はっ水性微細凹凸面上の流動抵抗低減に関する研究

金沢大学理工研究域ミクロンオーダーの規則的な凹凸形状を表面構造に持ち強いはっ水性を有する流路壁面で,流動抵抗の低減を実現するための基礎研究として,表面近傍の状態の観測や流れの計測を行った.本年度は,ニッケル製メッシュを型に用いて,数十ミクロンオーダの微細凹凸をアクリル樹脂表面上に加熱成型することにより,半導体プロセス技術を用いない安価な微細凹凸面作成法を考案した.前年度の数値解析で示唆された凹凸のスケールが大きいほど抵抗低減効果が大きいという推測により,この加熱成型法で数種類の凹凸サイズの試験面を作製した.表面のはっ水性は市販のはっ水剤を塗布することにより付与した.実験では,水滴の接触角,水中での空気層保持機能の経時変化や空気層の面積,及び層流域での流動抵抗を測定した.試験した微細凹凸面の中で凹凸が最も大きい100ミクロン間隔,50ミクロン角の突起を有する試験面において2%の流動抵抗低減を見出した.また,水中での空気保持機能に対しては凹凸のスケールのほか凸部と凹部の面積割合が影響し,表面上の水滴接触角により評価されるはっ水性と水中での空気保持機能との間の相違も見出した.凹部の比率が最も大きい突起間隔50ミクロン,14ミクロン角の微細凹凸面において水滴接触角が最大になったものの,突起のサイズに比べ間隔が過大であったため水中において凹部への浸水を生じさせ気体層を保持が不可能であった.本研究により,微細凹凸を有するはっ水面における流動抵抗低減現象の凹凸サイズ・形状と抵抗低減割合に関連性があることを示す事が出来た.ただし,抵抗低減割合は従来の研究などに比べ顕著ではなく,より望ましい微細凹凸サイズ・形状を精査することが今後の課題である.研究課題/領域番号:13750139, 研究期間(年度):2001-2002出典：「はっ水性微細凹凸面上の流動抵抗低減に関する研究」研究成果報告書　課題番号13750139（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（ https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-13750139/）を加工して作

Potent prion-like behaviors of pathogenic α-synuclein and evaluation of inactivation methods

The concept that abnormal protein aggregates show prion-like propagation between cells has been considered to explain the onset and progression of many neurodegenerative diseases. Indeed, both synthetic amyloid-like fibrils and pathogenic proteins extracted from patients’ brains induce self-templated amplification and cell-to-cell transmission in vitro and in vivo. However, it is unclear whether exposure to exogenous prion-like proteins can potentially cause these diseases in humans. Here, we investigated in detail the prion-like seeding activities of several kinds of pathogenic α-synuclein (α-syn), including synthetic fibrils and detergent-insoluble fractions extracted from brains of patients with α-synucleinopathies. Exposure to synthetic α-syn fibrils at concentrations above 100 pg/mL caused seeded aggregation of α-syn in SH-SY5Y cells, and seeded aggregation was also observed in C57BL/6 J mice after intracerebral inoculation of at least 0.1 μg/animal. α-Syn aggregates extracted from brains of multiple system atrophy (MSA) patients showed higher seeding activity than those extracted from patients with dementia with Lewy bodies (DLB), and their potency was similar to that of synthetic α-syn fibrils. We also examined the effects of various methods that have been reported to inactivate abnormal prion proteins (PrPSc), including autoclaving at various temperatures, exposure to sodium dodecyl sulfate (SDS), and combined treatments. The combination of autoclaving and 1% SDS substantially reduced the seeding activities of synthetic α-syn fibrils and α-syn aggregates extracted from MSA brains. However, single treatment with 1% SDS or generally used sterilization conditions proved insufficient to prevent accumulation of pathological α-syn. In conclusion, α-syn aggregates derived from MSA patients showed a potent prion-like seeding activity, which could be efficiently reduced by combined use of SDS and autoclaving

Thioredoxin interacting protein protects mice from fasting induced liver steatosis by activating ER stress and its downstream signaling pathways

Under normal conditions, fasting results in decreased protein disulfide isomerase (PDI) activity and accumulation of unfolded proteins, leading to the subsequent activation of the unfolded protein response (UPR)/autophagy signaling pathway to eliminate damaged mitochondria. Fasting also induces upregulation of thioredoxin-interacting protein (TXNIP) expression and mice deficient of this protein (TXNIP-KO mice) was shown to develop severe hypoglycemia, hyperlipidemia and liver steatosis (LS). In the present study, we aimed to determine the role of TXNIP in fasting-induced LS by using male TXNIP-KO mice that developed LS without severe hypoglycemia. In TXNIP-KO mice, fasting induced severe microvesicular LS. Examinations by transmission electron microscopy revealed mitochondria with smaller size and deformities and the presence of few autophagosomes. The expression of beta-oxidation-associated genes remained at the same level and the level of LC3-II was low. PDI activity level stayed at the original level and the levels of p-IRE1 and X-box binding protein 1 spliced form (sXBP1) were lower. Interestingly, treatment of TXNIP-KO mice with bacitracin, a PDI inhibitor, restored the level of LC3-II after fasting. These results suggest that TXNIP regulates PDI activity and subsequent activation of the UPR/autophagy pathway and plays a protective role in fasting-induced LS

Locating Congested Segments over the Internet Based on Multiple End-to-End Path Measurements

Since congestion is very likely to happen in the Internet, locating congested areas (path segments) along a congested path is vital to appropriate actions by Internet Service Providers to mitigate or prevent network performance degradation. We propose a practical method to locate congested segments by actively measuring one-way end-to-end packet losses on appropriate paths from multiple origins to multiple destinations, using a network tomographic approach. Then we conduct a long-term experiment measuring packet losses on multiple paths over the Japanese commercial Internet. The experimental results indicate that the proposed method is able to precisely locate congested segments. Some findings on congestion over the Japan Internet are also given based on the experimen