Pemodelan Pertumbuhan Ekonomi Provinsi Sumatera Utara Dengan Pendekatan Ekonometrika Spasial Data Panel

Salah satu indikator untuk melihat keberhasilan pembangunan suatu wilayah dapat dilihat dari pertumbuhan ekonominya. Dalam analisis pertumbuhan ekonomi, indikator yang menunjukkan pertumbuhan nyata ekonomi suatu wilayah adalah PDRB atas dasar harga konstan. Pertumbuhan ekonomi suatu wilayah memiliki kecenderungan berkaitan dengan wilayah sekitarnya, sehingga diperlukan model ekonometrika spasial yang dapat mengakomodasi adanya keterkaitan antar wilayah tersebut. Pada penelitian ini menggunakan pemodelan pertumbuhan ekonomi dengan model ekonometrika spasial data panel. Model spasial yang dibangun dalam penelitian ini yaitu Spatial Autoregressive Model (SAR) dan Spatial Error Model (SEM) dengan melibatkan model panel pooled, fixed effects dan random effects menggunakan prosedur estimasi maximum likelihood. Terdapat dua pembobot spasial yang digunakan, yaitu pembobot queen contiguity dan customize. Pembobot queen contiguity dibentuk berdasarkan ketersinggungan sisi sudut. Pembobot customize dibentuk berdasarkan faktor lain yaitu keterkaitan infrastuktur berupa jalan nasional, jalan provinsi serta Kota Medan sebagai pusat perekonomian. Model terbaik pada pemodelan pertumbuhan ekonomi kabupaten/kota di Provinsi Sumatera Utara adalah SAR pooled dengan pembobot queen contiguity, dengan variabel signifikan yang mempengaruhi pertumbuhan ekonomi kabupaten/kota di Provinsi Sumatera Utara adalah pendapatan asli daerah dengan elastisitas sebesar 0,4044, belanja modal dengan elastisitas sebesar 0,6144 dan rumah tangga pengguna listrik dengan elastisitas sebesar 0,6609

Actinic Skin Damage and Mortality - the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study

BACKGROUND: Exposure to sunlight may decrease the risk of several diseases through the synthesis of vitamin D, whereas solar radiation is the main cause of some skin and eye diseases. However, to the best of our knowledge, the association of sun-induced skin damage with mortality remains unknown. METHODOLOGY/PRINCIPAL FINDINGS: Subjects were 8472 white participants aged 25-74 years in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Cardiovascular disease mortality, cancer mortality, and all-cause mortality were obtained by either a death certificate or a proxy interview, or both. Actinic skin damage was examined and recorded by the presence and severity (absent, minimal, moderate, or severe) of overall actinic skin damage and its components (i.e., fine telangiectasia, solar elastosis, and actinic keratoses). Cox regression and Kaplan-Meier methods were applied to explore the associations. A total of 672 cancer deaths, 1500 cardiovascular disease deaths, and 2969 deaths from all causes were documented through the follow-up between 1971 and 1992. After controlling for potential confounding variables, severe overall actinic skin damage was associated with a 45% higher risk for all-cause mortality (95% CI: 1.22, 1.72; P<0.001), moderate overall skin damage with a 20% higher risk (95% CI: 1.08., 1.32; P<0.001), and minimal overall skin damage with no significant mortality difference, when compared to those with no skin damage. Similar results were obtained for all-cause mortality with fine telangiectasia, solar elastosis, and actinic keratoses. The results were similar for cancer and cardiovascular disease mortality. CONCLUSIONS: The present study gives an indication of an association of actinic skin damage with cardiovascular disease, cancer and all-cause mortality in white subjects. Given the lack of support in the scientific literature and potential unmeasured confounding factors, this finding should be interpreted with caution. More independent studies are needed before any practical recommendations can be made

Does the oxytocin receptor polymorphism (rs2254298) confer 'vulnerability' for psychopathology or 'differential susceptibility'? insights from evolution

The diathesis-stress model of psychiatric conditions has recently been challenged by the view that it might be more accurate to speak of 'differential susceptibility' or 'plasticity' genes, rather than one-sidedly focusing on individual vulnerability. That is, the same allelic variation that predisposes to a psychiatric disorder if associated with (developmentally early) environmental adversity may lead to a better-than-average functional outcome in the same domain under thriving (or favourable) environmental conditions. Studies of polymorphic variations of the serotonin transporter gene, the monoamino-oxidase-inhibitor A coding gene or the dopamine D4 receptor gene indicate that the early environment plays a crucial role in the development of favourable versus unfavourable outcomes. Current evidence is limited, however, to establishing a link between genetic variation and behavioural phenotypes. In contrast, little is known about how plasticity may be expressed at the neuroanatomical level as a 'hard-wired' correlate of observable behaviour. The present review article seeks to further strengthen the argument in favour of the differential susceptibility theory by incorporating findings from behavioural and neuroanatomical studies in relation to genetic variation of the oxytocin receptor gene. It is suggested that polymorphic variation at the oxytocin receptor gene (rs2254298) is associated with sociability, amygdala volume and differential risk for psychiatric conditions including autism, depression and anxiety disorder, depending on the quality of early environmental experiences. Seeing genetic variation at the core of developmental plasticity can explain, in contrast to the diathesis-stress perspective, why evolution by natural selection has maintained such 'risk' alleles in the gene pool of a population