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

WT and TLR4^−/− mice treated with streptozotocin display a similar profile of hyperglycemia (A) and changes in body weight (B) over a 24 week period including week 6 (WT n = 12; TLR4^−/− n = 9), week 12 (WT n = 10; TLR4^−/− n = 13), week 24 (WT n = 12; TLR4^−/− n = 12) for diabetes groups and non-diabetes controls were 5 mice per group.

<p>The data are present as the means ± SD.</p

TLR4 deficiency protected diabetic kidneys from interstitial fibrosis and tubular injury.

<p>(A) Significant interstitial collagen accumulation was evident in WT but not TLR4^−/− mice with diabetes at 12 and 24 weeks. (B) Illustration of representative sections of the histological changes on PSR staining for collagen. (C) Immunohistochemical staining showed upregulation of α-SMA in WT, but not TLR4^−/− mice, with diabetes as compared to non-diabetic controls at week 24. (D) Significant upregulation of KIM-1 was apparent in WT mice with diabetes, but attenuated in TLR4^−/− diabetic kidneys. The data are present as the means ± SEM; * <i>p</i><0.05; ** <i>p</i><0.01; *** <i>p</i><0.001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p

TLR4 deficiency suppressed inflammatory and fibrotic responses in diabetic kidney.

<p>The expression of endogenous TLR ligands was upregulated in WT-DN kidneys and TLR4^−/−diabetic kidneys at week 6 compared with WT non-diabetic controls. (A). Gene expression of IL-6 (A), TNF-α (B), CCL2 (C), CXCL10 (D), TGF-β (E) and fibronectin (F) were upregulated in WT mice with diabetes, but suppressed in TLR4^−/− mice with diabetes, as measured by RT-PCR. Data are presented as means ± SD; ** <i>p</i><0.01; *** <i>p</i><0.001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p

TLR4 deficiency reduced macrophage accumulation in diabetic nephropathy.

<p>Macrophage (CD68⁺ or F8/40⁺) accumulation was evident in WT mice with diabetes, but prevented by TLR4 deficiency in both the interstitial (A) and glomerular (B & C) compartments. Data are present as means ± SEM; * <i>p</i><0.05; *** <i>p</i><0.001.</p

TLR4 deficiency diminished glomerular injury in DN.

<p>WT diabetic mice showed significant glomerular injury including increased kidney to body weight ratio (A), glomerular volume (B), glomerular cellularity (C, week 24), glomerular mesangial matrix (D & E), decreased podocin staining (F) and WT1⁺ podocyte numbers (H & I) compared to non-diabetic WT controls. These were attenuated in TLR4^−/− diabetic mice. (E) Photomicrographs of representative sections of glomerular changes at 24 weeks on PAS staining (×400 magnification). (G) Representative sections of glomeruli were stained for podocin at week 24, with similar staining intensity evident in non-diabetic WT and TLR4^−/− mice but reduced staining in diabetic mice with a substantially greater reduction seen in WT versus TLR4^−/− diabetic mice. (I) Representative sections were stained for WT1 at week 24. The data are presented as the means ± SEM; * <i>p</i><0.05; *** <i>p</i><0.001; *** <i>p</i><0.0001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p

Expression of TLR4 and its endogenous ligands was upregulated in the early diabetic kidney in WT mice.

<p>mRNA expression of TLR4 and its ligands in kidney was upregulated at 10 weeks after diabetes induction (A & B). The data are presented as means ± SD; * <i>p</i><0.05; ** <i>p</i><0.01; *** <i>p</i><0.001. n = 7 per group. (C) Representative sections of kidney were stained with a rabbit anti-mouse-TLR4 polyclonal antibody in the top panels and a goat anti-mouse-TLR4 polyclonal antibody in the bottom panels.</p

TLR4 deficiency attenuated albuminuria in DN compared to WT mice at week 6, 12, and 24.

<p>The data are present as the means ± SD; ** <i>p</i><0.01; *** <i>p</i><0.001. The number of animals per group was described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097985#pone-0097985-g001" target="_blank">Figure 1</a>.</p

Additional file 3 of Conserved expression of transposon-derived non-coding transcripts in primate stem cells

Table of coordinates for table 1. (TXT 869 kb

Additional file 2 of Conserved expression of transposon-derived non-coding transcripts in primate stem cells

Table of values for figures 1 and 2 and table 1. (TXT 1220 kb