Omental leiomyosarcoma with unusual giant cells in a Beagle dog — Short communication

A 10-year-old castrated male Beagle dog was presented with a 2-month history of intermittent vomiting and abdominal pain. The dog was referred to the Veterinary Teaching Hospital at Iwate University for further evaluation, and a splenic tumour was suspected on the basis of ultrasonography and computed tomography. Surgery identified a large, solid, light-pink mass on the greater omentum with blood-coloured ascites in the abdominal cavity, and resection was performed. Microscopically, the mass comprised spindle-shaped tumour cells and scattered osteoclast-like giant cells. Most spindle-shaped cells were positive for vimentin, desmin, and smooth muscle actin (α-SMA), whereas osteoclast-like giant cells were positive only for vimentin. On the basis of histopathological and immunohistochemical findings, a diagnosis of leiomyosarcoma was made. To the best of our knowledge, this represents the first report of leiomyosarcoma associated with osteoclast-like giant cells developing from the greater omentum in a dog

Alternative methods to evaluate the protective ability of sunscreen against photo-genotoxicity

Numerous epidemiological investigations show that sunlight is carcinogenic to humans and that the use of sunscreen may be effective in decreasing the risk of skin cancer. The biological activity of a sunscreen is evaluated by its ability to protect human skin from erythema as represented by a Sun Protection Factor (SPF). We propose that the sunscreen's protective effect against sunlight-induced genotoxicity, including mutation, should also be taken into account. In this study we examined the protective ability of sunscreens against natural sunlight and UV-induced genotoxicity in Drosophila somatic cells. We prepared three kinds of sunscreen samples, each with an SPF value of 20, 40 or 60 and compared their protective activities with commercial sunscreens. When a sunscreen of SPF 20, 40 or 60 was pasted on the plastic cover of a petri dish in which Drosophila larvae were exposed to the sun or UV lamps, genotoxicity decreased as the SPF of the sunscreen increased, relative to levels of genotoxicity observed in samples without sunscreen. However, the protective abilities of sunscreens were unexpectedly not so different from each other. To reveal the relationship between the protective activity of sunscreen and the wavelength of light with which larvae were irradiated through the sunscreen, we measured the transmittance of light through the petri dish cover on which the sunscreen was pasted. Effective protection was demonstrated by removing components of light whose wavelengths were below 315 nm. We suggest, that the measurement of anti-genotoxic activity and the determination of the wavelengths of light transmitted through the sunscreen should be an alternative method for evaluating the effectiveness of a sunscreen.</p

2019 年度看護学部教育課程の改定について

紀要委員会企画Special Articles　本稿は、本学看護学部の2019 年度教育課程改定における活動内容の概要を記した。2012 年に教育課程変更を行って５年が経過したことや、教育職員免許法の改正により養護教諭課程の再課程認定に伴い、2019 年度に向けて看護学部教育課程の改定を行うことになった。2017 年度からカリキュラム検討委員会を中心に教育課程の検討を行い、２年間に渡って教育課程改定に向けて活動した内容をまとめた。2019 年度新教育課程としては、地域包括ケアシステムの推進に基づく社会の変遷にあわせた教育課程へと発展させるための学修内容の追加、本学の強みである充実した実習環境をもとに行われている臨地看護学実習を通して「生命の尊厳と隣人愛」に基づく教育理念を継続的に意識づけられるような教育課程を策定することができた。指定規則改正に伴う次の教育課程の改定に向けて、今回のプロセスが参考となることを期待する

ショウシャ セイシ ジュセイ マウス ラン ニ オケル p53 ノ テンシャ ヒイソンテキナ DNA ゴウセイ ノ ヨクセイ

京都大学0048新制・課程博士博士(医学)甲第11435号医博第2858号新制||医||894(附属図書館)23078UT51-2005-D185京都大学大学院医学研究科生理系専攻(主査)教授 藤堂 剛, 教授 武田 俊一, 教授 篠原 隆司学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDA

The involvement of cell cycle checkpoint-mutations in the mutagenesis induced in Drosophila by a longer wavelength light band of solar UV

Solar ultraviolet radiation is considered to be injurious rather than necessary for most organisms living on the earth. It is reported that the risk of skin cancer in humans increased by the depletion of the ozone layer. We have examined the genotoxicity of solar ultraviolet, especially the longer wavelengths light, using Drosophila. Recently, we have demonstrated that light of wavelengths up to 340 nm is mutagenic on Drosophila larvae. Using an excision repair-deficient Drosophila strain (mus201), we have obtained results suggesting that the lesion caused in larvae by the 320 nm-light irradiation may be similar to the damage induced by irradiation at 310 nm, and that light of 330 and 340 nm may induced damage different from that induced by 310 and 320 nm-light. To examine the difference in DNA damage induced by light of particular wavelength, we performed monochromatic irradiation on larvae of two Drosophila strains; one excision repair-deficient (mei-9) and another postreplication repair-deficient (mei-41). 310 and 320 nm-light was more mutagenic in the mei-9 strain than mei-41, whereas 330 and 340 nm-light was more mutagenic in mei-41 than in mei-9. It is demonstrated that the mei-41 gene is a homologue of the human atm gene which is responsible for a cell cycle checkpoint. This result suggests that 310-320 nm-light induces DNA damage that is subject to nucleotide excision repair (NER) and that 3300-360 nm-light causes damage to be recognized by the cell cycle checkpoint but it is not repairable by NER

Radiation induction of delayed recombination in Schizosaccharomyces pombe.

Ionizing radiation is known to induce delayed chromosome and gene mutations in the descendants of the irradiated tissue culture cells. Molecular mechanisms of such delayed mutations are yet to be elucidated, since high genomic complexity of mammalian cells makes it difficult to analyze. We now tested radiation induction of delayed recombination in the fission yeast Schizosaccharomyces pombe by monitoring the frequency of homologous recombination after X-irradiation. A reporter with 200 bp tandem repeats went through spontaneous recombination at a frequency of 1.0 x 10(-4), and the frequency increased dose-dependently to around 10 x 10(-4) at 500 Gy of X-irradiation. Although the repair of initial DNA damage was thought to be completed before the restart of cell division cycle, the elevation of the recombination frequency persisted for 8-10 cell generations after irradiation (delayed recombination). The delayed recombination suggests that descendants of the irradiated cells keep a memory of the initial DNA damage which upregulates recombination machinery for 8-10 generations even in the absence of DNA double-strand breaks (DSBs). Since radical scavengers were ineffective in inhibiting the delayed recombination, a memory by continuous production of DNA damaging agents such as reactive oxygen species (ROS) was excluded. Recombination was induced in trans in a reporter on chromosome III by a DNA DSB at a site on chromosome I, suggesting the untargeted nature of delayed recombination. Interestingly, Rad22 foci persisted in the X-irradiated population in parallel with the elevation of the recombination frequency. These results suggest that the epigenetic damage memory induced by DNA DSB upregulates untargeted and delayed recombination in S. pombe

Delayed and stage specific phosphorylation of H2AX during preimplantation development of gamma-irradiated mouse embryos

Within minutes of the induction of DNA double-strand breaks in somatic cells, histone H2AX becomes phosphorylated in the serine 139 residue at the damage site. The phosphorylated H2AX, designated as gamma-H2AX, is visible as nuclear foci in the irradiated cells which are thought to serve as a platform for the assembly of proteins involved in checkpoint response and DNA repair. It is known that early stage mammalian embryos are highly sensitive to radiation but the mechanism of radiosensitivity is not well understood. Thus, we investigated the damage response of the preimplantation stage development by analyzing focus formation of gamma-H2AX in mouse embryos gamma-irradiated in utero. Our analysis revealed that although H2AX is present in early preimplantation embryos, its phosphorylation after 3 Gy gamma-irradiation is hindered up to the two cell stage of development. When left in utero for another 24-64 h, however, these irradiated embryos showed delayed phosphorylation of H2AX. In contrast, phosphorylation of H2AX was readily induced by radiation in post-compaction stage embryos. It is possible that phosphorylation of H2AX is inefficient in early stage embryos. It is also possible that the phosphorylated H2AX exists in the dispersed chromatin structure of early stage embryonic pronuclei, so that it cannot readily be detected by conventional immunostaining method. In either case, this phenomenon is likely to correlate with the lack of cell cycle arrest, apoptosis and high radiosensitivity of these developmental stages