フィリピン・ルソン島地震の高密度震度分布調査

1990年7月16日午後4時26分(現地時間)にフィリピン・ルソン島の中央部に発生したフィリピン地震(M= 7.8) は，内陸部に発生した最大級の地震であり，延長約120km，水平平均ずれ量約5.0mに及ぶ左横ずれ断層が出現した。震度地は，首都マニラの北北東約110kmのDigdig断層上で，震度の深さは約25kmとされている。本地震において，多数の建物が被災し約2000名の死者と3500名の負傷者が発生し，全壊建物約22000棟，被災者約160万人に及び被害が発生した。この地震による被害は，地震断層に沿った広範囲の地域に発生したが，被害が比較的集中的に発生した地域は，震央近傍の地域より，むしろ上記地震断層の北西方向の末端部の西側に位置している地域に多数の被害建物が認められた。また，Lingayen湾に面した沿岸地域の沖積軟弱地盤地帯においては，顕著な液状化現象が発生し，多数の構造物に被害が認められた。しかし，残念ながら本地震の被災地域における強震観測記録は得られていない。本研究の目的は，アンケートによる震度推定法を用いて本地震の震源域を中心とする広い範囲の地域における震度(MM震度)を可能な限り高密度に推定し，強震記録に代わる情報のひとつとして各地の地震動の強さとその分布状況を推定することである。また，被害地域といえども，ごく狭い地域でさえ被害程度に大きな差を生じることは過去の地震において確認され，今回の地震においてもまた同様の傾向がみられた。そこで，可能な限り高密度の震度分布を推定し，被害分布などともにいわゆるサイミックマイクロゾーニングマップを作成することを最終的な目的としている。本報告は，これまでに分析ができた各地の震度分布の結果を示したのである。その結果，調査地域内の主要都市の推定震度では， La Union 州のAgoo町が最も大きく平均震度(MM震度)で10.7となり，次いでAringay町で9.8，Baguio市で8.8となるO 以下，Dagupan市で8.7，Cabanatuan市で7.8，San Carlos市で7.7，首都Manilaの北側に隣接するQuezon市で6.5と推定された。また，各州や主要都市における震度分布も明かとなっている。本調査により，1990年フィリピン地震の震源域における震度分布がほぼ明かとなり，震度分布は被害分布とよく対応し，地震動の強さを推測する上で重要な情報を提供するものと考えられる

Impact Properties of TiC Dispersed Molybdenum Alloys Exposed to 2273 K Heating

Ultra-fine grained molybdenum alloys with fine TiC particles at grain boundaries that were recently developed by the authors are very promising for the application to divertor components in advanced fusion devices. In order to examine the impact toughness and microstructural change of the alloys which were exposed to high temperature heating, miniaturized flat specimens, 1 mm by 1 mm by 20 mm, of both the alloys with TiC additions to 1.0 wt% and TZM alloy were subjected to vacuum heating up to 2273 K for 3.6 ks. The impact toughness was evaluated by three-point bending tests. It is shown that the developed alloys exhibit much improved toughness (lower ductile-to-brittle transition temperature and higher yield and maximum strengths) and the toughness increases both by increasing TiC content and by using mechanical alloying (MA) treatment for fabrication : the ductile-to-brittle transition temperature of the MA treated alloy with 1 wt% TiC is 75 K lower than that of TZM. In addition, the alloy with 1 wt% TiC shows no significant grain growth, though TEM observation indicate the occurrence of recrystallization

Development of Nanostructured Tungsten Based Materials Resistant to Recrystallization and/or Radiation Induced Embrittlement

Mitigation of embrittlement caused by recrystallization and radiation is the key issue of tungsten (W) based materials for use in the advanced nuclear system such as fusion reactor applications. In this paper, our nanostructured W materials development performed so far to solve the key issue is reviewed, including new original data. Firstly, the basic concept of mitigation of the embrittlement is shown. The approach to the concept has yielded ultra-fine grained, recrystallized (UFGR) W–(0.25–1.5) mass%TiC compacts containing fine TiC dispersoids (precipitates). The UFGR W–(0.25–1.5)%TiC exhibits favorable as well as unfavorable features from the viewpoints of microstructures and various thermo-mechanical properties including the response to neutron and ion irradiations. Most of the unfavorable features stem from insufficient strengthening of weak random grain boundaries (GBs) in the recrystallized state. The focal point on this study is, therefore, to develop a new microstructural modification method to significantly strengthen the random GBs. The method is designated as GSMM (GB Sliding-based Microstructural Modification) and has lead to the birth of toughened, fine-grained W–1.1%TiC in the recrystallized state (TFGR W–1.1TiC). The TFGR W–1.1TiC exhibits much improved thermo-mechanical properties. The applicability of TFGR W–1.1TiC to the divertor in ITER is discussed

Plasma Membrane and Nuclear Localization of G Protein–coupled Receptor Kinase 6A

G protein–coupled receptor (GPCR) kinases (GRKs) specifically phosphorylate agonist-occupied GPCRs at the inner surface of the plasma membrane (PM), leading to receptor desensitization. Here we show that the C-terminal 30 amino acids of GRK6A contain multiple elements that either promote or inhibit PM localization. Disruption of palmitoylation by individual mutation of cysteine 561, 562, or 565 or treatment of cells with 2-bromopalmitate shifts GRK6A from the PM to both the cytoplasm and nucleus. Likewise, disruption of the hydrophobic nature of a predicted amphipathic helix by mutation of two leucines to alanines at positions 551 and 552 causes a loss of PM localization. Moreover, acidic amino acids in the C-terminus appear to negatively regulate PM localization; mutational replacement of several acidic residues with neutral or basic residues rescues PM localization of a palmitoylation-defective GRK6A. Last, we characterize the novel nuclear localization, showing that nuclear export of nonpalmitoylated GRK6A is sensitive to leptomycin B and that GRK6A contains a potential nuclear localization signal. Our results suggest that the C-terminus of GRK6A contains a novel electrostatic palmitoyl switch in which acidic residues weaken the membrane-binding strength of the amphipathic helix, thus allowing changes in palmitoylation to regulate PM versus cytoplasmic/nuclear localization