130 research outputs found

    Eksistensi Hukum Adat dalam Melindungi Pelestarian Sasi Ikan Lompa di Desa Haruku Kabupaten Maluku Tengah

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    Penelitian ini bertujuan : (1) Pengaturan hukum adat sasi, (2) Upaya masyarakat mempertahankan dan menaati hukum adat sasi, (3) Eksistensi hukum adat sasi dalam hukum nasional. Lokasi penelitian dilakukan di Desa Haruku Kabupaten Maluku Tengah. Metode yang digunakan adalah metode studi kasus dengan cara pengambilan sampel adalah purposive sampling, yang dilaksanakan pada tanggal 12 Agustus 2011sampai 27 September 2011. Data yang digunakan meliputi data primer dan data sekunder. Pengumpulan data dilakukan dengan cara observasi, wawancara, dokumentasi, studi pustaka, dan metode analisisisi. Data dianalisis secara deskriptif kualitatif. Kesimpulan dalam penelitian ini bahwa: (1) Dalam sasiter dapat beberapa pengaturan hokum adat sasi mulai dari pengaturan pengelolaan, pemeliharaan, dan sampai pada waktu pemanenan. (2) Efektivitas masyarakat dalam menjaga hukum adat sangat kuat dari ribuan tahun lalu hingga tahun 2003 sampai 2007 terlihat masih terjaganya hukum adat dan tradisi sasi ikan lompa, akan tetapi tradisi hukum adat sasi sejak tahun 2008 hingga saat ini mulai mengalami penurunan hal ini dibuktikan dengan tidak terlihat lagi ikan lompa selama 4 tahun. (3) Eksistensi hukum adat sasi berisi peraturan-peraturan dan selalu mengikat masyarakatnya dalam menjaga lingkungan alam terutama laut sudah dilakukan sejak ribuan tahun lalu juga terdapat dalam hukum nasional Indonesia

    X-Efficiency of Commercial Banks in Kenya

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    This study sought to determine the X-efficiency of commercial banks in Kenya and to establish whether the X-efficiency of these banks is affected by economies of scale. The data set consisted of annual operation costs of banks including interest expense. Deposits and borrowed funds were the inputs, and the loans to customers and investment and other incomes were the outputs. The data was collected from 33 banks for the period 2000 to 2005. To measure the X-efficiency level of commercial banks in Kenya, the study applied the Stochastic Econometric Cost Frontier approach which involves the estimation of the cost function and the derivation of the X-efficiency estimate based on the deviation from the efficient cost frontier. The empirical results obtained showed that X-efficiency exists in the commercial banks in Kenya and that X-efficiency of the banks is affected by economies of scale. The results showed that the average level of X-efficiency in Kenya’s commercial banks industry is 18%. After controlling for scale differences, the average small bank is found to be relatively less efficient than the average large bank. The persistency of X-efficiency in relation to bank size was measured to determine if inefficient banks tend to remain inefficient over time. The results indicate that the average large bank inefficiency was more persistent than the average small bank inefficiency at the level of 23%. The results also show that bank size affects X-efficiency for large banks. These findings were consistent with the results found in other related studies in US Kwan and Eisenbeis, 1996), Hong Kong (Kwan, 2001) and Namibia (Ikhide, 2000)

    Causal Dependence Plots

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    Explaining artificial intelligence or machine learning models is increasingly important. To use such data-driven systems wisely we must understand how they interact with the world, including how they depend causally on data inputs. In this work we develop Causal Dependence Plots (CDPs) to visualize how one variable--an outcome--depends on changes in another variable--a predictor--along with any consequent causal changes in other predictor variables\textit{along with any consequent causal changes in other predictor variables}. Crucially, CDPs differ from standard methods based on holding other predictors constant or assuming they are independent. CDPs make use of an auxiliary causal model because causal conclusions require causal assumptions. With simulations and real data experiments, we show CDPs can be combined in a modular way with methods for causal learning or sensitivity analysis. Since people often think causally about input-output dependence, CDPs can be powerful tools in the xAI or interpretable machine learning toolkit and contribute to applications like scientific machine learning and algorithmic fairness

    PAX3-FOXO1 uses its activation domain to recruit CBP/P300 and shape RNA Pol2 cluster distribution

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    Activation of oncogenic gene expression from long-range enhancers is initiated by the assembly of DNA-binding transcription factors (TF), leading to recruitment of co-activators such as CBP/p300 to modify the local genomic context and facilitate RNA-Polymerase 2 (Pol2) binding. Yet, most TF-to-coactivator recruitment relationships remain unmapped. Here, studying the oncogenic fusion TF PAX3-FOXO1 (P3F) from alveolar rhabdomyosarcoma (aRMS), we show that a single cysteine in the activation domain (AD) of P3F is important for a small alpha helical coil that recruits CBP/p300 to chromatin. P3F driven transcription requires both this single cysteine and CBP/p300. Mutants of the cysteine reduce aRMS cell proliferation and induce cellular differentiation. Furthermore, we discover a profound dependence on CBP/p300 for clustering of Pol2 loops that connect P3F to its target genes. In the absence of CBP/p300, Pol2 long range enhancer loops collapse, Pol2 accumulates in CpG islands and fails to exit the gene body. These results reveal a potential novel axis for therapeutic interference with P3F in aRMS and clarify the molecular relationship of P3F and CBP/p300 in sustaining active Pol2 clusters essential for oncogenic transcription

    Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

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    Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

    Conjunctival Melanoma Targeted Therapy: MAPK and PI3K/mTOR Pathways Inhibition.

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    To analyze the activity of mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinases/mechanistic target of rapamycin (PI3K/mTOR) pathways in benign and malignant conjunctival melanocytic proliferations and explore whether specific inhibitors can suppress growth of conjunctival melanoma (CJM) cells. The presence of a BRAF V600E mutation and activation of ERK, MEK, S6, and AKT were assessed with immunohistochemistry in 35 conjunctival nevi and 31 melanomas. Three CJM cell lines were used: CRMM1, carrying the BRAF V600E mutation; CRMM2, harboring the NRAS Q61L mutation; and T1527A, with a BRAF G466E mutation. WST-1 assays were performed with a BRAF inhibitor (vemurafenib), two MEK inhibitors (trametinib, selumetinib), a PI3K inhibitor (pictilisib), and a dual PI3K/mTOR inhibitor (dactolisib). The phosphorylation of ERK, MEK, and S6 were tested with western blots and apoptosis with cleaved caspase-3 immunostaining. A BRAF V600E mutation was detected in 42.6% of nevi and in 35.5% of CJM. MEK and ERK activation were higher in CJM, occurring in 62.9% and 45.7% of the nevi and 90.3% and 96.8% of the CJM, respectively. There was also a significant increase in S6 activation in CJM (90.3%) compared with the nevi (20%). CRMM1 was sensitive to trametinib and the PI3K inhibitors but only marginally to vemurafenib. CRMM2 was moderately sensitive to pictilisib, whereas T1527A was resistant to all drugs tested. The MAPK pathway activity in CJM is increased, not only as a consequence of the BRAF V600E mutation. Targeted therapy may be useful for patients with CJM, especially those with activating BRAF mutations, whereas NRAS-mutated melanomas are relatively resistant
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