TiO2-Photocatalyzed Epoxidation of 1-Decene by H2O2 under Visible Light

1-Decene was converted to 1,2-epoxydecane on UV-irradiated TiO2 powder using molecular oxygen as the oxygen source. Other main products were nonanal and 2-decanone. For anatase-form TiO2 powders, the reaction rate was hardly affected by addition of hydrogen peroxide to the solution. In contrast, for rutile-form TiO2 powders, the rate of epoxide generation was significantly increased by addition of hydrogen peroxide. In this case, the reaction occurred under visible light as well as UV light. The selectivity of the production of 1,2-epoxydecane was higher under visible light than under UV light. The conversion efficiency of an incident photon to 1,2-epoxydecane was about 2% when irradiated with visible light in the range 440–480 nm. UV–visible diffuse reflection spectroscopy, Fourier transform infrared spectroscopy, and X-ray photoelectron spectroscopy suggested the generation of a Ti–η2-peroxide on rutile TiO2 surface after treatment with hydrogen peroxide. The initial step of the reaction under visible light was attributed to a photochemical reaction of this peroxide with 1-decene

Delaunay network using detour

計算機器（以下ノード）の位置関係により定義されるドロネーネットワークは，平面上で局所性を持つため，（i）対象領域の拡張に伴うネットワークの拡張性，（ii）ノードの位置に基づく地理的な経路選択，（iii）ノードの頻繁な参加・離脱に対する弾力性の保持などの面で有用である．そのため，アドホックネットワークを用いたアプリケーションにおいて応用性が広い．しかし，ノードの通信範囲に制限のある無線環境を考慮すると，ノードの位置に基づくドロネー図を直接的に構成できない．そこで本稿では，直接接続を持たないノード間に対して迂回経路による仮想リンクを定義し，無線環境でドロネー図を仮想的に構成するアルゴリズムを提案する．各ノードは，実行時の隣人までの接続通知に経路情報を繋ぎ合わせることで，迂回経路による仮想リンクを生成し，すべてのノード間で仮想的なドロネーネットワークを自律分散的に構成することができる．さらに，迂回経路は一般に2ノード間で複数存在するため，迂回経路の縮退アルゴリズムについても述べる．提案ネットワークの上で，欲張り法及びその拡張法を用いた経路選択法を提示し，本ネットワークのアプリケーションについても述べ，各ノードの維持負荷，迂回経路の効果などを定量的に検証する．DEWS2008 D7-2 電子情報通信学会 第19回データ工学ワークショップ 2008年3月9日～11日正式版リンクwww.ieice.org/~de/DEWS/DEWS2008/proceedings/files/d7//d7-2.pd

Evaluating the Need for and Effect of Percutaneous Transluminal Angioplasty on Arteriovenous Fistulas by Using Total Recirculation Rate per Dialysis Session (“Clearance Gap”)

The functioning of an arteriovenous fistula (AVF) used for vascular access during hemodialysis has been assessed mainly by dilution methods. Although these techniques indicate the immediate recirculation rate, the results obtained may not correlate with Kt/V. In contrast, the clearance gap (CL-Gap) method provides the total recirculation rate per dialysis session and correlates well with Kt/V. We assessed the correlation between Kt/V and CL-Gap as well as the change in radial artery (RA) blood flow speed in the fistula before percutaneous transluminal angioplasty (PTA) in 45 patients undergoing continuous hemodialysis. The dialysis dose during the determination of CL-Gap was 1.2 to 1.4 Kt/V. Patients with a 10% elevation or more than a 10% relative increase in CL-Gap underwent PTA (n＝45), and the values obtained for Kt/V and CL-Gap before PTA were compared with those obtained immediately afterward. The mean RA blood flow speed improved significantly (from 52.9 to 97.5cm/sec) after PTA, as did Kt/V (1.07 to 1.30) and CL-Gap (14.1% to －0.2%). A significant correlation between these differences was apparent (r＝－0.436 and p＝0.003). These findings suggest that calculating CL-Gap may be useful for determining when PTA is required and for assessing the effectiveness of PTA, toward obtaining better dialysis

Antioxidant and renoprotective activity of chitosan in nephrectomized rats.

The effect of chitosan on oxidative stress and chronic renal failure was investigated using 5/6 nephrectomized rats. The ingestion of chitosan over a 4-week period resulted in a significant decrease in total body weight, glucose, serum creatinine and indoxyl sulfate levels (P=0.0011, P=0.0006, P=0.0012, and P=0.0005, respectively), compared with the non-treated nephrectomized group. The ingestion of chitosan also resulted in a lowered ratio of oxidized to reduced albumin (P=0.003) and an increase in biological antioxidant potential (P=0.023). Interestingly, the oxidized albumin ratio was correlated with serum indoxyl sulfate levels in vivo. These results suggest that the ingestion of chitosan results in a significant reduction in the levels of pro-oxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation.The effect of chitosan on oxidative stress and chronic renal failure was investigated using 5/6 nephrectomized rats. The ingestion of chitosan over a 4-week period resulted in a significant decrease in total body weight, glucose, serum creatinine and indoxyl sulfate levels (P=0.0011, P=0.0006, P=0.0012, and P=0.0005, respectively), compared with the non-treated nephrectomized group. The ingestion of chitosan also resulted in a lowered ratio of oxidized to reduced albumin (P=0.003) and an increase in biological antioxidant potential (P=0.023). Interestingly, the oxidized albumin ratio was correlated with serum indoxyl sulfate levels in vivo. These results suggest that the ingestion of chitosan results in a significant reduction in the levels of pro-oxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation

Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress

Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy via a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration in vivo and C2C12 mice myoblast cells in vitro. In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of mitogen-activated protein kinase signaling pathways. In vitro, iron overload also suppressed the differentiation of C2C12 myoblast cells, but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis via oxidative stress, leading to an imbalance in skeletal muscle homeostasis