周産期遺伝看護実践のパフォーマンス向上を目指す教育プログラムの開発

University of Yamanashi (山梨大学)博士(看護学)医工博甲第448号thesi

A Study on the Timing of Realization and Recognition of Income from Stock Award : Focusing on Restricted Stock Units

亜細亜大学修士（法学）master thesi

Observation of b→dγ and Determination of |Vtd/Vts|

journal articl

COMPARISON OF SOMATIC MUTATION FREQUENCIES IN THE STAMEN HAIRS OF ONE MUTABLE AND 2 STABLE CLONES OF TRADESCANTIA TREATED WITH SMALL DOSES OF GAMMA-RAYS

Induced somatic pink mutation frequencies in the stamen hairs of Tradescantia KU 20 clone, a blue/pink heterozygote highly mutable spontaneously at lower temperature, were studied after treating with relatively small doses of Co-60 gamma rays (39 to 551 mGy or 3.9 to 55.1 rad), and were compared with those of two stable clones (non-mutable spontaneously), BNL 02 and KU 9, which are also blue/pink heterozygotes. It was found that the gamma-ray-induced mutation frequency in KU 20 clone was comparable (18.8 pink mutant events per 10(4) hair-cell divisions per Gy) to those in BNL 02 (12.2 and 21.2) and KU 9 (17.4) clones, when the spontaneous mutation frequencies of KU 20 clone were relatively low (at most about 5.7 and 2.3 times of BNL 02 and KU 9 clones, respectively). However, when the spontaneous mutation frequecies of KU 20 clone were much higher (up to about 65 and 27 times of BNL 02 and KU 9 clones, respectively), induced mutation frequency was significantly higher in KU 20 clone (58.8 pink mutant events per 10(4) hair-cell divisions per Gy) than in BNL 02 and KU 9 clones. The extent of increase in the gamma-ray-induced mutation frequency in the latter case was nevertheless very much less than the increase in the spontaneous mutation frequency, suggesting different mechanisms of initiation and repair of radiation-induced and spontaneous mutations.textapplication/pdfjournal articl

相知炭山計画

東京帝国大学工科大学種別:卒業論文thesi

集合住宅共用部のエネルギー消費特性とそのPV利用に関する研究

application/pdf三重大学大学院工学研究科博士前期課程建築学専攻91thesi

アーバニズムと社会的ネットワーク―名古屋調査による「下位文化」理論の検証―

1992-03departmental bulletin pape

Developmental requirement of gp130 signaling in neuronal survival and astrocyte differentiation.

gp130 is a signal-transducing receptor component used in common by the interleukin-6 (IL-6) family of hematopoietic and neurotrophic cytokines, including IL-6, IL-11, leukemia-inhibitory factor, ciliary neurotrophic factor, oncostatin-M, and cardiotrophin-1. We have examined in this study a role of gp130 in the nervous system by analyzing developmental cell death of several neuronal populations and the differentiation of astrocytes in gp130-deficient mice. A significant reduction was observed in the number of sensory neurons in L5 dorsal root ganglia and motoneurons in the facial nucleus, the nucleus ambiguus, and the lumbar spinal cord in gp130 ?/? mice on embryonic day 18.5. On the other hand, no significant neuronal loss was detectable on day 14.5, suggesting a physiological role of gp130 in supporting newly generated neurons during the late phase of development when naturally occurring cell death takes place. Moreover, expression of an astrocyte marker, GFAP, was severely reduced in the brain of gp130 ?/? mice. Our data demonstrate that gp130 expression is essential for survival of subgroups of differentiated motor and sensory neurons and for the differentiation of major populations of astrocytesin vivo.journal articl

BRK binding is required to suppress <i>dpp</i> expression

<p>BRK binding sites are located in the R domain of APRD (filled pentagons). SPR analysis shows BRK binding to the intact R domain (R). Mutation of BRK site 1 [<i>r(brk1)</i>] reduces binding incrementally, mutation of BRK site 2 [<i>r(brk2)</i>] reduces binding still further while mutation of both sites [<i>r(brk1,2)</i>] abolishes binding completely. The biophysical binding of BRK to its DNA sites correlates well with the biological responses caused by the same mutations. B: <i>dpp</i> expression is ventrally repressed in the intact APRD fragment (arrow). C: Mutation of both BRK sites leads to loss of repression and ventral expression of <i>dpp</i> (arrow). D: Mutation of a single BRK site leads to ventral expression of <i>dpp</i> (arrow).</p

Simultaneous binding of BRK and dTCF is required for <i>dpp</i> repression.

<p>A–H: 3^rd instar leg imaginal discs. Dorsal is up and Anterior is to the left. A–D: response of <i>dpp</i> reporters to dpp^blk GAL4 driven expression of WG. E–H: response of <i>dpp</i> reporters to dpp^blk GAL4 driven expression of BRK. A: Ectopic dorsal expression of <i>wg</i> represses APRD>lacZ expression. B: Ectopic <i>wg</i> expression does not repress the APRD <i>dpp</i> reporter when all 5 of the dTCF binding sites are mutated (indicated by A<i>p</i>R<i>d</i>). C: WG expression does not repress the APRD <i>dpp</i> reporter when the BRK binding sites are mutated (AP<i>r</i>D). D: WG expression does not repress the APRD <i>dpp</i> reporter when all the dTCF and BRK binding sites are mutated (A<i>prd</i>). E: Ectopic dorsal expression of BRK represses APRD>lacZ expression. F: Ectopic BRK expression does not repress the APRD <i>dpp</i> reporter when all 5 of the dTCF binding sites are mutated (A<i>p</i>R<i>d</i>). G: Ectopic BRK expression does repress the <i>dpp</i> reporter when the BRK sites are mutated, APrD H: Ectopic BRK expression does not repress the <i>dpp</i> reporter when all the dTCF and BRK binding sites are mutated, A<i>prd</i>.</p