EVALUASI KEBIJAKAN PEMERINTAH DI BAGIAN INFRASTRUKTUR UNTUK MENDUKUNG KOTA TIDORE KEPULAUAN SEBAGAI KOTA JASA BERBASIS AGROMARINE

Persiapan pembangunan dari segi fisik infrastruktur prioritas dapat melalui identifikasi potensi dan serta perencanaan induk dalam mendukung pengembangan Kota Tidore Kepulauan sebagai kota jasa berbasis agromarine. Dengan basis Agromarine yang merupakan percepatan dan mengoptimalkan pembangunan dan percepatan pemanfaatan sumber daya potensial dan unggulan di darat maupun di laut yang meliputi sektor perikanan, pariwisata, pertanian untuk mewujudkan kesejahteraan masyarakat. Infrastruktur menjadi faktor utama untuk mendukung terwujudnya Kota Tidore Kepulauan sebagai kota jasa berbasi agromarine, karena pola agromarine di tekankan harus didukung dengan pembangunan infrasktruktur yang memawadai. Tujuan penelitian ini adalah untuk mengetahui Kota Tidore Kepulauan menjadi kota jasa berbasis agromarine dengan mengidentifikasi dan mengevaluasi 5 bidang pendukung di program infrastruktur.Penelitian ini mengunakan metode analisis Deskrpitif Kualitatif dan evaluatif dengan mengidentifikasi data yang sudah ada di 5 bidang pada program infrastrukutur, dan mengevaluasi menggunakan parameter yang telah di tentukan.Hasil rangkaian analisis yang di lakukan, di peroleh bahwa 5 bidang khususnya program infrastruktur tahun 2016-2018 dari 5 bidang belum semua mencapai target (100%) di antaranya di bidang Petanian 2016, 33% 2017, 33%, 2018, 66%, di bidang perikanan 2016, 50%. 2017, 50%, 2018 50%, di bidang kelauatan 2016, 50%, 2017, 50%, 2018, 50%, di bidang pariwisata 2016, 66%, 2017, 33%, 2018, 66%, di bidang pekerjaan umum 2016, 42%, 2017, 50%, 2018, 65%. 5 bidang pada pogram Infrastruktur banyak yang belum sesuai dengan kebijakan yang di buat oleh pemerintah.Kata Kunci: Agromarine, Program, Infrastruktur, Kota Tidore Kepulauan

The Vehicle, Spring 1970, Vol. 12 no. 2

Vol. 12, No. 2 Table of Contents Prose short storyCarol Jean Baumgartepage 5 essayDan Franklinpage 8 short storyMary Yarbroughpage 21 Poetry Sara Brinkerhoffpage 20 Nick Dagerpage 18 E.S.page 17 Harry Fordpage 20 Melinda Gimbutpage 19 Ann Graffpage 20 Heather Hoebelpage 7 Becky McIntoshpage 20 John Metcalfpage 17 Mary Pipekpage 19 Cynthia C. Yohopage 17 Photography Dennis Hoaglundpages 5, 10, 21 Dale Huberpage 23 Scott Redfieldpages 7, 19 Tribute to the Ordinary Studentpage 11artMike DorseystoryNick Dagerhttps://thekeep.eiu.edu/vehicle/1022/thumbnail.jp

Policy Recommendations for Meeting the Grand Challenge to Achieve Equal Opportunity and Justice

This brief was created forSocial Innovation for America’s Renewal, a policy conference organized by the Center for Social Development in collaboration with the American Academy of Social Work & Social Welfare, which is leading theGrand Challenges for Social Work initiative to champion social progress. The conference site includes links to speeches, presentations, and a full list of the policy briefs

Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

The maintenance of normal body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time. Prior to the onset of AN, premorbid body mass index (BMI) spans the entire range from underweight to obese. After recovery, patients have reduced rates of overweight and obesity. As such, loci involved in body weight regulation may also be relevant for AN and vice versa. Our primary analysis comprised a cross-trait analysis of the 1000 single nucleotide polymorphisms (SNPs) with the lowest p-values in a genome-wide association meta-analysis (GWAMA) of AN (GCAN) for evidence of association in the largest published GWAMA for BMI (GIANT). Subsequently we performed sex-stratified analyses for these 1000 SNPs. Functional ex vivo studies on four genes ensued. Lastly, a look-up of GWAMA-derived BMI related loci was performed in the AN GWAMA. We detected significant associations (p-values < 5×10−5, Bonferroni corrected p < 0.05) for 9 SNP alleles at 3 independent loci. Interestingly, all AN susceptibility alleles were consistently associated with increased BMI. None of the genes (chr. 10: CTBP2, chr. 19: CCNE1, chr. 2: CARF and NBEAL1; the latter is a region with high linkage disequilibrium) nearest to these SNPs has previously been associated with AN or obesity. Sex-stratified analyses revealed that the strongest BMI signal originated predominantly from females (chr. 10 rs1561589; poverall: 2.47 × 10−06/pfemales: 3.45 × 10−07/pmales: 0.043). Functional ex vivo studies in mice revealed reduced hypothalamic expression of Ctbp2 and Nbeal1 after fasting. Hypothalamic expression of Ctbp2 was increased in diet induced obese (DIO) mice as compared to age-matched lean controls. We observed no evidence for associations for the look-up of BMI related loci in the AN GWAMA. A cross-trait analysis of AN and BMI loci revealed variants at three chromosomal loci with potential joint impact. The chromosome 10 locus is particularly promising given that the association with obesity was primarily driven by females. In addition, the detected altered hypothalamic expression patterns of Ctbp2 and Nbeal1 as a result of fasting and DIO implicate these genes in weight regulation

Systematic Review and Meta-Analysis: An Empirical Approach to Defining Treatment Response and Remission in Pediatric Obsessive-Compulsive Disorder

©. This manuscript version is made available under the CC-BY-NC 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the, Submitted, version of a Published Work that appeared in final form in Journal of the American Academy of Child and Adolescent Psychiatry. To access the final edited and published work see: https://doi.org/10.1016/j.jaac.2021.05.027Objective: A lack of universal definitions for response and remission in pediatric obsessive- compulsive disorder (OCD) has hampered the comparability of results across trials. To address this problem, we conducted an individual participant data diagnostic test accuracy meta-analysis to evaluate the discriminative ability of the Children’s Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) in determining response and remission. We also aimed to generate empirically derived cutoffs on the CY-BOCS for these outcomes. Method: A systematic review of PubMed, PsycINFO, Embase and CENTRAL identified 5,401 references, 42 randomized controlled clinical trials (RCTs) were considered eligible and 21 provided data for inclusion (N 1,234). A score ≤ 2 in the Clinical Global Impressions Improvement and Severity scales were chosen to define response and remission, respectively. A two-stage random-effects meta-analysis model was established. The area under the curve (AUC) and the Youden Index were computed to indicate the discriminative ability of the CY-BOCS and to guide for the optimal cutoff, respectively. Results: The CY-BOCS had sufficient discriminative ability to determine response (AUC 0.89) and remission (AUC 0.92). The optimal cutoff for response was a ≥ 35% reduction from baseline to posttreatment (sensitivity [95% CI] 83.9 [83.7, 84.1]; specificity [95% CI] 81.7 [81.5, 81.9]). The optimal cutoff for remission was a posttreatment raw score ≤ 12 (sensitivity [95% CI] 82.0 [81.8, 82.2]; specificity [95% CI] 84.6 [84.4, 84.8]). Conclusion: Meta-analysis identified empirically optimal cutoffs on the CY-BOCS to determine response and remission in pediatric OCD RCTs. Systematic adoption of standardized operational definitions for response and remission will improve comparability across trials for pediatric OCD

Improving Laboratory Animal Genetic Reporting: Lag-R Guidelines

The biomedical research community addresses reproducibility challenges in animal studies through standardized nomenclature, improved experimental design, transparent reporting, data sharing, and centralized repositories. The ARRIVE guidelines outline documentation standards for laboratory animals in experiments, but genetic information is often incomplete. To remedy this, we propose the Laboratory Animal Genetic Reporting (LAG-R) framework. LAG-R aims to document animals\u27 genetic makeup in scientific publications, providing essential details for replication and appropriate model use. While verifying complete genetic compositions may be impractical, better reporting and validation efforts enhance reliability of research. LAG-R standardization will bolster reproducibility, peer review, and overall scientific rigor

A genome-wide association study of anorexia nervosa.

Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets. Seventy-six (72 independent) single nucleotide polymorphisms were taken forward for in silico (two data sets) or de novo (13 data sets) replication genotyping in 2677 independent AN cases and 8629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication data sets comprised 5551 AN cases and 21 080 controls. AN subtype analyses (1606 AN restricting; 1445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01 × 10(-7)) in SOX2OT and rs17030795 (P=5.84 × 10(-6)) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76 × 10(-)(6)) between CUL3 and FAM124B and rs1886797 (P=8.05 × 10(-)(6)) near SPATA13. Comparing discovery with replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P=4 × 10(-6)), strongly suggesting that true findings exist but our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field

A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling

J. Kaprio, A. Palotie, A. Raevuori-Helkamaa ja S. Ripatti ovat työryhmän Eating Disorders Working Group of the Psychiatric Genomics Consortium jäseniä. Erratum in: Sci Rep. 2017 Aug 21;7(1):8379, doi: 10.1038/s41598-017-06409-3We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 x 10(-7); OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation.Peer reviewe

A genome-wide association study of anorexia nervosa

Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2,907 cases with AN from 14 countries (15 sites) and 14,860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery datasets. Seventy-six (72 independent) SNPs were taken forward for in silico (two datasets) or de novo (13 datasets) replication genotyping in 2,677 independent AN cases and 8,629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication datasets comprised 5,551 AN cases and 21,080 controls. AN subtype analyses (1,606 AN restricting; 1,445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01×10−7) in SOX2OT and rs17030795 (P=5.84×10−6) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76×10−6) between CUL3 and FAM124B and rs1886797 (P=8.05×10−6) near SPATA13. Comparing discovery to replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P= 4×10−6), strongly suggesting that true findings exist but that our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field

Shared genetic risk between eating disorder- and substance-use-related phenotypes:Evidence from genome-wide association studies

First published: 16 February 202