Hadronic decays of B→a1(1260)b1(1235)B \to a_1(1260) b_1(1235) in the perturbative QCD approach

We calculate the branching ratios and polarization fractions of the $B \to a_1 b_1$ decays in the perturbative QCD(pQCD) approach at leading order, where $a_1$($b_1$) stands for the axial-vector $a_1(1260)[b_1(1235)]$ state. By combining the phenomenological analyses with the perturbative calculations, we find the following results: (a) the large decay rates around $10^{-5}$ to $10^{-6}$ of the $B \to a_1 b_1$ decays dominated by the longitudinal polarization(except for the $B^+ \to b_1^+ a_1^0$ mode) are predicted and basically consistent with those in the QCD factorization(QCDF) within errors, which are expected to be tested by the Large Hadron Collider and Belle-II experiments. The large $B^0 \to a_1^0 b_1^0$ branching ratio could provide hints to help explore the mechanism of the color-suppressed decays. (b) the rather different QCD behaviors between the $a_1$ and $b_1$ mesons result in the destructive(constructive) contributions in the nonfactorizable spectator diagrams with $a_1(b_1)$ emission. Therefore, an interesting pattern of the branching ratios appears for the color-suppressed $B^0 \to a_1^0 a_1^0, a_1^0 b_1^0,$ and $b_1^0 b_1^0$ modes in the pQCD approach, $Br(B^0 \to b_1^0 b_1^0) > Br(B^0 \to a_1^0 b_1^0) \gtrsim Br(B^0 \to a_1^0 a_1^0)$, which is different from $Br(B^0 \to b_1^0 b_1^0) \sim Br(B^0 \to a_1^0 b_1^0) \gtrsim Br(B^0 \to a_1^0 a_1^0)$ in the QCDF and would be verified at future experiments. (c) the large naive factorization breaking effects are observed in these $B \to a_1 b_1$ decays. Specifically, the large nonfactorizable spectator(weak annihilation) amplitudes contribute to the $B^0 \to b_1^+ a_1^-(B^+ \to a_1^+ b_1^0\; {\rm and}\; B^+ \to b_1^+ a_1^0)$ mode(s), which demand confirmations via the precise measurements.Comment: 13 pages, 1 figure, 5 tables, revtex fil

TSVを考慮した3次元積層プロセッサ向けフロアプランナの提案とマルチコアプロセッサの配置設計

近年半導体技術の進歩により3次元積層技術が開発され、半導体チップの更なる性能向上が期待されている。 3次元積層実装を行うことによってトランジスタ数あたりのチップ面積（フットプリント）を減少させることが出来、さらにはモジュール（一定の機能をもったひとまとまりの回路）同士の幾何学的な距離が短くなり，平面配置に比べて配線長を短縮することが出来る。さらに、積層間の結線を行う際にチップ外に配線を通して結線するワイヤボンディングに代わり、積層内を貫通する電極であるTSVを用いる事で積層間配線長を短縮できるようになった。3次元積層技術の利点としてチップ面積の減少とそれに伴う歩留まりの向上、モジュール間配線の減少による高速化と消費電力の減少、バンド幅の増加、異なるプロセスの混在など数多くの利点が挙げられ、TSVによる柔軟な配線はこれらをさらに促進する。一方で3次元積層技術の問題点は、設計の難化、製造コストの増大、熱密度の増加が挙げられる。柔軟な層間配線を可能とするTSVだが、通常配線に比べれば100?1000倍程度の大きさとなる。更に総配線長はTSVがどこに配置されるかによって大きく変化する。しかし、従来の手法ではモジュール位置が優先され，TSVの配置が最適化されない。そこで本論文では複数のTSVをまとめて扱い，TSV配置を準最適化する探索配置アルゴリズムを提案する。我々の手法ではTSVを配置するための場所を仮想的なモジュール、「TSVモジュール」として他のモジュールと同様に探索アルゴリズムに従って準最適化する。提案システムの評価ではシングルコアプロセッサ、マルチコアプロセッサについてフロアプランを取得した。 これらの評価を行い、TSVモジュールを導入することでいままでより配線が向上したフロアプランを得ることが出来た。これはシングルコアだけではなくマルチコアでも同様なことが言えた。また、従来のシーケンスペアではホワイトスペースが出来ないような位置にTSVモジュールが存在することで、本来の手法では配置されないような場所にもTSVを配置するのに適した場所が存在する事がわかった。電気通信大学201

Minimum energy broadcast on rectangular grid wireless networks

The minimum energy broadcast problem is to assign a transmission range to each node in an ad hoc wireless network to construct a spanning tree rooted at a given source node such that any non-root node resides within the transmission range of its parent. The objective is to minimize the total energy consumption, i.e., the sum of the δth powers of a transmission range (δ<1). In this paper, we consider the case that δ=2, and that nodes are located on a 2-dimensional rectangular grid. We prove that the minimum energy consumption for an n-node k×l-grid with n=kl and k≤l is at most nπ+O(n k0.68) and at least nπ+Ω(nk)-O(k). Our bounds close the previously known gap of upper and lower bounds for square grids. Moreover, our lower bound is n3-O(1) for 3≤k≤18, which matches a naive upper bound within a constant term for k≡0(mod3). © 2011 Elsevier B.V. All rights reserved

A personal tourism navigation system to support traveling multiple destinations with time restrictions

AINA2004 : The 18th International Conference on Advanced Information Networking and Applications , Mar 29 -31, 2004 , Fukuoka, JapanWe propose a personal navigation system (called PNS) which navigates a tourist through multiple destinations efficiently. In our PNS, a tourist can specify multiple destinations with desired arrival/stay time and preference degree. The system calculates the route including part of the destinations satisfying tourist's requirements and navigates him/her. For the above route search problem, we have developed an efficient route search algorithm using a genetic algorithm. We have designed and implemented the PNS as a client-server system so that the portable device users can use the PNS through the Internet. Experiments using general map data and PDAs show that our PNS can calculate a semioptimal route almost in real-time

Axillary artery injury combined with delayed brachial plexus palsy due to compressive hematoma in a young patient: a case report

<p>Abstract</p> <p>Introduction</p> <p>Axillary artery injury in the shoulder region following blunt trauma without association with either shoulder dislocation or fracture of the humeral neck has been previously reported. Axillary artery injury might also be accompanied with brachial plexus injury. However, delayed onset of brachial plexus palsy caused by a compressive hematoma associated with axillary injury after blunt trauma in the shoulder region has been rarely reported. In previous reports, this condition only occurred in old patients with sclerotic vessels. We present a case of a young patient who suffered axillary artery injury associated with brachial plexus palsy that occurred tardily due to compressive hematoma after blunt trauma in the shoulder region without association of either shoulder dislocation or humeral neck fracture.</p> <p>Case presentation</p> <p>A 16-year-old male injured his right shoulder in a motorbike accident. On initial physical evaluation, the pulses on the radial and ulnar arteries in the affected arm were palpable. Paralysis developed later from 2 days after the injury. Functions in the right arm became significantly impaired. Angiography showed complete occlusion of the axillary artery. Magnetic resonance imaging demonstrated a mass measuring 4 × 5 cm that was suspected to be a hematoma compressing the brachial plexus in a space between the subscapular muscle and the pectoralis minor muscle. Surgery was performed on the third day after injury. In intraoperative observations, the axillary artery was occluded with thrombus along 5 cm; a subscapular artery was ruptured; the brachial plexus was compressed by the hematoma. After evacuation of the hematoma, neurolysis of the brachial plexus, and revascularization of the axillary artery, the patient had an excellent functional recovery of the affected upper limb, postoperatively.</p> <p>Conclusion</p> <p>Surgeons should be aware that axillary artery injuries may even occur in young people after severe blunt trauma in the shoulder region and can be associated with secondary brachial plexus injury due to a hematoma. For treatment in cases with progressive nervous deficit after trauma, not only reconstruction of the injured artery but also immediate evacuation of the hematoma, and exploration of the brachial plexus are necessary to avoid irreversible neurological damage.</p

骨巨細胞腫における骨芽細胞系分化マーカーの発現パターン

取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1725号 , 学位授与年月日 : 平成17年12月31日, 学位授与大学 : 金沢大

Suppression of cell cycle progression by Jun dimerization protein (JDP2) involves down-regulation of cyclin A2

We report here a novel role for Jun dimerization protein-2 (JDP2) as a regulator of the progression of normal cells through the cell cycle. To determine the role of JDP2 in vivo, we generated Jdp2 knock-out (Jdp2KO) mice by targeting exon 1 to disrupt the site of initiation of transcription. The healing of wounded skin of Jdp2KO mice proceeded more rapidly than that of control mice and more proliferating cells were found at wound margins. Fibroblasts derived from embryos of Jdp2KO mice proliferated more rapidly and formed more colonies than wild-type fibroblasts. JDP2 was recruited to the promoter of the gene for cyclin A2 (ccna2) at a previously unidentified AP-1 site. Cells lacking Jdp2 had elevated levels of cyclin A2 mRNA. Moreover, reintroduction of JDP2 resulted in repression of transcription of ccna2 and of cell cycle progression. Thus, transcription of the gene for cyclin A2 appears to be a direct target of JDP2 in the suppression of cell proliferation