High-temperature creep strength and room-temperature fracture toughness of MoSiBTiC alloy

Quite recently, the author and his coworkers have developed a new high-temperature material based on Mo-Si-B alloys with TiC addition for ultrahigh temperature applications. The alloys are produced not by powder sintering but by casting, and the constituent phases are of Mo solid solution, Mo5SiB2 (T2), (Ti, Mo)C and (Mo, Ti)2C. The density is reduced to less than 9.0 g/cm3, which is comparable to that of Ni-base superalloys. The high-temperature compressive strength is much stronger than that of commercial heat-resistant molybdenum alloys such as TZM and MHC in a wide high-temperature range. In this paper, the recent progress of our research and development of the MoSiBTiC alloys is reviewed focusing on high-temperature creep strength and room temperature fracture toughness. The alloy having a primary phase during solidification of (Ti, Mo)C and thus a higher (Ti, Mo)C volume fraction was examined for tensile creep properties, and it was found that the alloy showed typical tensile creep curves accompanying transient, steady-state and acceleration creep stages in all the test conditions. The creep strength was relatively good, for example, the rupture time at 1350 °C under 170 MPa was about 750 h. The stress exponents, n, in the temperature range of 1400 – 1600 °C and the stress range of 100 – 300 MPa were ≈ 3 while it was 5 – 6 at 1350 °C, suggesting that the rate-controlling process of creep deformation is different between at and below 1350 °C and at and above 1400 °C in the stress range. Room-temperature fracture toughness of the MoSiBTiC alloys was measured by three-point or four-point bending tests using Chevron-notched specimens. The alloy having the primary phase of (Ti, Mo)C showed the fracture toughness value of better than 15 MPa(m)1/2 at room temperature. The value was better than that of the alloy having a primary phase of Moss and thus a higher Moss volume fraction. The obtained results indicated that (Ti, Mo)C phase works for improving not only high-temperature strength but also room-temperature fracture toughness

画像解析と機械学習によるトマトの自動生育診断および高速フェノタイピングに関する研究

学位の種別: 課程博士審査委員会委員 : (主査)東京大学教授 二宮 正士, 東京大学教授 溝口 勝, 東京大学教授 小林 和彦, 東京大学教授 河鰭 実之, 三重大学大学院生物資源学研究科教授 亀岡 孝治University of Tokyo(東京大学

Treatment resistance of rheumatoid arthritis relates to infection of periodontal pathogenic bacteria: a case-control cross-sectional study

Recent studies have shown that periodontitis is associated with rheumatoid arthritis (RA) and periodontal bacteria, such as Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) are involved in the pathogenesis of RA via citrullinated proteins. Smoking has also been shown to be involved in the pathogenesis of RA; however, the extent of this involvement is still poorly understood. In addition, RA and polymyalgia rheumatica (PMR) are sometimes difficult to differentiate; however, the relationship between PMR and the factors from smoking and periodontal bacteria is unclear. The aim of this study was to clarify the relationship between periodontal pathogenic bacterial infections and smoking in patients with RA or PMR. This case-control study included 142 patients with untreated RA or PMR. This study evaluated the serum antibody titers against periodontal pathogenic bacterial antigens and an anti-citrullinated peptide antibody (ACPA). In patients with RA, the relationship between antibody titers and disease activity of RA and response after 3 months of treatment was also investigated. Additionally, the effects of smoking were evaluated. Although there was no significant difference in serum antibody titer against periodontal pathogenic bacteria between the ACPA-positive RA group and the ACPA-negative PMR group, we found an association between the elevated antibody titer against Pg and the degree of ACPA value, especially between negative group and high-value positive group (>= 100 U/mL). The antibody titers against Aa and Pg did not differ depending on disease activity score 28 (DAS28) at baseline; however, patients with high antibody titers had poor RA therapeutic response as judged by DAS28 after 3 months. We could not find any association between smoking and any of these parameters. Periodontal pathogenic bacteria, especially Pg, are associated with elevated ACPA levels. Our findings suggest that Pg and Aa infections interfere with the therapeutic response of RA

The Expression Level of HIV-1 Vif Is Optimized by Nucleotide Changes in the Genomic SA1D2prox Region during the Viral Adaptation Process

HIV-1 Vif plays an essential role in viral replication by antagonizing anti-viral cellular restriction factors, a family of APOBEC3 proteins. We have previously shown that naturally-occurring single-nucleotide mutations in the SA1D2prox region, which surrounds the splicing acceptor 1 and splicing donor 2 sites of the HIV-1 genome, dramatically alter the Vif expression level, resulting in variants with low or excessive Vif expression. In this study, we investigated how these HIV-1 variants with poor replication ability adapt and evolve under the pressure of APOBEC3 proteins. Adapted clones obtained through adaptation experiments exhibited an altered replication ability and Vif expression level compared to each parental clone. While various mutations were present throughout the viral genome, all replication-competent adapted clones with altered Vif expression levels were found to bear them within SA1D2prox, without exception. Indeed, the mutations identified within SA1D2prox were responsible for changes in the Vif expression levels and altered the splicing pattern. Moreover, for samples collected from HIV-1-infected patients, we showed that the nucleotide sequences of SA1D2prox can be chronologically changed and concomitantly affect the Vif expression levels. Taken together, these results demonstrated the importance of the SA1D2prox nucleotide sequence for modulating the Vif expression level during HIV-1 replication and adaptation

Carbon Dioxide Emissions from Hydrogen Vehicles : Is a Hydrogen-based Society Realistic?

二酸化炭素の排出が地球温暖化にどの程度影響しているかは議論の余地の残るところではあるが，現時点で商用化されている水素自動車（燃料電池車）は走行時に二酸化炭素を排出しないので，地球温暖化防止に有効であると広く認識されている．しかし，水素は，工業的には天然ガスから製造されているので製造時点で二酸化炭素が排出される．そこで，水素自動車が実質的に排出する二酸化炭素量を推計し，ガソリン車，ハイブリッド車，電気自動車が排出する二酸化炭素量と比較して考察した．ここで，電気自動車については発電時の排出量であるので，各国の電力ミックスに大きく依存する．比較考察した結果，日本の場合，水素自動車と電気自動車の二酸化炭素排出量は，現時点ではほぼ同量であるが，政府が2030年に目標としている電力ミックスで考えるとむしろ電気自動車の方が少なくなることがわかった．したがって，水素ステーションなどに膨大な設備投資を行って取り扱いが難しく非常に危険な水素で走行する水素自動車の普及を推進するより，現時点でもかなり普及している電気自動車の更なる普及を促進する方が合理的である．本稿では，最後に，水素の製造や発電の際に排出される二酸化炭素の地中への貯留手法であるCCSの現状と実現性についても言及した．Hydrogen-fuel vehicles do not emit carbon dioxide while running: however, carbon dioxide is emitted during the hydrogen production process. In this study, the amount of carbon dioxide produced by hydrogen vehicles was estimated, and compared to the carbon dioxide emissions of gasoline, hybrid, electric vehicles. Although the quantity of carbon dioxide produced by electric vehicles depends on the power mix, in Japan, electric vehicle and hydrogen vehicle emissions are currently almost the same. However, by 2030, electric vehicle carbon dioxide emissions, are expected to be lower than those of hydrogen vehicles, when the power mix will reach current government targets. The government is currently promoting the use of hydrogen vehicles, but high capital investment will be required for the necessary hydrogen refueling stations. Above all, hydrogen is a very dangerous gas that can explode due to minor errors. Conversely, electric vehicles have already gained popularity and do not carry the same risks. For these reasons, it is more reasonable to promote the use of electric rather than hydrogen vehicles. Finally, this study considers the current situation and feasibility of carbon dioxide capture and storage

The fungal metabolite (+)-terrein abrogates osteoclast differentiation via suppression of the RANKL signaling pathway through NFATc1

Pathophysiological bone resorption is commonly associated with periodontal disease and involves the excessive resorption of bone matrix by activated osteoclasts. Receptor activator of nuclear factor (NF)-κB ligand (RANKL) signaling pathways have been proposed as targets for inhibiting osteoclast differentiation and bone resorption. The fungal secondary metabolite (+)-terrein is a natural compound derived from Aspergillus terreus that has previously shown anti-interleukin-6 properties related to inflammatory bone resorption. However, its effects and molecular mechanism of action on osteoclastogenesis and bone resorption remain unclear. In the present study, we showed that 10 µM synthetic (+)-terrein inhibited RANKL-induced osteoclast formation and bone resorption in a dose-dependent manner and without cytotoxicity. RANKL-induced messenger RNA expression of osteoclast-specific markers including nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), the master regulator of osteoclastogenesis, cathepsin K, tartrate-resistant acid phosphatase (Trap) was completely inhibited by synthetic (+)-terrein treatment. Furthermore, synthetic (+)-terrein decreased RANKL-induced NFATc1 protein expression. This study revealed that synthetic (+)-terrein attenuated osteoclast formation and bone resorption by mediating RANKL signaling pathways, especially NFATc1, and indicated the potential effect of (+)-terrein on inflammatory bone resorption including periodontal disease

The Fungal Metabolite (+)-Terrein Abrogates Ovariectomy-Induced Bone Loss and Receptor Activator of Nuclear Factor-kappa B Ligand-Induced Osteoclastogenesis by Suppressing Protein Kinase-C alpha/beta II Phosphorylation

Osteoporosis is a common disease characterized by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. Severe bone loss due to osteoporosis triggers pathological fractures and consequently decreases the daily life activity and quality of life. Therefore, prevention of osteoporosis has become an important issue to be addressed. We have reported that the fungal secondary metabolite (+)-terrein (TER), a natural compound derived from Aspergillus terreus, has shown receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclast differentiation by suppressing nuclear factor of activated T-cell 1 (NFATc1) expression, a master regulator of osteoclastogenesis. TER has been shown to possess extensive biological and pharmacological benefits; however, its effects on bone metabolism remain unclear. In this study, we investigated the effects of TER on the femoral bone metabolism using a mouse-ovariectomized osteoporosis model (OVX mice) and then on RANKL signal transduction using mouse bone marrow macrophages (mBMMs). In vivo administration of TER significantly improved bone density, bone mass, and trabecular number in OVX mice (p < 0.01). In addition, TER suppressed TRAP and cathepsin-K expression in the tissue sections of OVX mice (p < 0.01). In an in vitro study, TER suppressed RANKL-induced phosphorylation of PKC alpha/beta II, which is involved in the expression of NFATc1 (p < 0.05). The PKC inhibitor, GF109203X, also inhibited RANKL-induced osteoclastogenesis in mBMMs as well as TER. In addition, TER suppressed the expression of osteoclastogenesis-related genes, such as Ocstamp, Dcstamp, Calcr, Atp6v0d2, Oscar, and Itgb3 (p < 0.01). These results provide promising evidence for the potential therapeutic application of TER as a novel treatment compound against osteoporosis

Mechanisms With Clinical Implications for Atrial Fibrillation–Associated Remodeling: Cathepsin K Expression, Regulation, and Therapeutic Target and Biomarker

Background: The cysteine protease cathepsin K (CatK) has been implicated in the pathogenesis of cardiovascular disease. We sought to determine the link between atrial fibrillation (AF) and plasma CatK levels and to investigate the expression of and therapeutic target for CatK in vivo and in vitro. Methods and Results: Plasma CatK and extracellular matrix protein peptides (intact procollagen type I of N‐terminal propeptide; carboxyl‐terminal telopeptide of type I collagen [ICTP]) were measured in 209 consecutive patients with AF (paroxysmal AF, 146; persistent AF, 63) and 112 control subjects. In addition, the regulation of CatK expression was investigated in vivo and vitro. Patients with AF had higher plasma CatK and ICTP levels than did control subjects. Patients with persistent AF had higher levels of plasma CatK and ICTP than did patients with paroxysmal AF. CatK was correlated with ICTP concentration and left atrial diameter in all subjects. In rabbits, superoxide production, CatK activity, fibrosis, and the levels of atrial tissue angiotensin II, angiotensin type 1 receptor, gp91phox, phospho‐p38 mitogen‐activated protein kinase, and CatK were greater in those with tachypacing‐induced AF than in controls, and these changes were reversed with angiotensin type 1 receptor antagonist. Olmesartan and mitogen‐activated protein kinase inhibitor decreased the CatK expression induced by angiotensin II in rat neonatal myocytes. Conclusions: These data indicated that increased plasma CatK levels are linked with the presence of AF. Angiotensin type 1 receptor antagonist appears to be effective in alleviating atrial fibrosis in a rabbit AF model, partly reducing angiotensin type 1 receptor‐p38mitogen‐activated protein kinase‐dependent and ‐independent CatK activation, thus preventing AF