48 research outputs found

    Additional file 1 of Estimating Phred scores of Illumina base calls by logistic regression and sparse modeling

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    Supplementary information about the elastic net model. This file contains the following sections: S1 - Introduction to the elastic net model and its advantages. S2 - Results of the elastic net mode include training time, coefficients, consistency and empirical discrimination power. Table S1 - The coefficients of 74 predicted features of the elastic net model. Figure S1 - The consistency of the elastic net model with three different training sets. Figure S2 - The empirical discrimination power of the elastic net model with three different training sets. (PDF 164 kb

    The emergence of noncoding RNAs as Heracles in autophagy

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    <p>Macroautophagy/autophagy is a catabolic process that is widely found in nature. Over the past few decades, mounting evidence has indicated that noncoding RNAs, ranging from small noncoding RNAs to long noncoding RNAs (lncRNAs) and even circular RNAs (circRNAs), mediate the transcriptional and post-transcriptional regulation of autophagy-related genes by participating in autophagy regulatory networks. The differential expression of noncoding RNAs affects autophagy levels at different physiological and pathological stages, including embryonic proliferation and differentiation, cellular senescence, and even diseases such as cancer. We summarize the current knowledge regarding noncoding RNA dysregulation in autophagy and investigate the molecular regulatory mechanisms underlying noncoding RNA involvement in autophagy regulatory networks. Then, we integrate public resources to predict autophagy-related noncoding RNAs across species and discuss strategies for and the challenges of identifying autophagy-related noncoding RNAs. This article will deepen our understanding of the relationship between noncoding RNAs and autophagy, and provide new insights to specifically target noncoding RNAs in autophagy-associated therapeutic strategies.</p

    Marketing Strategy Proposal of Cooperative

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    This Diploma Thesis deals with marketing strategy of Brisk, production cooperative. It contains theoretical knowledge from the field of marketing. The practical part focuses on the analysis of the current situation of the cooperative. Based on the information from marketing analyzes are recommended proposals for the imporvement of marketing policy of the cooperative

    Induction of phosphorylation and acetylation by acetyl-CoA.

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    <p>A. Induction of acetyl-CoA in mitochondria by palmitate. Mitochondria were isolated from cells after palmitate treatment (300 μM) at 1, 4 and 16 h, and then used in the concentration assay of acetyl-CoA. B. Induction of PDH phosphorylation in mitochondria lysate by acetyl-CoA at different concentrations indicated. The phosphorylation was determined by Western blotting and the quantified signal was expressed in bar figure C. Induction of acetylation by acetyl-CoA. Mitochondria lysate was treated with acetyl-CoA at multiple dosages for 30 mins at 37°C. Acetylation was determined in mitochondrial protein by Western blotting. The experiments were performed three times with consistent results, and the representative blots are shown. The acetylation signal of highlighted bands was quantified individually, combined together and expressed in fold change in the bar figure. The result represents mean ± SE (n = 3). * p<0.05 compared with the control.</p

    Protection of mitochondria function by β-oxidation inhibitor.

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    <p>A. Inhibition of oxygen consumption rate (OCR) by palmitate. OCR was examined in mitochondria after palmitate treatment of cells at times indicated. B. Protection of mitochondrial function by Etomoxir (ET, 50 μM). ET was used to block β-oxidation in cells in the presence of palmitate (300 μM, 4 h). Freshly isolated mitochondria were used in the assays. In the bar figure, the result represents mean ± SE (n = 3). * p<0.05 compared with the control.</p

    Statistical testings of the reported region with its adjacent area.

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    <p>Statistical testings of the reported region with its adjacent area.</p

    Plots of copy number loss candidates and their adjacency.

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    <p>In each plot, x-axis shows the loci on the Chromosome 11; y-axis shows the read depth; purple dot is read depth for corresponding loci; orange vertical line is the reported copy number loss boundary; pink dashed line is the loci of probe on SNP microarray.</p

    Comparison of copy number losses from 1000 Genome Project and CNVhac calling.

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    <p>Comparison of copy number losses from 1000 Genome Project and CNVhac calling.</p

    Comparison of copy number losses from Hapmap Project and CNVhac calling.

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    <p>Comparison of copy number losses from Hapmap Project and CNVhac calling.</p

    Induction of protein acetylation by ATP.

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    <p>A. Acetylation of mitochondrial protein. Cells were treated with palmitate (300 μM) in cell culture and acetylation was tested in isolated mitochondria at multiple time points. B. Acetylation inhibition by the β-oxidation inhibitor ET. The acetylation was determined in mitochondrial lysate following pre-treatment of cells with ET (50 μM) and palmitate (300 μM for 4 hr). C. Induction of acetylation by ATP. Mitochondrial lysate was incubated with ATP at multiple dosages for 30 minutes at 37°C. Acetylation was determined in the mitochondrial proteins by Western blotting. In this figure, the acetylation signal of highlighted bands was quantified individually, combined together and expressed in fold change in the bar figure. In the bar figure, the result represents mean ± SE (n = 3). * p<0.05 compared with the control (0 point).</p
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