カフェイン酸フェネチルエステル（CAPE）がラット象牙芽細胞様細胞のVEGF発現と産生に与える影響

Caffeic acid phenethyl ester (CAPE), the main component of propolis, has various biological activities including anti-inflammatory effect and wound healing promotion. Odontoblasts located in the outermost layer of dental pulp play crucial roles such as production of growth factors and formation of hard tissue termed reparative dentin in host defense against dental caries. In this study, we investigated the effects of CAPE on the upregulation of vascular endothelial growth factor (VEGF) and calcification activities of odontoblasts, leading to development of novel therapy for dental pulp inflammation caused by dental caries. CAPE significantly induced mRNA expression and production of VEGF in rat clonal odontoblast-like KN-3 cells cultured in normal medium or osteogenic induction medium. CAPE treatment enhanced nuclear factor-kappa B (NF-κB) transcription factor activation, and furthermore, the specific inhibitor of NF-κB significantly reduced VEGF production. The expression of VEGF receptor- (VEGFR-) 2, not VEGFR-1, was up regulated in KN-3 cells treated with CAPE. In addition, VEGF significantly increased mineralization activity in KN-3 cells. These findings suggest that CAPE might be useful as a novel biological material for the dental pulp conservative therapy

Pachychoroid neovasculopathy and age-related macular degeneration.

Pachychoroid neovasculopathy is a recently proposed clinical entity of choroidal neovascularization (CNV). As it often masquerades as neovascular age-related macular degeneration (AMD), it is currently controversial whether pachychoroid neovasculopathy should be distinguished from neovascular AMD. This is because its characteristics have yet to be well described. To estimate the relative prevalence of pachychoroid neovasculopathy in comparison with neovascular AMD and to investigate the phenotypic/genetic differences of the two diseases, we evaluated 200 consecutive Japanese patients who agreed to participate in the genetic study and diagnosed with pachychoroid neovasculopathy or neovascular AMD. Pachychoroid neovasculopathy was observed in 39 individuals (19. 5%), which corresponds to one fourth of neovascular AMD. Patients with pachychoroid neovasculopathy were significantly younger (p = 5. 1 × 10[−5]) and showed a greater subfoveal choroidal thickness (p = 3. 4 × 10[−14]). Their genetic susceptibility to AMD was significantly lower than that of neovascular AMD; ARMS2 rs10490924 (p = 0. 029), CFH rs800292 (p = 0. 013) and genetic risk score calculated from 11 AMD susceptibility genes (p = 3.8 × 10[−3]). Current results implicate that the etiologies of the two conditions must be different. Thus, it will be necessary to distinguish these two conditions in future studie

歯髄象牙芽細胞の自然免疫反応におけるNOD1の役割

Caries-related pathogens are first recognized by odontoblasts and induce inflammatory events that develop to pulpitis. Generally, initial sensing of microbial pathogens is mediated by pattern recognition receptors, such as Toll-like receptor and nucleotide-binding oligomerization domain (NOD); however, little is known about NODs in odontoblasts. In this study, the levels of NODs expressed in rat odontoblastic cell line, KN-3, were assessed by flow cytometry and the levels of chemokines in NOD-specific ligand-stimulated KN-3 cells were analyzed by real-time PCR and ELISA. The signal transduction pathway activated with NOD-specific ligand was assessed by blocking assay with specific inhibitors and reporter assay. In KN-3 cells, the expression level of NOD1 was stronger than that of NOD2 and the production of chemokines, such as CINC-1, CINC-2, CCL20, and MCP-1, was upregulated by stimulation with NOD1-specific ligand, but not with NOD2-specific ligand. CINC-2 and CCL20 production by stimulation with NOD1-specific ligand was reduced by p38 MAPK and AP-1 signaling inhibitors. Furthermore, the reporter assay demonstrated AP-1 activation in NOD1-specific ligand-stimulated KN-3 cells. These findings indicated that NOD1 expressed in odontoblasts functions to upregulate the chemokines expression via p38-AP-1 signaling pathway and suggested that NOD1 may play important roles in the initiation and progression of pulpitis

Geometry of the Philippine Sea plate subducting beneath the westernmost Nankai Trough

SSS035-06発表要旨 / 日本地球惑星科学連合2011年大会（2011年5月22日～5月27日, 幕張メッセ国際会議場） / 日本惑星科学連合の許諾に基づき本文ファイルを掲

構造研究に基づく南海トラフ（西部）地震発生帯のプレート形状および速度構造の3次元モデル

Great interplate earthquakes have repeatedly occurred in pairs along the Nankai Trough. In order to reduce a great deal of damage to coastal area from both strong ground motion and tsunami generation, it is necessary to understand rupture synchronization and segmentation of the Nankai megathrust earthquake. For a precise estimate of the rupture zone of the Nankai megathrust event based on the knowledge of realistic earthquake cycles and variations of magnitude, it is important to know the geometry and property of the plate boundary of the subduction seismogenic zone. To improve a physical model of the Nankai Trough seismogenic zone, the large-scale high-resolution wide-angle and reflection (MCS) seismic studies, and long-term observation have been conducted since 2008. Marine active source seismic data have been acquired along grid two-dimensional profiles having the total length of ~800km per year. A three-dimensional seismic tomography using active and passive seismic data observed both land and ocean bottom stations have been also performed. This study is part of 'Research concerning Interaction Between the Tokai, Tonankai and Nankai Earthquakes' funded by Ministry of Education, Culture, Sports, Science and Technology, Japan. The seismic survey was conducted off the Tokai area including the onshore survey across the eastern Kii Peninsula in 2012, the final year of this project. Compiling those studies provides a three-dimensional plate geometry and velocity structure models of the western Nankai Trough at the moment. Although their reliability and resolution should be evaluated, these models can be applied to a numerical simulation to examine if the observed rupture zone of the historical event can be reproduced. We will also try to construct more fine-scale model for the entire Nankai Trough area.SSS31-P15ポスター要旨 / 日本地球惑星科学連合2013年大会（2013年5月19日～5月24日, 幕張メッセ国際会議場） / 日本惑星科学連合の許諾に基づき本文ファイルを掲載http://www.godac.jamstec.go.jp/darwin/cruise/kairei/kr10-11/ehttp://www.godac.jamstec.go.jp/darwin/cruise/kairei/kr11-09/