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

Determination of weights for calculating the weighted averages of similar experiments.

<p>(A) Example of how correlations between inhibitors and stimuli were calculated. The two colored columns represent the vector of phosphoprotein values obtained under all experimental conditions, sorted in an arbitrary but defined way. In the case of the mTOR inhibitor, data for the IGF-I stimulus is missing; these data are to be predicted. Similarly, in the case of the MEK inhibitor, data for the INFg stimulus is missing. The data in common (dashed box) was used to calculate the Spearman rank correlation coefficient. (B) Graphic representation of the normalized correlation coefficients relating inhibitors (top) and stimuli (bottom). The matrices are asymmetric because correlation coefficients were separately normalized for each inhibitor (stimulus), setting the maximum in a row to 1 (yellow) and the minimum to 0 (black). Other values were based on the correlation coefficient, scaling linearly between the minimum and maximum values in the row.</p

Visualization of the data provided to predictors for the phosphoprotein sub-challenge.

<p>Phosphoprotein levels were been normalized such that values above the median for all values are yellow and those below the median are red. Each column is one of the phosphoproteins, clustered based on similarity in expression. Rows correspond to experiments, sorted in an arbitrary hierarchical manner (cell type, time point, stimulus type, and inhibitor type). The white rows that appear to subdivide the dataset represent the missing data to be predicted.</p

PPARG Binding Landscapes in Macrophages Suggest a Genome-Wide Contribution of PU.1 to Divergent PPARG Binding in Human and Mouse

<div><h3>Background</h3><p>Genome-wide comparisons of transcription factor binding sites in different species can be used to evaluate evolutionary constraints that shape gene regulatory circuits and to understand how the interaction between transcription factors shapes their binding landscapes over evolution.</p> <h3>Results</h3><p>We have compared the PPARG binding landscapes in macrophages to investigate the evolutionary impact on PPARG binding diversity in mouse and humans for this important nuclear receptor. Of note, only 5% of the PPARG binding sites were shared between the two species. In contrast, at the gene level, PPARG target genes conserved between both species constitute more than 30% of the target genes regulated by PPARG ligand in human macrophages. Moreover, the majority of all PPARG binding sites (55–60%) in macrophages show co-occupancy of the lineage-specification factor PU.1 in both species. Exploring the evolutionary dynamics of PPARG binding sites, we observed that PU.1 co-binding to PPARG sites appears to be important for possible PPARG ancestral functions such as lipid metabolism. Thus we speculate that PU.1 may have guided utilization of these species-specific PPARG conserved binding sites in macrophages during evolution.</p> <h3>Conclusions</h3><p>We propose a model in which PU.1 sites may have served as “anchor” loci for the formation of new and functionally relevant PPARG binding sites throughout evolution. As PU.1 is an essential factor in macrophage biology, such an evolutionary mechanism would allow for the establishment of relevant PPARG regulatory modules in a PU.1-dependent manner and yet permit for nuanced regulatory changes in individual species.</p> </div

Composition of PPARG bound cis-regulatory modules is conserved between human and mouse macrophages.

<p>A) Overlap between PPARG/RXR and PU.1 ChIP-seq peaks. Significance of overlap was calculated using proportion test. B) PPARG/RXR ChIP-Seq enrichment at PPARG/RXR sites without and with PU.1 overlap. C) Proportion of PPARG/RXR binding sites in human and mouse macrophages that are co-occupied by PU.1. D) Venn-diagram depicting the numbers of species-specific and retained PU.1 binding sites in human and mouse macrophages.</p

Global identification of PPARG and RXR binding sites in human macrophages.

<p>A) Table displaying the number identified PPARG peaks. PPARG/RXR peaks represent PPARG peaks that are supported by enrichment in the RXR ChIP-Seq library (RXR here represents RXRA, RXRB and RXRG). B) PPARG and RXR binding profiles across the locus for PDK4 in THP-1 cells. Plotted are the tag counts obtained from the respective ChIP-Seq libraries. C) Distribution of PPARG/RXR binding sites relative to annotated genes obtained from UCSC Genome Browser (built hg18/NCBI36; RefGene table). D) Motif identified <i>de novo</i> at PPARG/RXR binding sites using CisFinder.</p

Conservation reveals functional PPARG/RXR target genes.

<p>A) Association of PPARG/RXR binding sites with RSG regulated genes in THP-1 cells. Significance of enrichment over background was calculated using Fisher's exact test. B) Venn diagram representing the overlap between PPARG/RXR bound genes and RSG regulated genes across the different conservation categories. Indicated are the numbers of genes exclusive to the respective gene sets. C) Proportion of non-conserved, indirectly and directly shared target genes that are induced by RSG. Significance was calculated using Fisher's exact test. D) Bar plot showing the ratio of expected versus observed number of genes associated with the biological process category ‘lipid metabolic processes’ obtained from PANTHER for human-specific, indirectly and directly shared target genes.</p

PPARG binding is poorly conserved between human and mouse macrophages.

<p>A) Overlap of PPARG bindings sites between human and mouse macrophages. Comparison is based on murine binding sites lifted over to the human genome. 1548 out of 1961 PPARG binding sites in mouse aligned to the human genome. B) Tag counts from human PPARG library at different genomic loci in the human genome and mouse genome. Retained binding sites, human-specific sites and mouse-specific binding sites. Mouse and Human-specific sites in the human and mouse genome refer to the orthologous loci of mouse-specific or human-specific sites in the original genomes. For better visualization outliers were omitted from plot. C) Sequence conservation at human-specific and retained PPARG/RXR sites. Shown is the distribution of PhastCons scores for both categories. Significance was calculated using two-tailed t-test D) Pie chart summarizing the proportion of PPARG/RXR site that are retained and/or show sequence conservation (i.e. overlap with PhastCons element). E) Proportion of PPARG/RXR sites in human macrophages containing a PPARG motif compared to the proportion of sites with motif after liftOver to the mouse genome. The orthologous regions in the mouse genome are separated into PPARG bound and not bound. ‘Random’ shows the expected motif frequency for randomly distributed intervals with a matched size distribution. F) Distribution of PPARG/RXR binding sites in regard to TSS of RefGenes. Displayed are the distributions of human-specific and conserved PPARG/RXR sites.</p

Identification of human-specific and shared PPARG/RXR target genes.

<p>A) Grouping of PPARG/RXR targets genes in human macrophages based on PPARG binding in mouse. Displayed is the number of genes that are human-specific, indirectly, and directly shared PPARG/RXR target genes. Only PPARG binding sites in proximity to genes (<100 kb to TSS) were taken into consideration. B) and C) Enrichment of PPARG binding in homologous regions proximal to <i>SLAMF9/Slamf9</i> and <i>NR1H3/Nr1h3</i> in human and mouse macrophages (upper and lower panel, respectively). <i>SLAMF9/Slamf9</i> represents an indirectly shared PPARG target gene while <i>NR1H3/Nr1h3</i> represents a directly shared target gene. Browser tracks for mouse are shown in reversed direction to facilitate easier comparison between human and mouse.</p

Pu.1 potentially restricts binding site selection for PPARG during binding site turnover.

<p>A) Scheme depicting a potential scenario for PU.1-associated PPARG binding site turnover. B) Average numbers of PU.1 binding sites in proximity to human-specific, indirectly shared, and directly shared PPARG target genes (<100 kb of TSS). Significance was calculated using two-tailed t-test. C) Proportion of conserved PU.1 binding sites at PPARG/RXR-PU.1 binding sites in human macrophages. Comparison was made between sites at human-specific and indirectly shared targets and significance was calculated using Fisher's exact test D) Human PPARG/RXR binding sites co-bound by PU.1 and adjacent to indirectly shared genes were split into sites containing conserved PU.1 binding sites and human-specific PU.1 binding sites, respectively. PPARG and PU.1 motifs were identified at orthologous loci in human and mouse. E) Shown is the locus for a PPARG/RXR binding site in human macrophages adjacent to <i>ALOX5AP</i> and its orthologous region in mouse. Binding for PU.1 and PPARG is shown at orthologous regions in human and mouse. Sequence alignments demonstrate conservation and loss/gain of binding motifs.</p