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The purpose of this study was to evaluate marginal leakage of composite resin restoration from cavities prepared by Er:YAG laser. The observation of the dentin surface after the application of laser irradiation was performed by LSM, the cutting surface showed a rough surface similar to scales, and exposed dentinal tubules were observed without striations or a smeared layer formation that were observed when using a rotary cutting device. Leakage tests revealed no significant differences in the marginal seal for both enamel and dentin between cavities prepared by Er:YAG laser irradiation and when using an air-turbine. In this study, the usefulness of cavity preparation by Er:YAG laser irradiation in composite resin restoration was suggested.  相似文献   
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Clinical and Experimental Nephrology - We investigated whether butyrylcholinesterase (BChE) was independently related to the overall survival (OS) of patients on maintenance hemodialysis (MHD)....  相似文献   
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The apical junctional complex consists of adherens junctions (AJs) and tight junctions (TJs) in polarized epithelial cells, which are attached to each other to form a sheet. Actin filaments (F‐actin) are associated with AJs and TJs and required for the formation and maintenance of this complex. l‐Afadin is an F‐actin‐binding protein, which is localized at AJs through binding to the cell adhesion molecule nectin, and regulates the formation of AJs and TJs. However, the role of the F‐actin‐binding activity of l‐afadin for the formation of the apical junctional complex remains unknown. We generated here the cultured EpH4 mouse mammary epithelial cells in which afadin was genetically ablated. In the Ca2+ switch assay, the formation of both AJs and TJs was markedly impaired in the afadin‐deficient cells. Re‐expression of l‐afadin in the afadin‐deficient cells fully restored the formation of both AJs and TJs, but the re‐expression of the l‐afadin mutant lacking the FAB domain did not completely restore the formation of AJs or TJs. These results indicate that the F‐actin‐binding activity of l‐afadin is required for enhancing the formation of both AJs and TJs.  相似文献   
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Metabolic acidosis is the serious acid-base balance disorder complicated in diabetes mellitus. The pathogenesis and treatment of various type of metabolic acidosis (Keto-acidosis, lactic acidosis, hyperchloremic acidosis and type IV renal tubular acidosis) are discussed. Metabolic acidosis in the diabetic patient is associated with an increased anion-gap caused by the presence of organic anion (beta-hydroxybutyrate, acetoacetate, and lactate). The rise in anion-gap usually equals the fall in plasma bicarbonate. With appropriate therapy, progressive decline in the anion-gap is one of the best indications of successful treatment. If hyperchloremic acidosis is established, appropriate infusion of hypochloremic rehydration fluid may be useful.  相似文献   
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The effects of reaction environments on the radical-scavenging mechanisms of ascorbic acid (AscH2) were investigated using 2,2-diphenyl-1-picrylhydrazyl radical (DPPH) as a reactivity model of reactive oxygen species. Water-insoluble DPPH was solubilized by β-cyclodextrin (β-CD) in water. The DPPH-scavenging rate of AscH2 in methanol (MeOH) was much slower than that in phosphate buffer (0.05 M, pH 7.0). An organic soluble 5,6-isopropylidene-l-ascorbic acid (iAscH2) scavenged DPPH much slower in acetonitrile (MeCN) than in MeOH. In MeOH, Mg(ClO4)2 significantly decelerated the DPPH-scavenging reaction by AscH2 and iAscH2, while no effect of Mg(ClO4)2 was observed in MeCN. On the other hand, Mg(ClO4)2 significantly accelerated the reaction between AscH2 and β-CD-solubilized DPPH (DPPH/β-CD) in phosphate buffer (0.05 M, pH 6.5), although the addition of 0.05 M Mg(ClO4)2 to the AscH2–DPPH/β-CD system in phosphate buffer (0.05 M, pH 7.0) resulted in the change in pH of the phosphate buffer to be 6.5. Thus, the DPPH-scavenging reaction by iAscH2 in MeCN may proceed via a one-step hydrogen-atom transfer, while an electron-transfer pathway is involved in the reaction between AscH2 and DPPH/β-CD in phosphate buffer solution. These results demonstrate that the DPPH-scavenging mechanism of AscH2 are affected by the reaction environments.  相似文献   
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The present study was designed to investigate the influence of modifiable risk factors (body weight and lifestyle) for bone loss on bone mineral density (BMD). We examined age-specific changes in metacarpal BMD, and its associations with body mass index and lifestyle among 532 community-dwelling postmenopausal Japanese women. Measurements of the second metacarpal BMD were obtained from the hand radiographs using computer-assisted radiographic absorptiometry. Body height and weight were measured, and body mass index (BMI) was calculated. Physical activity index was calculated using validated questionnaire. Daily calcium intake and amount of ingested alcohol were estimated by semiquantitative food frequency questionnaire. Current smoking status was obtained by questionnaire. Metacarpal BMD decreased significantly with increasing age. Simple correlation analysis indicated that metacarpal BMD correlated significantly with BMI and physical activity index. On the other hand, metacarpal BMD did not correlate with calcium intake and alcohol drinking. Metacarpal BMD in current smokers was not different from that in nonsmokers. Multiple regression analysis showed that increasing age was associated with decreased metacarpal BMD and greater BMI increased metacarpal BMD. However, physical activity, calcium intake, alcohol drinking and current smoking were not significant determinants of metacarpal BMD. Our findings suggest that maintenance of adequate body mass (prevention for leanness) is important for prevention of postmenopausal bone loss.  相似文献   
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