Jmjd3</i> induces perinatal lethality associated with defective lung development. Tissue and stage-specific deletion revealed that Jmjd3 is dispensable in the later stage of embryonic lung development. <i>Jmjd3</i> ablation downregulates the expression of genes critical for lung development and function, including <i>AQP-5</i> and <i>SP-B</i>. Jmjd3-mediated alterations in gene expression are associated with locus-specific changes in the methylation status of H3K27 and H3K4. Furthermore, Jmjd3 is recruited to the <i>SP-B</i> promoter through interactions with the transcription factor Nkx2.1 and the epigenetic protein Brg1. Taken together, these findings demonstrate that <i>Jmjd3</i> plays a stage-dependent and locus-specific role in the mouse lung development. Our study provides molecular insights into the mechanisms by which Jmjd3 regulates target gene expression in the embryonic stages of lung development.</p></div

    Relative H3K4me3 enrichment on functional parts of genes in LD.

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    <p>(A) Peaks overlapping gene feagures in tender group; (B) Peak overlapping gene features in tough group.</p

    Normal PcG protein activities are required for the PRE-mediated transcriptional repression.

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    <p>Knocking down SUZ12 decreased the binding of PRC1 proteins at the endogenous SLC (<b>A</b>) and endogenous A3 (<b>B</b>) regions. ChIP assays were performed using the indicated antibodies, with chromatin from HeLa cells transfected with pREP4-Puro-siSUZ12 or the control vector. ChIP DNA was analyzed by qPCR using primers specific for the SLC-PRE and A3-PRE regions (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036365#pone-0036365-t001" target="_blank">Table 1</a>). The specificity of ChIP experiment was confirmed by evaluating PcG binding at a region upstream of the <i>BRG1</i> gene locus, which showed very low level of PcG proteins in both the control and SUZ12 knockdown cells. (<b>C</b>) Knocking down SUZ12 in HeLa cells increased the expression of the endogenous <i>SLC17A7</i> (SLC locus) and <i>HoxA3</i> (A3 locus) genes but not the <i>HoxA13</i> (A13 locus) gene. Total RNAs were isolated from HeLa cells transfected with pREP4-Puro-siSUZ12 or a control vector and selected with puromycin. The expression level of the genes was determined by qRT-PCR analysis.</p

    The demethylase activity of Jmjd3 is required for the regulation of <i>SP-B</i> expression.

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    <p>(<b>A</b>) WT, but not mutant, Jmjd3 enhanced NKx2.1 and Brg1-mediated <i>SP-B</i> promoter activity. Data are presented as the mean ± SD from three independent experiments. *<i>P</i><0.05 (Student's <i>t</i> test). (<b>B</b>) qPCR analysis of <i>SP-B</i> expression in Jmjd3-specific shRNA-expressing H441 cells transfected with WT or mutant <i>Jmjd3</i>. Data are presented as the mean ± SD from three independent experiments. (<b>C</b>) Immunoblot analysis of SP-B protein in Jmjd3-specific shRNA-expressing H441 cells transfected with WT or mutant <i>Jmjd3</i>. (<b>D</b>) A proposed model explaining how Jmjd3 specifically upregulates SP-B expression by interacting with Nkx2.1 and Brg1 in the SP-B promoter.</p
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