1.Disability-adjusted Life Years for 313 Diseases and Injuries: the 2012 Korean Burden of Disease Study.
Jihyun YOON ; In Hwan OH ; Hyeyoung SEO ; Eun Jung KIM ; Young Hoon GONG ; Minsu OCK ; Dohee LIM ; Won Kyung LEE ; Ye Rin LEE ; Dongwoo KIM ; Min Woo JO ; Hyesook PARK ; Seok Jun YOON
Journal of Korean Medical Science 2016;31(Suppl 2):S146-S157
This study is part of a 5-year research project on the national burden of diseases, injuries, and risk factors in Korea. Using disability-adjusted life years (DALYs), a metric introduced by the 1990 Global Burden of Disease (GBD) project, we performed a comprehensive and detailed assessment of the magnitude and distribution of both fatal and non-fatal health problems in the Korean population. The concept and general approach were consistent with the original GBD study, with some methodological modifications to make the study more suitable for Korea. We computed DALYs for 313 causes in both sexes and nine age groups using the entire population's medical records and newly generated Korean disability weights. In 2012, the dominant disease burden was non-communicable diseases, which accounted for 85.21% of total DALYs, while injuries accounted for 7.77% and communicable, maternal, neonatal, and nutritional disorders for 7.02%. Of the total DALYs, 88.67% were from years lived with disability and 11.32% were from years of life lost due to premature mortality. Diabetes mellitus was the leading cause of DALYs, followed by low back pain, chronic obstructive pulmonary disease, ischemic heart disease, ischemic stroke, cirrhosis of the liver, falls, osteoarthritis, motorized vehicle with three or more wheels, and self-harm. The results reported here identify key health challenges and opportunities for future health interventions and policy changes, and provide information that will help assess the major public health issues in Korea, a nation faced with one of the world's most rapidly ageing populations.
Accidental Falls
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Child
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Diabetes Mellitus
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Fibrosis
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Health Policy
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Humans
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Korea
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Liver
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Low Back Pain
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Medical Records
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Mortality, Premature
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Myocardial Ischemia
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Nutrition Disorders
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Osteoarthritis
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Public Health
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Pulmonary Disease, Chronic Obstructive
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Risk Factors
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Stroke
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Weights and Measures
2.Sphingosine-1-phosphate hinders the osteogenic differentiation of dental pulp stem cells in association with AKT signaling pathways.
Bongkun CHOI ; Ji-Eun KIM ; Si-On PARK ; Eun-Young KIM ; Soyoon OH ; Hyuksu CHOI ; Dohee YOON ; Hyo-Jin MIN ; Hyung-Ryong KIM ; Eun-Ju CHANG
International Journal of Oral Science 2022;14(1):21-21
Sphingosine-1-phosphate (S1P) is an important lipid mediator that regulates a diverse range of intracellular cell signaling pathways that are relevant to tissue engineering and regenerative medicine. However, the precise function of S1P in dental pulp stem cells (DPSCs) and its osteogenic differentiation remains unclear. We here investigated the function of S1P/S1P receptor (S1PR)-mediated cellular signaling in the osteogenic differentiation of DPSCs and clarified the fundamental signaling pathway. Our results showed that S1P-treated DPSCs exhibited a low rate of differentiation toward the osteogenic phenotype in association with a marked reduction in osteogenesis-related gene expression and AKT activation. Of note, both S1PR1/S1PR3 and S1PR2 agonists significantly downregulated the expression of osteogenic genes and suppressed AKT activation, resulting in an attenuated osteogenic capacity of DPSCs. Most importantly, an AKT activator completely abrogated the S1P-mediated downregulation of osteoblastic markers and partially prevented S1P-mediated attenuation effects during osteogenesis. Intriguingly, the pro-inflammatory TNF-α cytokine promoted the infiltration of macrophages toward DPSCs and induced S1P production in both DPSCs and macrophages. Our findings indicate that the elevation of S1P under inflammatory conditions suppresses the osteogenic capacity of the DPSCs responsible for regenerative endodontics.
Cell Differentiation
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Cell Proliferation
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Cells, Cultured
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Dental Pulp/metabolism*
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Lysophospholipids
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Osteogenesis
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Proto-Oncogene Proteins c-akt/metabolism*
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Signal Transduction
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Sphingosine/analogs & derivatives*
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Stem Cells