677 research outputs found

    Trends in Avoidable Death over 20 Years in Korea

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    To evaluate the achievement of health care services in Korea independent of other socioeconomic factors, we observed the time trend of avoidable death between 1983 and 2004. A list of avoidable causes of death was constructed based on the European Community Atlas of "Avoidable Death". We calculated sex- and age-standardized mortality rates of Korean aged 1-64 yr using data of the Korea National Statistical Office. The avoidable mortality rate (per 100,000 persons) decreased from 225 to 84 in men and from 122 to 41 in women. Accordingly, the proportion of avoidable deaths among all classifiable deaths was reduced by 8.1% in men and 6.4% in women. However, mortality rates from some preventable causes such as ischemic heart disease and malignant neoplasms of lung, breast, cervix, and colorectum have been on the rise. Mortality preventable by appropriate medical care showed the greatest reduction (by 77.8%), while the mortality preventable by primary prevention showed the least reduction (by 50.0%). These findings suggest that health care service has significantly contributed to the improvement of health in Korea. However, more effective intervention programs would be needed given the less reduction in mortality avoidable by primary or secondary prevention than expected and unexpectedly increasing mortality from several preventable causes

    Markedly enhanced intratumoral spread and antitumor effect of oncolytic adenovirus expressing decorin

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    With the aim of improving viral distribution and tumor penetration, we have engineered decorin expressing replication-incompetent (dl-LacZ-DCNG) and -competent (Ad-[DELTA]E1B-DCNG) adenoviruses. In both tumor spheroids and established solid tumors in vivo, administration of dl-LacZ-DCNG resulted in greater transduction efficiency and viral spread throughout the tumor mass. Ad-[DELTA]E1B-DCNG also enhanced viral distribution and tumor spread, leading to an increased anti-tumor effect and survival advantage. Upon histological analysis, Ad-[DELTA]E1B-DCNG also elicited greater percentage of apoptotic cells and extensive necrosis compared to those from untreated or control virus-treated tumors. Furthermore, Ad-[DELTA]E1B-DCNG substantially decreased extracellular matrix components within the tumor tissue, while normal tissue adjacent to the tumor was not affected. Finally, intratumoral administration of Ad-[DELTA]E1B-DCNG did not enhance but inhibited the formation of pulmonary metastases of B16BL6 melanoma cells in mice. Taken together, these data demonstrate the utility of decorin as a dispersion agent and suggest its utility and potential in improving the efficacy of replicating adenovirus-mediated cancer gene therapy

    Differential effect of NF-κB activity on β-catenin/Tcf pathway in various cancer cells

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    Abstractβ-Catenin/Tcf and NF-κB pathways play an important role in biological functions. We determined the underlying mechanisms of differential interaction between two pathways in various human cancer cell lines. NF-κB positively regulated β-catenin/Tcf pathways in human glioblastoma, whereas it has an opposite effect on β-catenin/Tcf pathways in colon, liver, and breast cancer cells. Expression of lucine zipper tumor suppressor 2 (lzts2) was positively regulated by NF-κB activity in colon, liver, and breast cancer cells, whereas negatively regulated in glioma cells. Downregulation of lzts2 increased the β-catenin/Tcf promoter activity and inhibited NF-κB-induced modulation of the nuclear translocation of β-catenin. These data indicate that the differential crosstalk between β-catenin/Tcf and NF-κB pathway in various cancer cells is resulted from the differences in the regulation of NF-κB-induced lzts2 expression

    Effect of software version and parameter settings on the marginal and internal adaptation of crowns fabricated with the CAD/CAM system

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    Objective This study investigated the marginal and internal adaptation of individual dental crowns fabricated using a CAD/CAM system (Sirona’s BlueCam), also evaluating the effect of the software version used, and the specific parameter settings in the adaptation of crowns.Material and Methods Forty digital impressions of a master model previously prepared were acquired using an intraoral scanner and divided into four groups based on the software version and on the spacer settings used. The versions 3.8 and 4.2 of the software were used, and the spacer parameter was set at either 40 μm or 80 μm. The marginal and internal fit of the crowns were measured using the replica technique, which uses a low viscosity silicone material that simulates the thickness of the cement layer. The data were analyzed using a Friedman two-way analysis of variance (ANOVA) and paired t-tests with significance level set at

    Insulin-inducible SMILE inhibits hepatic gluconeogenesis

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    The role of a glucagon/cAMP-dependent protein kinase–inducible coactivator PGC-1α signaling pathway is well characterized in hepatic gluconeogenesis. However, an opposing protein kinase B (PKB)/Akt-inducible corepressor signaling pathway is unknown. A previous report has demonstrated that small heterodimer partner–interacting leucine zipper protein (SMILE) regulates the nuclear receptors and transcriptional factors that control hepatic gluconeogenesis. Here, we show that hepatic SMILE expression was induced by feeding in normal mice but not in db/db and high-fat diet (HFD)-fed mice. Interestingly, SMILE expression was induced by insulin in mouse primary hepatocyte and liver. Hepatic SMILE expression was not altered by refeeding in liver-specific insulin receptor knockout (LIRKO) or PKB β-deficient (PKBβ−/−) mice. At the molecular level, SMILE inhibited hepatocyte nuclear factor 4–mediated transcriptional activity via direct competition with PGC-1α. Moreover, ablation of SMILE augmented gluconeogenesis and increased blood glucose levels in mice. Conversely, overexpression of SMILE reduced hepatic gluconeogenic gene expression and ameliorated hyperglycemia and glucose intolerance in db/db and HFD-fed mice. Therefore, SMILE is an insulin-inducible corepressor that suppresses hepatic gluconeogenesis. Small molecules that enhance SMILE expression would have potential for treating hyperglycemia in diabetes

    Establishment of Passive Energy Conservation Measure and Economic Evaluation of Fenestration System in Nonresidential Building of Korea

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    ECO2 (building energy efficiency rating program) and passive energy conservation measures (ECMs) were established as a basic study for targeted methodologies and decision support systems development in Korea to meet national regulations. The primary energy consumption and economic evaluation of nonresidential buildings was performed. Passive ECMs were classified as planning and performance elements. The planning elements are the window-to-wall ratio (WWR) and horizontal shading angle. The performance elements are the thermal transmittance (U-value) of the walls, roof, and floor and the U-value and solar heat gain coefficient (SHGC) of windows. This study focused on the window-to-wall ratio and the U-value and solar heat gain coefficient of windows. An economic efficiency database for the constructed alternatives was built; the target building was set and the Passive ECM List for the target building was derived. The energy consumption evaluation and economic evaluation were performed for each of the constructed alternatives, and a methodology for guiding energy efficiency decisions was proposed based on the performance evaluation results, and the optimal Passive ECM List for the target building was derived

    JNK pathway is involved in the inhibition of inflammatory target gene expression and NF-kappaB activation by melittin

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    <p>Abstract</p> <p>Background</p> <p>Bee venom therapy has been used to treat inflammatory diseases including rheumatoid arthritis in humans and in experimental animals. We previously found that bee venom and melittin (a major component of bee venom) have anti-inflammatory effect by reacting with the sulfhydryl group of p50 of nuclear factor-kappa B (NF-κB) and IκB kinases (IKKs). Since mitogen activated protein (MAP) kinase family is implicated in the NF-κB activation and inflammatory reaction, we further investigated whether activation of MAP kinase may be also involved in the anti-inflammatory effect of melittin and bee venom.</p> <p>Methods</p> <p>The anti-inflammatory effects of melittin and bee venom were investigated in cultured Raw 264.7 cells, THP-1 human monocytic cells and Synoviocytes. The activation of NF-κB was investigated by electrophoretic mobility shift assay. Nitric oxide (NO) and prostaglandin E<sub>2 </sub>(PGE<sub>2</sub>) were determined either by Enzyme Linked Immuno Sorbent Assay or by biochemical assay. Expression of IκB, p50, p65, inducible nitric oxide synthetase (iNOS), cyclooxygenase-2 (COX-2) as well as phosphorylation of MAP kinase family was determined by Western blot.</p> <p>Results</p> <p>Melittin (0.5–5 μg/ml) and bee venom (5 and 10 μg/ml) inhibited lipopolysaccharide (LPS, 1 μg/ml) and sodium nitroprusside (SNP, 200 μM)-induced activation of c-Jun NH2-terminal kinase (JNK) in RAW 264.7 cells in a dose dependent manner. However, JNK inhibitor, anthra [1,9-cd]pyrazole-6 (2H)-one (SP600215, 10–50 μM) dose dependently suppressed the inhibitory effects of melittin and bee venom on NF-κB dependent luciferase and DNA binding activity via suppression of the inhibitory effect of melittin and bee venom on the LPS and SNP-induced translocation of p65 and p50 into nucleus as well as cytosolic release of IκB. Moreover, JNK inhibitor suppressed the inhibitory effects of melittin and bee venom on iNOS and COX-2 expression, and on NO and PGE<sub>2 </sub>generation.</p> <p>Conclusion</p> <p>These data show that melittin and bee venom prevent LPS and SNP-induced NO and PGE<sub>2 </sub>production via JNK pathway dependent inactivation of NF-κB, and suggest that inactivation of JNK pathways may also contribute to the anti-inflammatory and anti-arthritis effects of melittin and bee venom.</p
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