PERBUATAN MELAWAN HUKUM YANG DILAKUKAN OLEH PENGUASA DI ERA DIGITAL

Indonesia adalah negara demokrasi yang juga menganut ideologi negara kesejahteraan. Ideologi ini berdampak pada cara negara beroperasi, yang menjadi semakin penting dan berkembang. Semakin meluasnya pelaksanaan tugas dan wewenang pemerintah ternyata telah menimbulkan beberapa kemunduran bagi masyarakat luas, khususnya di bidang hukum publik. Penelitian ini bermaksud untuk dapat memahami bagaimana pengertian kegiatan melawan hukum yang dilakukan oleh pemerintah, serta bagaimana proses penyelesaiannya di dunia digital seperti sekarang ini. Secara khusus, penelitian ini akan melihat bagaimana konsep yang berhubungan satu sama lain. Karena semakin banyak orang yang menyadari kesulitan hukum di negara ini sebagai akibat dari globalisasi digital. Dalam penelitian ini metode penelitian deskriptif dipadukan dengan pendekatan yuridis normatif analitis. Selain itu, metode penelitian kepustakaan digunakan untuk mencari data guna mengetahui bagaimana perbuatan melawan hukum oleh penguasa atau pemerintah. Temuan penyelidikan menunjukkan bahwa pihak berwenang seharusnya dimintai pertanggungjawaban atas kegiatan ilegal yang mereka lakukan karena tindakan ini terkait langsung dengan pelanggaran hukum dan melibatkan semacam tindakan melebihi atau menyalahgunakan kekuasaan yang diberikan kepada mereka. Tindakan tersebut dapat berupa tindakan secara terang terangan, dan atau secara terselubung, yang dimana tindakan tersebut dapat merugikan masyarakat pada aspek berbagai pihak dan juga Pemerintah itu sendiri. Kata Kunci : PMHP, Hukum, Negara, Masyaraka

Genetic Architecture and Biology of Youth-Onset Type 2 Diabetes

The prevalence of youth-onset type 2 diabetes (T2D) and childhood obesity has been rising steadily1, producing a growing public health concern1 that disproportionately affects minority groups2. The genetic basis of youth-onset T2D and its relationship to other forms of diabetes are unclear3. Here we report a detailed genetic characterization of youth-onset T2D by analysing exome sequences and common variant associations for 3,005 individuals with youth-onset T2D and 9,777 adult control participants matched for ancestry, including both males and females. We identify monogenic diabetes variants in 2.4% of individuals and three exome-wide significant (P \u3c 2.6 × 10−6) gene-level associations (HNF1A, MC4R, ATXN2L). Furthermore, we report rare variant association enrichments within 25 gene sets related to obesity, monogenic diabetes and β-cell function. Many youth-onset T2D associations are shared with adult-onset T2D, but genetic risk factors of all frequencies—and rare variants in particular—are enriched within youth-onset T2D cases (5.0-fold increase in the rare variant and 3.4-fold increase in common variant genetic liability relative to adult-onset cases). The clinical presentation of participants with youth-onset T2D is influenced in part by the frequency of genetic risk factors within each individual. These findings portray youth-onset T2D as a heterogeneous disease situated on a spectrum between monogenic diabetes and adult-onset T2D

Exome sequencing of 20,791 cases of type 2 diabetes and 24,440 controls

Protein-coding genetic variants that strongly affect disease risk can yield relevant clues to disease pathogenesis. Here we report exome-sequencing analyses of 20,791 individuals with type 2 diabetes (T2D) and 24,440 non-diabetic control participants from 5 ancestries. We identify gene-level associations of rare variants (with minor allele frequencies of less than 0.5%) in 4 genes at exome-wide significance, including a series of more than 30 SLC30A8 alleles that conveys protection against T2D, and in 12 gene sets, including those corresponding to T2D drug targets (P = 6.1 × 10−3) and candidate genes from knockout mice (P = 5.2 × 10−3). Within our study, the strongest T2D gene-level signals for rare variants explain at most 25% of the heritability of the strongest common single-variant signals, and the gene-level effect sizes of the rare variants that we observed in established T2D drug targets will require 75,000–185,000 sequenced cases to achieve exome-wide significance. We propose a method to interpret these modest rare-variant associations and to incorporate these associations into future target or gene prioritization efforts