Properties of Recycled Aggregate Made of Demolished Concrete Debris

Demolished Concrete debris has been recycled mainly for roadbeds and backfill. Improvement of the quality is necessary in order to use the concrete debris as recycled aggregate for concrete. The basis of the improvement purpose is to remove mortar and cement paste that adhered to the rock aggregate. Improvement method in this study is based on abrasion and crushing action. For the equipment, Los Angeles Machine in JIS A 1121 and forced mixing type mixer in JIS A8603 were used. In the raw material put into both testing equipment, 40mm recycled coarse aggregate used as a roadbed was used. Various impurities such as small amount of asphalt and fiber in the aggregate with large amount coarse debris were included in visual observation and under the microscope. At quality and energy consumption of improved recycled aggregate, there were differences between both testing equipments. For example, 3 time the time of Los Angeles machine was needed in the mixer in order to obtain the recycled aggregate of the quality of the same water absorption

2021年8月の記録的大雨をもたらした寒冷渦と熱帯起源のテレコネクション

主催 山﨑哲 (海洋研究開発機構研究員); 共催 向川均 (京都大学大学院理学研究科教授); 共催 廣岡俊彦 (九州大学大学院教授); 共催 渡部雅浩 (東京大学大気海洋研究所教授); 共催 榎本剛 (京都大学防災研究所教授

15-7-11 :着衣快適性評価システムの開発

The purpose of this study is clarify the clothing comfort of suits and shirts. The comfort of these goods was evaluated at five levels by the paired comparison method. And the EMG value and the clothing pressure were measured.Article先進ファイバー工学研究教育拠点研究成果報告書 10: 169-170(2004)research repor

15-7-11 : 着衣快適性評価システムの開発

The purpose of this study is clarify the clothing comfort of suits and shirts. The comfort of these goods was evaluated at five levels by the paired comparison method. And the EMG value and the clothing pressure were measured.Article先進ファイバー工学研究教育拠点研究成果報告書 11: 172-173(2005)research repor

アルデヒド類のHPLC分析用蛍光誘導体化試薬4-(5,6-ジメトキシ-2-フタルイミジニル)フェニルスルホニルヒドラジド

アルデヒド類の定量のための高感度なHPLC用蛍光誘導体化試薬として4-(5,6-ジメトキシ-2-フタルイミジニル)フェニルスルホニルヒドラジドを開発した。本試薬はアルデヒド類と反応して発蛍光性のヒドラゾンを生成し、ヒドラゾン類は逆相系HPLC-蛍光検出法により分離された。モデル化合物としてp-トルアルデヒド及びヘプタナールを用いて誘導体化反応条件について検討した。誘導体化反応は塩酸酸性下、室温、60分で完了した。誘導体化率は102.3%であった。検出限界(S/N=3)はp-トルアルデヒド及びヘプタナールでそれぞれ80及び6fmol/注入量であった。A highly sensitive fluorescent labeling reagent, 4-(5,6-dimethoxy-2-phthalimidinyl) phenylsulfonyl hydrazide, for determination of aldehydes in HPLC was developed. The reagent reacts with aldehydes to form corresponding fluorescent hydrazones, which were separated by reversed phase HPLC with fluorescence detection. The labeling reaction conditions were examined by using p-tolualdehyde and heptanal as model compounds. The reaction proceeded in the presence of hydrochloric acid at room temperature and was completed within 60 min. The labeling yield was 102.3 %. The detection limits (S/N=3) for p-tolualdehyde and heptanal were 80 and 6 fmol/injection, respectively

Deletion of both p62 and Nrf2 spontaneously results in the development of nonalcoholic steatohepatitis

Nonalcoholic steatohepatitis (NASH) is one of the leading causes of chronic liver disease worldwide. However, details of pathogenetic mechanisms remain unknown. Deletion of both p62/Sqstm1 and Nrf2 genes spontaneously led to the development of NASH in mice fed a normal chow and was associated with liver tumorigenesis. The pathogenetic mechanism (s) underlying the NASH development was investigated in p62:Nrf2 double-knockout (DKO) mice. DKO mice showed massive hepatomegaly and steatohepatitis with fat accumulation and had hyperphagia-induced obesity coupled with insulin resistance and adipokine imbalance. They also showed dysbiosis associated with an increased proportion of gram-negative bacteria species and an increased lipopolysaccharide (LPS) level in feces. Intestinal permeability was elevated in association with both epithelial damage and decreased expression levels of tight junction protein zona occludens-1, and thereby LPS levels were increased in serum. For Kupffer cells, the foreign body phagocytic capacity was decreased in magnetic resonance imaging, and the proportion of M1 cells was increased in DKO mice. In vitro experiments showed that the inflammatory response was accelerated in the p62:Nrf2 double-deficient Kupffer cells when challenged with a low dose of LPS. Diet restriction improved the hepatic conditions of NASH in association with improved dysbiosis and decreased LPS levels. The results suggest that in DKO mice, activation of innate immunity by excessive LPS flux from the intestines, occurring both within and outside the liver, is central to the development of hepatic damage in the form of NASH

Nuclear factor (erythroid derived 2)-like 2 activation increases exercise endurance capacity via redox modulation in skeletal muscles

Sulforaphane (SFN) plays an important role in preventing oxidative stress by activating the nuclear factor (erythroid derived 2)-like 2 (Nrf2) signalling pathway. SFN may improve exercise endurance capacity by counteracting oxidative stress-induced damage during exercise. We assessed running ability based on an exhaustive treadmill test (progressive-continuous all-out) and examined the expression of markers for oxidative stress and muscle damage. Twelve- to 13-week-old Male wild-type mice (Nrf2+/+) and Nrf2-null mice (Nrf2−/−) on C57BL/6J background were intraperitoneally injected with SFN or vehicle prior to the test. The running distance of SFN-injected Nrf2+/+ mice was significantly greater compared with that of uninjected mice. Enhanced running capacity was accompanied by upregulation of Nrf2 signalling and downstream genes. Marker of oxidative stress in SFN-injected Nrf2+/+ mice were lower than those in uninjected mice following the test. SFN produced greater protection against muscle damage during exhaustive exercise conditions in Nrf2+/+ mice than in Nrf2−/− mice. SFN-induced Nrf2 upregulation, and its antioxidative effects, might play critical roles in attenuating muscle fatigue via reduction of oxidative stress caused by exhaustive exercise. This in turn leads to enhanced exercise endurance capacity. These results provide new insights into SFN-induced upregulation of Nrf2 and its role in improving exercise performance