Income Classification Provisions in Income Tax Act and Aggregation of Profit and Loss among Income Classification

亜細亜大学修士（法学）master thesi

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

journal articl

SYNERGISTIC EFFECTS OF METHYL METHANESULFONATE AND X-RAYS IN INDUCING SOMATIC MUTATIONS IN THE STAMEN HAIRS OF TRADESCANTIA CLONES, KU-27 AND BNL-4430

Young inflorescences of Tradescantia clones KU 27 and BNL 4430, the both of which are blue/pink heterozygotes and have been demonstrated to be highly sensitive to alkylating agents, were exposed either to aqueous solutions of methyl methanesulfonate (MMS) for 16hr alone (at 0.005 to 0.02% for KU 27 and at 0.006% for BNL 4430) or to acute 150 kVp X rays alone (161 to 531 mGy for KU 27 and 501 to 976 mGy for BNL 4430), or in combinations (134 to 448 mGy for KU 27 and 458 to 865 mGy for BNL 4430 after the 0.005% MMS treatment). The induced somatic pink mutation frequencies per hair-cell division were studied and compared, and clone BNL 4430 was found to be nearly two times more sensitive to MMS than clone KU 27, while the X-ray-induced mutation frequencies in the latter was about 1.5 times higher than those in the former. The lower sensitivity to MMS of clone KU 27 (as compared with BNL 4430) was nevertheless about 5.6 times higher as compared with the responses of clone BNL 02 to MMS reported earlier, proving the high sensitivities of the two clones used in the present study. Clear synergistic effects of MMS and X rays were observed in the both clones, indicating that the mechanisms of inducing mutations are common at least in part between MMS and X rays.textapplication/pdfjournal articl

高雄炭坑計画

東京帝国大学工科大学種別:卒業論文thesi

<翻訳>ドイツにおける労働裁判所の機能と名誉裁判官の役割

2008-03-25金井, 幸子[訳]departmental 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

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

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

Identification of dTCF binding sites required for <i>dpp</i> ventral repression

<p>A,B: dTCF binding sites in the <i>dpp</i> regulatory region from 109.4–112.8 kb were mapped by DNase I footprinting using dTCF protein as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000142#s2" target="_blank">methods</a> section <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000142#pone.0000142-vandeWetering1" target="_blank">[22]</a>. The approximate positions of the protected sites are indicated by stars. DNase I footprinting of the region containing the distal cluster (D) reveals 3 protected sites (sites 3, 4; 5) indicated by the bars in A and B. Similar footprints identified two sites in the proximal cluster (sites 1; 2 = P) and no footprints or gel shifts were detected in the A or R regions (not shown). Duplicate lanes represent independent reactions. Lanes 1; 7 are the GA sequencing ladder. All lanes utilize a 1∶1 dilution of bacterial extract containing empty expression vector or protein expressing vector and the same concentration of DNaseI except lane 4. Lanes 2 and 6 are no protein controls. Lane 3 uses an extract expressing human LEF1 protein. Lanes 4 and 5 use an extract expressing dTCF with lane 4 containing a 3 times higher concentration of DNase. C–E: 3rd instar leg imaginal discs. Dorsal is up, anterior is to the left. <i>dpp</i> lacZ expression is monitored by immunofluorescence. C: The 2.8 kb APRD <i>dpp</i> enhancer fragment with all 5 dTCF sites intact is repressed ventrally (bracket). D: Mutation of all 5 dTCF sites (A<i>p</i>R<i>d</i>) eliminates ventral repression (bracket). E: Mutation of just the 3 distal dTCF sites (APR<i>d</i>) is sufficient to eliminate ventral repression (bracket).</p