Problematika Penyelesaian Sengketa Kewenangan Lembaga Negara Oleh Mahkamah Konstitusi

According to Article 24C verse (1) of the 1945 Constitution, Constitutional court has an authority to examine the dispute among the state institution in which its authority is given by the constitution directly. But there is a certain problem in practice which is related to definition of “state institution” and “authorities are granted the Constitution” in the 1945 Constitution. This condition opens a debate the interpretation in executing the settlement on authority dispute among the institutions. In addition, should be considered the settlement of disputes the authority of institutions, whose authority derived from regulation other than the Constitution Menurut ketentuan Pasal 24C ayat (1) UUD NRI Tahun 1945, penyelesaian sengketa kewenangan lembaga negara yang kewenangannya diberikan oleh UUD merupakan kewenangan Mahkamah Konstitusi. Namun dalam praktiknya, proses penyelesaian sengketa kewenangan lembaga negara menghadapi problem tersendiri seiring tidak adanya batasan ruang lingkup dan definisi “lembaga negara” dan frasa “kewenangannya diberikan UUD” secara pasti dalam UUD NRI Tahun 1945. Situasi ini pada akhirnya menimbulkan multitafsir yang berpotensi mengakibatkan tidak efektifnya penyelesaian sengketa kewenangan lembaga negara di Indonesia. Selain itu, perlu dipikirkan mekanisme penyelesaian sengketa kewenangan lembaga yang kewenangannya bersumber dari peraturan selain UUD

Mitochondrial function following ethanol exposure: Cardiomyocyte mitochondrial membrane potential (MMP) in FVB and ADH mice with or without acute ethanol exposure.

<p>JC-1 fluorochrome was shown as the ratio of red to green fluorescence. CCCP was used a positive control. Mean ± SEM, n = 9–14 cells per group, * p<0.05 <i>vs.</i> FVB, # p<0.05 <i>vs.</i> FVB-EtOH group.</p

Histological analyses following ethanol exposure: Histological analyses hearts from FVB and ADH mice with or without ethanol exposure.

<p>A - D: H&E staining micrographs of transverse sections of left ventricular myocardium (x 400) from FVB, FVB-EtOH, ADH and ADH-EtOH groups; E: Quantitative analysis of cardiomyocyte cross-sectional (transverse) area using measurements of ∼150 cardiomyocytes from 3–5 mice per group. Mean ± SEM, * p<0.05 <i>vs.</i> FVB, # p<0.05 <i>vs.</i> FVB-EtOH group.</p

Mitochondrial death pathway in myocardium following ethanol exposure: Expression of pro-caspase-9 (B), cytosolic pro-caspase-9 (C), cytosolic cytochrome C (D), cytosolic pro-caspase-8 (E) and cytosolic AIF (F) in myocardium from FVB and ADH mice with or without acute ethanol exposure.

<p>Panel A depicts representative gels using specific antibodies. Mean ± SEM, n = 4–8 samples per group, all samples were in duplicates with the average being used, * p<0.05 <i>vs.</i> FVB group.</p

Effect of ethanol exposure on cardiac function: Effect of acute ethanol exposure on cardiac contractile function using a Langendorff perfusion system in FVB and ADH mice.

<p>A: Left ventricular developing pressure (LVDP); B and C: Maximal velocity of pressure development (+dP/dt) and decline (−dP/dt). Mean ± SEM, n = 5–10 hearts per group, * p<0.05 <i>vs.</i> FVB, # p<0.05 <i>vs.</i> FVB-EtOH group.</p

Mitochondrial O₂^•− generation following ethanol exposure: Mitochondrial O₂^•− generation using the MitoSOX Red probe in cardiomyocytes from FVB and ADH mice with or without acute ethanol exposure.

<p>Cohorts of non-ethanol-treated FVB cardiomyocytes were incubated with the ADH enzymatic metabolite of ethanol, acetaldehyde (ACA, 100 µM), for 4 hrs at 37°C prior to MitoSOX Red measurement. A–E: Representative fluorescence images (40x) from FVB, FVB-EtOH, ADH, ADH-EtOH and FVB-ACA groups. F: Pooled data. Mean ± SEM, n = 15–20 fields per group, * p<0.05 <i>vs.</i> FVB, # p<0.05 <i>vs.</i> FVB-EtOH group.</p

Protein Tyrosine Phosphatase 1B and Insulin Resistance: Role of Endoplasmic Reticulum Stress/Reactive Oxygen Species/Nuclear Factor Kappa B Axis

<div><p>Obesity-induced endoplasmic reticulum (ER) stress has been proposed as an important pathway in the development of insulin resistance. Protein-tyrosine phosphatase 1B (PTP1B) is a negative regulator of insulin signaling and is tethered to the ER-membrane. The aim of the study was to determine the mechanisms involved in the crosstalk between ER-stress and PTP1B. PTP1B whole body knockout and C57BL/6J mice were subjected to a high-fat or normal chow-diet for 20 weeks. High-fat diet feeding induced body weight gain, increased adiposity, systemic glucose intolerance, and hepatic steatosis were attenuated by PTP1B deletion. High-fat diet- fed PTP1B knockout mice also exhibited improved glucose uptake measured using [³H]-2-deoxy-glucose incorporation assay and Akt phosphorylation in the skeletal muscle tissue, compared to their wild-type control mice which received similar diet. High-fat diet-induced upregulation of glucose-regulated protein-78, phosphorylation of eukaryotic initiation factor 2α and c-Jun NH₂-terminal kinase-2 were significantly attenuated in the PTP1B knockout mice. Mice lacking PTP1B showed decreased expression of the autophagy related protein p62 and the unfolded protein response adaptor protein NCK1 (non-catalytic region of tyrosine kinase). Treatment of C2C12 myotubes with the ER-stressor tunicamycin resulted in the accumulation of reactive oxygen species (ROS), leading to the activation of protein expression of PTP1B. Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFκB p65 and was required for ER stress-mediated expression of PTP1B. Our data suggest that PTP1B is induced by ER stress via the activation of the ROS-NFκB axis which is causes unfolded protein response and mediates insulin resistance in the skeletal muscle under obese condition.</p></div

Genetic Diversity, Linkage Disequilibrium and Selection Signatures in Chinese and Western Pigs Revealed by Genome-Wide SNP Markers

<div><p>To investigate population structure, linkage disequilibrium (LD) pattern and selection signature at the genome level in Chinese and Western pigs, we genotyped 304 unrelated animals from 18 diverse populations using porcine 60 K SNP chips. We confirmed the divergent evolution between Chinese and Western pigs and showed distinct topological structures of the tested populations. We acquired the evidence for the introgression of Western pigs into two Chinese pig breeds. Analysis of runs of homozygosity revealed that historical inbreeding reduced genetic variability in several Chinese breeds. We found that intrapopulation LD extents are roughly comparable between Chinese and Western pigs. However, interpopulation LD is much longer in Western pigs compared with Chinese pigs with average r²_0.3 values of 125 kb for Western pigs and only 10.5 kb for Chinese pigs. The finding indicates that higher-density markers are required to capture LD with causal variants in genome-wide association studies and genomic selection on Chinese pigs. Further, we looked across the genome to identify candidate loci under selection using <em>F_ST</em> outlier tests on two contrast samples: Tibetan pigs versus lowland pigs and belted pigs against non-belted pigs. Interestingly, we highlighted several genes including <em>ADAMTS12</em>, <em>SIM1</em> and <em>NOS1</em> that show signatures of natural selection in Tibetan pigs and are likely important for genetic adaptation to high altitude. Comparison of our findings with previous reports indicates that the underlying genetic basis for high-altitude adaptation in Tibetan pigs, Tibetan peoples and yaks is likely distinct from one another. Moreover, we identified the strongest signal of directional selection at the <em>EDNRB</em> loci in Chinese belted pigs, supporting <em>EDNRB</em> as a promising candidate gene for the white belt coat color in Chinese pigs. Altogether, our findings advance the understanding of the genome biology of Chinese and Western pigs.</p> </div

Data from: Genetic Diversity, Linkage Disequilibrium and Selection Signatures in Chinese and Western Pigs Revealed by Genome-Wide SNP Markers

Dataset corresponds to the article: "Genetic Diversity, Linkage Disequilibrium and Selection Signatures in Chinese and Western Pigs Revealed by Genome-Wide SNP Markers" Huashui Ai, Lusheng Huang, Jun Ren. For any correspondence, please address Lusheng Huang ([email protected]) Complete dataset contains 52,556 SNP genotypes for 304 individuals. Info_sample.txt file contains information about location (Origin) and population (POPname) for each sample. 304IDs.maf0.05.geno0.1.* files contains genotypes for samples included for all analyses in the paper (PLINK format)

Morphometry and fasting glucose of C57BL/6 and PTP1BKO female mice fed with a ND or a HFD for a 20 week period.

<p>Values are mean ± SEM, n = 5–6 mice per group, ^* p<0.05 vs. C57BL/6 ND group, ^† p<0.05 vs. PTP1BKO ND, ^‡ p<0.05 vs. C57BL/6 HFD group.</p