type: misc

label: url

en: 家庭の安全・安心科学 ―家庭における微生物汚染とその対策― --- 紫外線を使った身の回りにある電化製品とその利用の注意点

en: Journal of Antibacterial and Antifungal Agents

ja: 日本防菌防黴学会誌


en: 近紫外線発光ダイオードを用いた殺菌システム

ja: 近紫外線発光ダイオードを用いた殺菌システム

en: 食品分野における非加熱殺菌技術

ja: 食品分野における非加熱殺菌技術


en: 臨床スポーツ医学, 運動習慣形成と脳内神経伝達物質

ja: 臨床スポーツ医学, 運動習慣形成と脳内神経伝達物質

en: 臨床スポーツ医学

ja: 臨床スポーツ医学


en: 侵襲時の栄養評価法

ja: 侵襲時の栄養評価法

en: 機能性食品と薬理栄養

ja: 機能性食品と薬理栄養


en: Control of hypertension in metabolic syndrome

ja: メタボリック症候群における高血圧の管理

en: Metabolic syndrome includes abdominal obesity, hyperlipidemia, diabetes, and hypertension. All, but hypertension, are obviously related to metabolism. However, hypertension might result from, at least in part, abdominal obesity, because adipose tissue produces bioactive mediators (adipocytokines)which increase blood pressure. In treatment of hypertension, we should concern insulin resistance, which is a major risk factor of cardiovascular events. Angiotensin converting enzyme inhibitor is known to improve insulin resistance, but results of angiotensin receptor blocker in animal studies are controversial. In clinical trial, there are many established data that ARBs prevent new onset of diabetes mellitus, suggesting that this agent also has a beneficial effect on glucose metabolism. Short acting Ca-antagonists, such as nifedipine, decrease insulin sensitivity, but long-acting Ca-antagonists increase it. βblockers decrease insulin sensitivity but those with α-blocking action improve insulin resistance. Recent study, ARB is more potent to reduce cardiovascular risk in those with obesity than in those with normal body weight, suggesting some drugs are more effective in metabolic syndrome. Thus, when we chose antihypertensive drugs in treating patients with metabolic syndrome, we have to choose proper drugs in addition to modify life-style.

en: Shikoku Acta Medica

ja: 四国医学雑誌


en: The phytoestrogen ginsensoside Re activates potassium channels of vascular smooth muscle cells through PI3K/Akt and nitric oxide pathways

en: In vascular smooth muscle cells, large-conductance Ca(2+)-activated K(+) channels (K(Ca) channels) play a pivotal role in determining membrane potential, and thereby the vascular tone. Ginsenoside Re, a phytochemical from ginseng, is reported to activate this channel, but its precise mechanism is unsolved. Patch clamp studies showed that ginsenoside Re activates K(Ca) channels in the arterial smooth muscle cell line A10 in a dose-dependent manner. The channel-opening effect of ginsenoside Re was inhibited by 1 microM L-NIO, an inhibitor of eNOS, but not by 3 microM SMTC, an inhibitor of nNOS, indicating that ginsenoside Re activated K(Ca) channels through activation of eNOS. SH-6 (10 microM), an Akt inhibitor, and wortmannin, a PI3-kinase inhibitor, completely blocked activation of K(Ca) channels by ginsenoside Re, indicating that it activates eNOS via a c-Src/PI3-kinase/Akt-dependent mechanism. In addition, the ginsenoside Re-induced activation of eNOS and K(Ca) channel was blocked by 10 microM ICI 182, 780, an inhibitor of membrane estrogen receptor-alpha, suggesting that eNOS activation occurs via a non-genomic pathway of this receptor. In conclusion, ginsenoside Re releases NO via a membrane sex steroid receptors, resulting in K(Ca) channel activation in vascular smooth muscle cells, promoting vasodilation and preventing severe arterial contraction.

en: The Journal of Medical Investigation : JMI


en: 筋肉をつけるための栄養学

ja: 筋肉をつけるための栄養学

en: The Journal of Therapy

ja: 治療


en: 肝疾患の病変と栄養管理-解決すべき問題点 「肝硬変への分割食と就寝前軽食-その効果と課題」

en: 日本病態栄養学会誌

ja: 日本病態栄養学会誌