Cluster structures in Oxygen isotopes

Cluster structure of 16O,18O and 20O is investigated by the antisymmettrized molecular dynamics (AMD) plus generator coordinate method (GCM). We have found the K^{\pi}=0$_2^+$ and 0$_1^-$ rotational bands of 18O that have the prominent 14C+\alpha cluster structure. Clustering systematics becomes richer in 20O. We suggest the K^{\pi}=0$_2^+$ band that is the mixture of the 12C+\alpha+4n and 14C+6He cluster structures, and the K^{\pi}=0$_1^-$ band that has the 14C+6He cluster structure. The K^{\pi}=0$_3^+$ and 0$_2^-$ bands that have the prominent 16C+\alpha cluster structure are also found.Comment: 9pages, 9figure

Role of the imprinted allele of the Cdkn1c gene in mouse neocortical development

Imprinted genes are expressed from only one allele in a parent of origin–specific manner. The cyclin-dependent kinase inhibitor p57^{kip2} is encoded by an imprinted gene Cdkn1c, with the paternal allele being silenced. The possible expression and function of the paternal allele of Cdkn1c have remained little studied, however. We now show that the paternal allele of the Cdkn1c gene is expressed at a low level in the developing mouse neocortex. Surprisingly, the central nervous system-specific conditional deletion of the paternal allele (pat cKO) at the Cdkn1c locus resulted in a marked reduction in brain size. Furthermore, pat cKO gradually reduced the number of neural stem-progenitor cells (NPCs) during neocortical development, and thus reduced the number of upper-layer neurons, which were derived from late-stage NPCs. Our results thus show that the paternal allele of the Cdkn1c locus plays a key role in maintenance of NPCs during neocortical development

Area-Specific Regulation of Quiescent Neural Stem Cells by Notch3 in the Adult Mouse Subependymal Zone

In the adult mammalian brain, neural stem cells (NSCs) generate new neurons throughout the mammal's lifetime. The balance between quiescence and active cell division among NSCs is crucial in producing appropriate numbers of neurons while maintaining the stem cell pool for a long period. The Notch signaling pathway plays a central role in both maintaining quiescent NSCs (qNSCs) and promoting cell division of active NSCs (aNSCs), although no one knows how this pathway regulates these apparently opposite functions. Notch1 has been shown to promote proliferation of aNSCs without affecting qNSCs in the adult mouse subependymal zone (SEZ). In this study, we found that Notch3 is expressed to a higher extent in qNSCs than in aNSCs while Notch1 is preferentially expressed in aNSCs and transit-amplifying progenitors in the adult mouse SEZ. Furthermore, Notch3 is selectively expressed in the lateral and ventral walls of the SEZ. Knockdown of Notch3 in the lateral wall of the adult SEZ increased the division of NSCs. Moreover, deletion of the Notch3 gene resulted in significant reduction of qNSCs specifically in the lateral and ventral walls, compared with the medial and dorsal walls, of the lateral ventricles. Notch3 deletion also reduced the number of qNSCs activated after antimitotic cytosine β-D-arabinofuranoside (Ara-C) treatment. Importantly, Notch3 deletion preferentially reduced specific subtypes of newborn neurons in the olfactory bulb derived from the lateral walls of the SEZ. These results indicate that Notch isoforms differentially control the quiescent and proliferative steps of adult SEZ NSCs in a domain-specific manner. SIGNIFICANCE STATEMENT In the adult mammalian brain, the subependymal zone (SEZ) of the lateral ventricles is the largest neurogenic niche, where neural stem cells (NSCs) generate neurons. In this study, we found that Notch3 plays an important role in the maintenance of quiescent NSCs (qNSCs), while Notch1 has been reported to act as a regulator of actively cycling NSCs. Furthermore, we found that Notch3 is specifically expressed in qNSCs located in the lateral and ventral walls of the lateral ventricles and regulates neuronal production of NSCs in a region-specific manner. Our results indicate that Notch3, by maintaining the quiescence of a subpopulation of NSCs, confers a region-specific heterogeneity among NSCs in the adult SEZ

酸素活性種を含む金属錯体の合目的創製および精密機能制御

金沢大学理工研究域本研究では,生体系で酸素分子活性化反応を行う非ヘム金属タンパク質で観測,推定されている反応中間体(酸素活性種を含む遷移金属錯体)を,合目的に創製し,それらの精密機能制御を通してこれら金属タンパクの機能発現機構の解明を目指した.1)酸素活性種を含む銅錯体:三脚型四座配位子を用いて,配位子のメチル基の水酸化反応における反応中間体を単離し,X線結晶構造解析により構造を明らかにした.2)酸素活性種を含む鉄錯体:二核化配位子を含む二核鉄(II)錯体を用いて非ヘム二核鉄酵素の機能モデル研究を行った.二核鉄パーオキソ錯体の架橋基が安息香酸の場合は,酸素分子運搬体であるヘムエリスリンに類似した可逆的酸素化挙動を示し,架橋基がトリフェニル酢酸架橋の場合は,トルエンモノオキシゲナーゼに類似した配位子のフェニル基の水酸化反応を行うことを明らかにし,酸素分子との反応の精密機能制御に成功した.3)酸素活性種を含む銅錯体:6-メチルピリジル基をサイドアームに有する二核化配位子の二核銅錯体を用いて,配位子の芳香環のNIHシフトを伴う水酸化反応の反応中間体を観測することに初めて成功し,その中間体は(μ-η^2:η^2-peroxo)dicopper(II)種であることを明らかにした.研究課題/領域番号:18750044, 研究期間(年度):2006 – 2007出典：「酸素活性種を含む金属錯体の合目的創製および精密機能制御」研究成果報告書　課題番号18750044（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-18750044/)を加工して作

Trans,trans,trans-Diethanoldiquinaldinatoiron(II)

金沢大学理学部金沢大学大学院自然科学研究科物質創成The title complex, trans,trans,trans-[FeII(C10H 6NO2)2-(C2H6O) 2], is centrosymmetric and the quinaldinate ligands form five-membered chelate rings. The geometry of the complex is distorted octahedral, with a trans-FeN2O4 chromophore. The hydroxy H atom forms an intermolecular hydrogen bond with the carbonyl O atom of the quinaldinate ligand. © 2003 International Union of Crystallography Printed in Great Britain - all rights reserved