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Exposure of mice to a high dose of estrogens including diethylstilbestrol (DES) during the neonatal period modifies the developmental plan of the genital tract, which leads to various permanent changes in physiology, morphology and gene expression. These changes include development of an abnormal vaginal epithelium lined with hyperplastic mucinous cells accompanied by Tff1 gene expression in mice. Here, the influence of vitamin D on the direct effect of estrogen on the developing mouse vagina was examined. The mid-vagina of neonatal mice was cultured in a serum-free medium containing estradiol-17β (E2) and various concentrations of 1,25-dihydroxyvitamin D3 (1,25(OH)2D) ex vivo and then was transplanted under the renal capsule of ovariectomized host mice for 35 days. Exposure to E2 alone caused the vaginal tissue to develop estrogen-independent epithelial hyperplasia and to express TFF1 mRNA, while addition of a low nanomolar amount of 1,25(OH)2D added at the same time as E2 to the culture medium attenuated the effects of estrogen. Expression of vitamin D receptor was also evident in the neonatal mouse vagina. Interestingly, addition of 25-hydroxyvitamin D3, a pro-activated form of vitamin D, at the micromolar level was found to be potent in disrupting the developmental effects of E2, while cholecalciferol was not at least at the dose examined. Correspondingly, expression of Cyp27B1, a kidney-specific 25-hydroxyvitamin D hydroxylase, was evident in the neonatal mouse vagina when examined by RT-PCR. In addition, simultaneous administration of 1,25(OH)2D successfully attenuated DES-induced ovary-independent hyperplasia in the vagina in neonatal mice in vivo. Thus, manipulation of vitamin D influenced the harmful effects of estrogens on mouse vaginal development.

The larval habitat of the terrestrial firefly, Luciola parvula, was investigated at five points in the campus of Nagoya University in 2007, 2008, and 2010. By using bait trap, the specimens were captured at the northern area of Ichi-no-tani and the east side of Toyoda Auditorium, but not at Ni-no-tani area, near paddy field, and the area around Building B of the Graduate school of Science. The result suggests that L. parvula inhabits in the area around Ichi-no-tani and Toyoda Auditorium. To identify the precise distributions, further studies are necessary.

石鹸水とストローでできる自然現象として、「シャボン玉」がある。シャボン玉は、子供の頃に誰でも一度は遊んだことがあるだろう。このシャボン玉はこれまで多くの研究者が興味を持ち、数多くの研究がなされている。ところで、シャボン玉を作るために必要な石鹸水とストローを用いると、もうひとつ違った現象を見ることができる。それが、「Antibubble」である。Antibubbleとは、液面に衝突した液柱(jet)が、液面と一体化することなく液中に潜り込んで液滴に分裂する現象、およびその液滴のことであり、簡単に言えば「水の中のシャボン玉」である。このAntibubbleは石鹸水に限らず、油、スプレー液やさらにはコーヒー、ビールなど、我々のごく身近なもので見ることができる。しかし、このAntibubbleは我々の身近で起こる現象にもかかわらず、その研究は最近まであまり行われていない。本研究は、Antibubbleの生成過程をモデル化することを目的として行った。そして、剛体近似とjetの不安定性を用いた簡単なモデルでこの現象を表すことに成功した。本研究で構築したモデルは次のようなものである。まず、生成の過程を二つの段階に分ける。そして、それぞれの段階において次のように考える。・jetがある深さまで潜り込む間:剛体円柱と近似して「剛体の運動方程式」を解く。・潜り込んだ後くびれてAntibubbleとなる間:jetが不安定になってくびれるとして「jetの不安定性」の議論を行う。最後に、その二つの段階を合わせ、Antibubbleの生成過程モデルとした。この生成過程モデルを用いることで、Antibubbleの半径や生成時間など、Antibubbleの生成に関する様々なパラメータを導出することができた。また、このモデルから導出された各パラメータの理論値と実験値を比較した結果、このモデルが線形近似の範囲で現象をよく表しており、モデルとして妥当であることが示された。, この論文は国立情報学研究所の電子図書館事業により電子化されました。

Mammary gland development is controlled by a dynamic interplay between endocrine hormones and locally produced factors. Biogenic monoamines (serotonin, dopamine, norepinephrine, and others) are an important class of bioregulatory molecules that have not been shown to participate in mammary development. Here we show that mammary glands stimulated by prolactin (PRL) express genes essential for serotonin biosynthesis (tryptophan hydroxylase [TPH] and aromatic amine decarboxylase). TPH mRNA was elevated during pregnancy and lactation, and serotonin was detected in the mammary epithelium and in milk. TPH was induced by PRL in mammosphere cultures and by milk stasis in nursing dams, suggesting that the gene is controlled by milk filling in the alveoli. Serotonin suppressed beta-casein gene expression and caused shrinkage of mammary alveoli. Conversely, TPH1 gene disruption or antiserotonergic drugs resulted in enhanced secretory features and alveolar dilation. Thus, autocrine-paracrine serotonin signaling is an important regulator of mammary homeostasis and early involution.

We have previously performed suppression subtractive hybridization to identify genes that were induced during prolactin (PRL)-driven lobuloalveolar development of the mammary gland. This suggested that cortactin-binding protein 90 (CBP90), which is known to be a brain-specific protein that binds to cortactin, was expressed under the regulation of PRL in the mammary glands (preliminary observation). In this study, the expression of CBP90 was examined in the mammary glands of mice under manipulated hormonal circumstances. PRL treatment by 9 days of pituitary grafting induced CBP90 expression in the normal mammary glands but not in the cleared fat pads, while cortactin was expressed constitutively in both the normal mammary glands and the cleared fat pads. Unlike milk proteins, longer treatment with PRL (36 days of pituitary grafting) did not increase the expression level of CBP90 mRNA, while it slightly increased the cortactin mRNA level. Mammary CBP90 mRNA expression was induced by pituitary grafting but not by progesterone treatment in PRL-deficient mice, while pituitary grafting induced mammary CBP90 expression in ovariectomized PRL-deficient mice only when estrogen and progesterone were appropriately supplemented to permit the formation of alveolar buds. The CBP90 protein was detected by immunohistochemistry in the luminal epithelium of the alveolar buds and more faintly in the ductal epithelium. Thus, from the unique expression pattern, CBP90 may be useful as a molecular marker for the hormone-stimulated development of mammary alveolar buds.

本研究は、軽量コンクリートの実構造物への適用技術の検討として、軽量骨材を用いた鉄筋コンクリート梁（以下、RC梁）の力学的性状に焦点をあて、実験および解析的検討を行ったものである。, This study aims at researching experimentally mechanical properties of both right-weight concrete and reinforced light-weight concrete beams using high performance artificial aggregates.