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京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第21991号 / 医博第4505号 / 新制||医||1037(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 武田 俊一, 教授 坂井 義治, 教授 松田 道行 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

The aim of this thesis is to design nature trail in Lažánecko - Heroltický karst and by that increase the attractiveness of the area. The theoretical part is devoted to information and rules related to the creation of a nature trail, including specification of problems that may arise in the course of its implementation. Subsequently, nature trails from the surrounding area are analyzed as part of the field survey. In practical part is created design of educational trail that included project documentation, specific location and description of every stop.

Thema of the thesis is to analyse actual state and predict future application of english yew (Taxus baccata L.) in forest sites at chosen parts of PLA Moravský kras. Structure of parent stand and natural regeneration is analyzed on locations of interest Habrůvecká tůň, Lažánky, Sloup and Macocha. There was measured height, dbh, height of the crown, projection of the crown and space situations were drawned for mature individuals. In case of natural regeneration every individual was measured for height, distance from assumed parent tree, age and damage by game. At locations of interest were analysed 82 mature individuals. Height ranges from 1,7 to 13,4 m and dbh ranges from 4,1 to 33,7 cm. Natural regeneration containing 260 individuals was found near 35 mature yews and 58% was younger than 5 years. Damage by browsing was observed at 51 individuals, respectively 19,6 % of population. Mostly, trees older than 5 years are damaged. Damage is often repetitive. Only two individuals from natural regeneration are higher than 1m. From research is apparent negative influence of game on natural regeneration. Future of yew population in PLA Moravský Kras is conditioned to elimination of negative influence of game, which can be achieved by lowering numbers of game or suitable protection of trees.

京都大学 / 新制・課程博士 / 博士(医学) / 甲第23608号 / 医博第4795号 / 新制||医||1055(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 妹尾 浩, 教授 中島 貴子, 教授 戸井 雅和 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

Indiana University-Purdue University Indianapolis (IUPUI) / Pancreatic ductal adenocarcinoma (PDAC) is currently the fourth leading cause of cancer-related death in the United States, and is characterized by key driver mutations (e.g. KRAS, TP53, CDKN2A, and SMAD4), elevated expression of growth factors such as TGF-βs and the EGF receptor (EGFR), a markedly desmoplastic stroma, and a propensity to develop multi-organ metastases and chemoresistance. Consistent with its aggressive nature, the 5-year survival rate for PDAC is 8-9%, which demonstrates an urgent need to develop novel therapies. High expression levels of microRNA-10b (miR-10b) in PDAC tissues are associated with decreased patient survival and earlier appearance of metastatic disease following neoadjuvant chemoradiotherapy. miR-10b downregulates the expression of transcription coactivator Tat-Interacting Protein 30 (TIP30) by targeting its 3’UTR. TIP30 has multiple reported functions. TIP30 suppresses tumor formation and metastasis, forms a complex that regulates EGFR trafficking and degradation, and transcriptionally upregulates pro-apoptotic genes. Alterations in TIP30 have been reported in multiple human cancers, including pancreatic cancer. We hypothesized that Tip30-deficiency accelerates PDAC progression and metastasis in a murine model of PDAC. To test this hypothesis, we crossed mice with oncogenic Kras (KC) localized to the pancreas epithelium, with Tip30-deficient mice (K30C). We compared PDAC histopathology between Tip30-heterozygous (K30+/-C) and Tip30-null (K30-/-C) mice. Tip30-heterozygosity accelerated PDAC-lesion-associated pancreatic cancer cell (PCC) pulmonary seeding. By contrast, total loss of Tip30 enhanced PCC micrometastatic seeding to the liver and hepatic metastasis. K30+/-C mice also presented with an early, increased penetrance of lung lesions and lung adenocarcinoma; and PCCs isolated from K30+/-C pancreata exhibited increased EGFR protein levels. These findings suggest that TIP30 deficiency can have a dose-dependent effect on organotropic metastasis and EGFR levels in PCCs. Future studies will delineate the molecular consequences of TIP30 loss in PDAC and contribute to a broader understanding of pancreatic cancer metastasis. / 2020-08-05

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第18853号 / 医博第3964号 / 新制||医||1007(附属図書館) / 31804 / 京都大学大学院医学研究科医学専攻 / (主査)教授 山田 泰広, 教授 武田 俊一, 教授 野田 亮 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第20239号 / 医博第4198号 / 新制||医||1019(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 妹尾 浩, 教授 野田 亮, 教授 武藤 学 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

京都大学 / 新制・課程博士 / 博士(医学) / 甲第24804号 / 医博第4996号 / 新制||医||1067(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 武藤 学, 教授 藤田 恭之, 教授 川口 義弥 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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