著者
室井 喜景 石井 利明
出版者
公益社団法人 日本薬理学会
雑誌
日本薬理学会年会要旨集 第95回日本薬理学会年会 (ISSN:24354953)
巻号頁・発行日
pp.1-P-029, 2022 (Released:2022-03-21)

Maternal care is indispensable for survival of neonates in mammals. Lactating females consume a large amount of energy for nurturing their pups by lactation. Management of energy expenditure through lactation is important for survival of themselves and pups. We previously reported that the orexigenic neuropeptide neuropeptide Y in the dorsal raphe nucleus (DRN) regulated maternal care, depending on food intakes of lactating females. In the present study, we investigated the neuronal mechanism for regulating maternal care by melanocortin 3 and 4 receptors (MC 3/4R), which was regulated by the anorexigenic neuropeptide alpha-melanocyte-stimulating hormone (α-MSH) and the orexigenic neuropeptide agouti-related peptide (AgRP) in an opposing manner. Neuronal processes immunoreactive to adrenocorticotropic hormone, which was a precursor of α-MSH, or AgRP, were distributed in the DRN. Furthermore, the pre-synaptic marker synaptophysin was co-localized with ACTH or AgRP in the DRN. We next investigated how the MC3/4R antagonist SHU 9119 affected maternal care. Injection of 100 pmol SHU 9119 into the DRN prevented maternal care in fed dams. Additionally, we examined whether the agonist melanotan II could affect maternal care following fasting for 8 h. Fasting for 8 h abolished maternal care in lactating females. But injection of 100 pmol melanotan II into the DRN partially recovered maternal care. These results indicate that MC3/4R signaling in the DRN regulates maternal care depending on feed intake in lactating mice.
著者
大塚 雄司 原澤 信介 杉浦 仁 小池 美由紀 秋元 秀郎 石井 利明 阿部田 ひろみ 岡部 龍也 久代 登志男 上松瀬 勝男
出版者
Japanese Society of Nephrology
雑誌
日本腎臓学会誌 (ISSN:03852385)
巻号頁・発行日
vol.42, no.8, pp.619-624, 2000

Previous studies have shown that hypertension causes endothelial dysfunction. To study the influence of exogenous nitric oxide (NO) on endothelial dysfunction produced by hypertension, we administered a non-depressor dose of nipradilol to two-kidney, one clip renovascular hypertensive rats (2K1C). Sprague-Dawley rats underwent either sham surgery (G-l) or clipping of the left renal artery. From day seven, 2K1C were randomized into 3 groups, placebo treatment (G-2), nipradilol treament (G-3, ) and propranolol treatment (G-4). Urinary NO<SUP>-</SUP><SUB>2</SUB> +N0<SUP>-</SUP><SUB>3</SUB> (NOx) excretion (UNOxV) was measured 4 weeks after clipping, and then, acetylcholine (Ach), A23187, or sodium nitroprusside (SNP) -induced relaxation were measured in the aorta. Blood pressure was increased in G-2, G-3, and G-4 compared to G-1. UNOxV was lower in G-2, G-3, and G-4 compared to G-1, but UNOxV was higher in G-3 compared to G-2 and G-4. Although Ach or A23187-induced relaxation was significantly decreased in isolated artery from G-2, G-3, and G-4 compared with those from G-1. Ach- or A23187-induced relaxation was improved in G-3. SNP induced relaxation did not differ among the 4 groups. These results suggest that exogenous NO from nipradilol reduces the endothelial dysfunction caused by hypertension without changing the blood pressure.
著者
石井 利明 平田 英二 大屋 隆生 Ishii Toshiaki Hirata Eiji Ohya Takao
雑誌
【全国大会】平成19年電気学会全国大会論文集
巻号頁・発行日
pp.107-108, 2007-03-15

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