リン ナイ ビキコウ ガ ノネズミ ルイ ノ ホカクリツ ニ オヨボス エイキョウ

静岡県富士宮市麓の針葉樹植林地において,ノネズミ類の捕獲率に林内微気候が及ぼす影響を調べるために232台のワナを設置し,2007年5-11月の42夜に1夜につき4回の見回り調査を行った。ヒメネズミApodemus argenteusは延べ699回,アカネズミA. speciosusは66回捕獲された。降雨時と非降雨時の捕獲率には有意な違いは見られなかったが,降雨量20mm/h以上の時には捕獲されなかった。夜間の時間帯別捕獲率は,夜明け前後を除いて違いが見られなかった。夜間の気温や湿度は捕獲率に影響していなかった。捕獲率に最も大きく影響する要因は繁殖に伴う個体数変動であり,捕獲率は両種ともに5-6月に高く,その後漸減した。The influence of in-canopy microclimates on capture rates of small rodents was investigated at a coniferous plantation in Fujinomiya city, Japan. We installed 232traps and inspected them 4times per night for 42 nights from May to November 2007. A total of 699 captures were recorded for Apodemus argenteus and 66 for A. speciosus. Capture rates were not significantly different between rainy nights and non-rainy nights, except for heavy rainfall (>20mm/h) occasions. Capture rates of three time zones of a night (after sunset, before midnight, and after midnight) were not significantly different, but the rate around dawn became low. Ambient temperature and humidity were not influential factors for capture rates. Population fluctuation caused by breeding was the major factor that affected capture rates

老化マーカー分子glutathione S-transferase theta 1(GSTT1)の発現機構に関する研究

University of Tokyo (東京大学

Spontaneous transformation of human granulosa cell tumours into an aggressive phenotype: a metastasis model cell line

Abstract Background Granulosa cell tumours (GCTs) are frequently seen in menopausal women and are relatively indolent. Although the physiological properties of normal granulosa cells have been studied extensively, little is known about the molecular mechanism of GCT progression. Here, we characterise the unique behavioural properties of a granulosa tumour cell line, KGN cells, for the molecular analysis of GCT progression. Methods Population doubling was carried out to examine the proliferation capacity of KGN cells. Moreover, the invasive capacity of these cells was determined using the in vitro invasion assay. The expression level of tumour markers in KGN cells at different passages was then determined by Western blot analysis. Finally, the growth and metastasis of KGN cells injected subcutaneously (s.c.) into nude mice was observed 3 months after injection. Results During in vitro culture, the advanced passage KGN cells grew 2-fold faster than the early passage cells, as determined by the population doubling assay. Moreover, we found that the advanced passage cells were 2-fold more invasive than the early passage cells. The expression pattern of tumour markers, such as p53, osteopontin, BAX and BAG-1, supported the notion that with passage, KGN cells became more aggressive. Strikingly, KGN cells at both early and advanced passages metastasized to the bowel when injected s.c. into nude mice. In addition, more tumour nodules were formed when the advanced passage cells were implanted. Conclusion KGN cells cultured in vitro acquire an aggressive phenotype, which was confirmed by the analysis of cellular activities and the expression of biomarkers. Interestingly, KGN cells injected s.c. are metastatic with nodule formation occurring mostly in the bowel. Thus, this cell line is a good model for analysing GCT progression and the mechanism of metastasis in vivo.</p

Metachronous pancreatic cancer originating from disseminated founder pancreatic intraductal neoplasias (PanINs)

Abstract Clonal populations originated from benign‐looking ‘founder cells' may spread widely within pancreas instead of being localized in situ before frank pancreatic ductal adenocarcinoma (PDA) can be detected. Metachronous PDA is not common event, and we here sought to define potent origin of multiple PDAs developed in a woman using advanced genetics technologies. Curative resection of pancreatic head tumour was performed; however, ‘recurrent' lesions in the remnant pancreas were found 3.5 years later and total pancreatectomy was subsequently performed. The metachronous lesions were morphologically similar to the primary PDA. Using a next‐generation sequencing and digital PCR, all three PDAs were shown to possess rare somatic mutations in KRAS (p.T58I & p.Q61H). Curiously, identical KRAS mutations were found in low‐grade ‘intraepithelial' lesions, which localized in normal area of the pancreas and one of them possessed p53 mutation, which was also found in the PDAs. The footprint of the tumour evolution marked by mutational profiling supports a human correlate to the mouse models of ‘dissemination' occurring at the earliest stages of pancreatic neoplasia