KEBIJAKAN PENGAWASAN DAN PENGENDALIAN PENDUDUK: Era Otonomi Khusus Di Provinsi Papua

The provincial government is currently processing the document of the Governor of the Regulation and Control of Population growth in Papua province. Human Resources Development Agency (BPSDM) Papua province is doing some work programs in order to prepare and establish regulations in question. Population policy is an implementation of Law No. 21 of 2001 on Special Autonomy for Papua Province and Papua Provincial Regulation (Perdasi) No. 15 of 2008 on population. The focus of this rule is more dominant set the field of migration as the dominant factor causing population growth in Papua. It is planned that this rule would regulate the field of birth and death also, because in theory the cause of population growth is not only influenced the migration aspects but also aspects of death and rebirth. The difference between outmigration and inmigration is net migration. If inmigration then the addition of more residents in the region, and vice versa. If born population more than the death of the accretion occurs naturally (natural increase of), and vice versa, so regulation of the Governor's supervision and control of population growth should regulate the field of migration, births and deaths of the population

Phenotypic and genotypic characterisation of Neisseria gohorrhoeae isolates from New Zealand with reduced susceptibility to ceftriaxone : a thesis submitted to the College of Health in partial fulfilment of the requirements for the Master of Science in Microbiology at Massey University, New Zealand

Objectives Currently, ceftriaxone is the last remaining drug recommended for empirical treatment of gonorrhoea. Neisseria gonorrhoeae with reduced susceptibility to ceftriaxone have been isolated worldwide in countries such as Japan, France, Spain, Slovenia, Australia and Sweden. These have led to treatment failures and the emergence of ceftriaxone-resistant N. gonorrhoeae. Various mutations in penA (mosaic and nonmosaic), which encodes the penicillin-binding protein 2 (PBP2), have been reported to be the primary reason for reduced ceftriaxone susceptibility, but it can be reduced further by mutations in mtrR, porBIB and ponA. In this study, we aimed to determine the antimicrobial resistance patterns of New Zealand isolates of N. gonorrhoeae with reduced susceptibility to ceftriaxone and to characterise the penA, mtrR, porBIB and ponA in the isolates. Methods A total of 28 N. gonorrhoeae isolates with elevated ceftriaxone MIC (0.03 to 0.12 mg/L), collected from 2012 to 2015 and obtained from the Institute of Environmental Science and Research (ESR), were examined in this study. Samples came from laboratories in Auckland (26), Wellington (1) and Taranaki (1). The antimicrobial resistance of penicillin G, tetracycline, ciprofloxacin, azithromycin and ceftriaxone were determined through antimicrobial susceptibility test, using minimum inhibitory concentration (MIC) test strips. Polymerase chain reactions (PCRs) and sequencing to identify specific mutations in penA, mtrR, porBIB and ponA, that are associated with elevated minimum inhibitory concentrations (MICs) to ceftriaxone, were undertaken. The association between the phenotypic and genotypic results was investigated by comparing the presence of the number of mutated genes and the MIC level of ceftriaxone. Results Based on the AST results using MIC test strips and interpreted using The European Committee on Antimicrobial Susceptibility Testing (EUCAST) criteria, 23 out of 28 isolates (82%) showed reduced susceptibility to ceftriaxone, with MICs of 0.03 to 0.06 mg/L. All of the isolates were resistant to ciprofloxacin, while 36%, 25% and 7% were resistant to penicillin G, tetracycline and azithromycin, respectively. Two azithromycin-resistant N. gonorrhoeae isolates were observed, and isolate 264 (azithromycin MIC: 4mg/L) also exhibited reduced susceptibility to ceftriaxone (MIC: 0.03 mg/L). A total of 21% (6/28) of the isolates produced ß- lactamase. The 23 isolates that conveyed reduced ceftriaxone susceptibility were found to harbour three or four mutated genes (penA, mtrR and/or porBIB and ponA). Reduced susceptibility to ceftriaxone among N. gonorrhoeae isolates in this study was associated with mosaic PBP2 (encoded by penA) with G545S/A501V mutations, with nonmosaic PBP2 with an A501V mutation, plus the presence of mutation in mtrR promoter with G120 and A121 alterations in PorBIB. A total of 65% (15/23) of the N. gonorrhoeae isolates with reduced susceptibility to ceftriaxone harboured mosaic PBP2 XXXIV, a pattern found in N. gonorrhoeae associated with ceftriaxone treatment failures in Europe and Australia. The current study also revealed that the partial sequences of four mosaic PBP2 (M-2, M-3, M-4, M-5) were different from the common mosaic PBP2 sequences reported in various studies. Conclusion There is an association between the phenotypic and genotypic character of N. gonorrhoeae isolates expressing reduced susceptibility to ceftriaxone in this study population. Furthermore, the presence of important mosaic PBP2 that link to ceftriaxone treatment failure might be circulating among N. gonorrhoeae isolates in New Zealand . Keywords: Neisseria gonorrhoeae, ceftriaxone, reduced susceptibility, New Zealan

Antibodies Against β2-Glycoprotein I Complexed With an Oxidised Lipoprotein Relate to Intima Thickening of Carotid Arteries in Primary Antiphospholipid Syndrome

To explore whether antibodies against β2-glycoprotein I (β2GPI) complexed to 7-ketocholesteryl-9-carboxynonanoate (oxLig-1) and to oxidised low-density lipoproteins (oxLDL) relate to paraoxonase activity (PONa) and/or intima media thickness (IMT) of carotid arteries in primary antiphospholipid syndrome (PAPS). As many as 29 thrombotic patients with PAPS, 10 subjects with idiopathic antiphospholipid antibodies (aPL) without thrombosis, 17 thrombotic patients with inherited thrombophilia and 23 healthy controls were investigated. The following were measured in all participants: β2GPI−oxLDL complexes, IgG anti-β2GPI−oxLig-1, IgG anti-β2GPI−oxLDL antibodies (ELISA), PONa, (para-nitrophenol method), IMT of common carotid (CC) artery, carotid bifurcation (B), internal carotid (IC) by high resolution sonography. β2GPI−oxLDL complex was highest in the control group (p < 0.01), whereas, IgG anti-β2GPI−oxLig1 and IgG anti-β2GPI−oxLDL were highest in PAPS (p < 0.0001). In healthy controls, β2GPI−oxLDL complexes positively correlated to IMT of the IC (p = 0.007) and negatively to PONa after correction for age (p < 0.03). PONa inversely correlated with age (p = 0.008). In PAPS, IgG anti-2GPI−oxLig-1 independently predicted PONa (p = 0.02) and IMT of B (p = 0.003), CC, (p = 0.03) and of IC (p = 0.04). In PAPS, PONa inversely correlated to the IMT of B, CC and IC (p = 0.01, 0.02 and 0.003, respectively). IgG anti-2GPI−oxLig-1 may be involved in PAPS related atherogenesis via decreased PON activity

MAGISTER KEBIJAKAN PUBLIK DAN PEMBANGUNAN ERA OTSUS PAPUA

Progress and problems of regional development in Papua special autonomy to the era, including the implications for public policy and the central government had made this region. Various public policies implemented since the former Dutch East Indies colony was integrated into the 1962's the Republic of Indonesia. A variety of public policy at the positive and negative implications for regional development and community development. Similarly, the 2001 special autonomy has also developed a variety of public policy. It is not known for certain whether public policies that have been through a process step that is true or not, according to the rules of science to public policy. Moreover, knowledge of public policy that is multi-disciplinary and inter-discipline can be said is a relatively new field of science in the curriculum of higher education in Indonesia. Until 2012 in Indonesia there are 5 (five) universities are here opened master in public policy sciences, and the fourth is Cenderawasih University by developing field of study Master (S2) of public policy at the beginning of 2012 which is the efforts of some academics in the field of development science and support the process of national development policies and the regio

The Impact of Sleep Quality on Energy Intake, Eating Behavior, and Physical Activity

Title from PDF of title page, viewed on September 9, 2015Thesis advisor: Jennifer D. LundgrenVitaIncludes bibliographic references (pages 75-86)Thesis (M.A.)--Department of Psychology. University of Missouri--Kansas City, 2015Obesity is associated with numerous health risks and is prevalent across all stages of the lifespan, although it tends to increase with age. As such, the college years are an important time for the development of obesity. Sleep behavior is a possible factor that may contribute to obesity; however, most studies that have examined this relationship have focused on sleep duration and not on sleep quality. Because the restorative nature of sleep depends on its quality in addition to quantity, it is important to measure sleep quality. The purpose of this study was to examine the impact of sleep quality on energy intake, eating behavior, and physical activity in a college sample. Participants completed self-report questionnaires measuring their sleep quality, dietary intake, eating behaviors, and physical activity. It was hypothesized that poor-quality sleepers would consume less protein and more carbohydrates, fat, and total calories compared to good-quality sleepers. It was also predicted that poor-quality sleepers would demonstrate increased hunger, disinhibition, and dietary restraint compared to good-quality sleepers. Finally, it was hypothesized that poor-quality sleepers would demonstrate lower frequencies of moderate, hard, and very hard physical activity compared to good-quality sleepers. These findings will contribute to the existing literature on sleep and obesity and will be important in the development of health promotion programs for college students.Introduction -- Review of literature -- Methodology -- Results -- Appendix A. Pittsburgh Sleep Quality index -- Appendix B. Dietary recall -- Appendix C. Three-factor eating questionnaire -- Appendix D. Night eating questionnaire -- Appendix E. Seven-day physical activity recall -- Appendix F. State trait anxiety inventory -- Appendix G. Beck Depression Inventory -- Appendix H. Perceived stress scal

Can We Be Trained to Eat Healthy? The Effects of an Attentional Bias Modification Program on Eating Behavior

Title from PDF of title page viewed August 17, 2018Dissertation advisor: Jennifer D. LundgrenVitaIncludes bibliographical references (pages 105-121)Thesis (Ph.D.)--Department of Psychology. University of Missouri--Kansas City, 2018The prevalence of overweight (OW) and obesity (OB) has significantly increased over the past four decades. OW and OB are complex in nature and arise from a multitude of factors and their interactive effects. Based on etiological models of OW and OB, interventions to reduce excess body weight have been developed, including population- and individual-level approaches. Current interventions are limited, however, in that they lack focus on how environmental factors (e.g., food cues) interact with biology (e.g., neural reward systems) to influence individual health-related behaviors (e.g., food consumption) through mechanisms such as attentional bias. Attentional bias modification (ABM) programs have been developed to train individuals to either attend to or avoid certain food cues in the environment, yet research in this area is underdeveloped. The purpose of this dissertation was to evaluate the effect of a single-session ABM training designed to promote healthy eating on eating behavior as a potential intervention that targets an individual’s response to the obesogenic environment. This dissertation addressed the limitations of previous ABM studies in that it examined differential effects of the program on attention to food cues and eating behavior among individuals with varying body mass indices (i.e., healthy weight vs. OW/OB).Introduction -- Review of the literature -- Methodology -- Results -- Discussion -- Appendix A. Screening questionnaire -- Appendix B. Study information sheet consent form -- Appendix C. Demographics questionnaire -- Appendix D. Three-factor eating questionnaire -- Appendix E. Food rating scal