Manajemen Program Siaran Lokal Aceh TV Dalam Upaya Penyebarluasan Syariat Islam Dan Pelestarian Budaya Lokal

Managing broadcasting management is not easy. Managing the broadcasting business is a difficult and challenging. This research aims to analyze the activity of management and organizational performance ACEH TV television media in an effort to disseminate the Islamic Sharia and Preservation of Local Culture in Aceh. This research is descriptive qualitative. Informants of this research is managing director, program director, executive producer, cameraman / reporter, as well as additional informants Regional Chairman of the Indonesian Broadcasting Commission (KPID) Aceh, Aceh Province Department of Islamic Law, and local media observers. The location of this research is in Banda Aceh, Aceh province. Sampling was done purposively. Data collected through observation, interviews, and documentation. Data were analyzed by analysis of an interactive model of Miles and Huberman. The results showed that the ACEH TV as the medium of television that is broadcasting management ACEH have done according to a local television broadcasting standard. Agenda setting function of mass media performed in the ACEH TV dissemination of Islamic Shariah in Aceh and local culture to influence the people of Aceh to implement Islamic Sharia and also maintain the culture and local wisdom Aceh. It can be seen from all the programs that are aired ACEH TV is a program of local cultural nuances of Islamic law. There are still some shortcomings in running broadcasting broadcasting technology such as lack of equipment that is increasingly sophisticated. The results of image editing is very simple, and some programs presenter still looks stiff when in front of the camera

Novel insights into systemic autoimmune rheumatic diseases using shared molecular signatures and an integrative analysis

<p>We undertook this study to identify DNA methylation signatures of three systemic autoimmune rheumatic diseases (SARDs), namely rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis, compared to healthy controls. Using a careful design to minimize confounding, we restricted our study to subjects with incident disease and performed our analyses on purified CD4⁺ T cells, key effector cells in SARD. We identified differentially methylated (using the Illumina Infinium HumanMethylation450 BeadChip array) and expressed (using the Illumina TruSeq stranded RNA-seq protocol) sites between cases and controls, and investigated the biological significance of this SARD signature using gene annotation databases. We recruited 13 seropositive rheumatoid arthritis, 19 systemic sclerosis, 12 systemic lupus erythematosus subjects, and 8 healthy controls. We identified 33 genes that were both differentially methylated and expressed (26 over- and 7 under-expressed) in SARD cases versus controls. The most highly overexpressed gene was <i>CD1C</i> (log fold change in expression = 1.85, adjusted <i>P</i> value = 0.009). In functional analysis (Ingenuity Pathway Analysis), the top network identified was lipid metabolism, molecular transport, small molecule biochemistry. The top canonical pathways included the mitochondrial L-carnitine shuttle pathway (<i>P</i> = 5E-03) and PTEN signaling (<i>P</i> = 8E-03). The top upstream regulator was HNF4A (<i>P</i> = 3E-05). This novel SARD signature contributes to ongoing work to further our understanding of the molecular mechanisms underlying SARD and provides novel targets of interest.</p

Additional file 1 of An evaluation of methods correcting for cell-type heterogeneity in DNA methylation studies

Contains plots showing simulated effect sizes among 500 CpGs in simulation scenario 1, and QQ plots for p values of several simulation scenarios. (PDF 771 kb

Proportion of significant SNPs separated from regulatory region by a recombination hotspot (as in Figure 4).

<p>A hotspot has been simulated between the transcript locus and the regulatory rSNP as illustrated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038667#pone-0038667-g004" target="_blank">Figure 4</a>.</p

Empirical False Positive Rate estimates.

<p>Percent of SNPs showing <i>p</i>-values below 0.01, after randomly assigning AI to 5, 10, 15, 20 and 29 individuals out of the 54 considered (based on the set of Ge et al.). Based on 20 whole genome scans for 10, 15 and 20 AI individuals and on 20 scans of chromosomes 1 to 4 for 5 and 29 AI individuals.</p

Sets of possible genotypes under complete and incomplete linkage disequilibrium.

<p>Under complete LD for genealogical positions below (<b>A</b>), parallel (<b>B</b>) and above (<b>C</b>), there are always two genotypes characterizing AI-individuals and only one type of A-site homozygote present (AA or aa). Under equilibrium or incomplete linkage disequilibrium (<b>D</b>) all four haplotypes involving R and A sites are present and thus potentially all ten resulting genotypes as well.</p

Four possible mutational pathways creating three distinct sets of three haplotypes.

<p>Depending on the sequence of mutations starting with the ancestral haplotype on the left, we obtain three sets of haplotypes, referred to as below, parallel and above to reflect the position of the <i>A</i>-site vs. <i>R</i>-site mutation on the genealogy shown on the right. These genealogical positions can be modified by recombination. We assume no recurrent mutations.</p

Manhattan plots of <i>p</i>-values from the contingency test.

<p>(<b>A</b>) for all autosomes using HapMap2 polymorphisms and AI data for LRRIQ3; (<b>B</b>) using HapMap3 polymorphisms and AI data for TAPBP; and (<b>C</b>) using 1000 genomes sequences for chromosome 6 and the same AI data for TAPBP.</p

Ideograms of linear regression and binomial haplotype-based tests, and of contingency genotype-based test.

<p>How AI results are used in the three tests with hypothetical SNPs, SNP1 and SNP2, chosen such that SNP1 is not linked to the R-site whereas SNP2 is.</p

Phase switch errors in AI individuals due to rephasing (%).

<p>Phase switch errors between the direction of AI and the original haplotype phase of R and r alleles observed after rephasing (using PHASE) the simulation data for different r frequencies.</p