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No Effect of High Fat Diet-Induced Obesity on Spontaneous Reporter Gene Mutations in gpt Delta Mice
Takasu, Shinji,Ishii, Yuji,Matsushita, Kohei,Kuroda, Ken,Kijima, Aki,Kodama, Yukio,Ogawa, Kumiko,Umemura, Takashi Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.17
A large number of epidemiological studies have demonstrated that obesity is a risk factor for several human cancers. Several animal studies using rodents with diet-induced or genetic obesity have also demonstrated that obesity can promote tumor development. However, the effects of obesity on the early stages of carcinogenesis, and especially on the spontaneous occurrence of somatic gene mutations, remain unclear. To investigate the effects of obesity on the rate of spontaneous gene mutations, we performed reporter gene mutation assays in liver, kidney, and colon, organs in which obesity appears to be associated with cancer development on the basis of epidemiological or animal studies, in mice with high fat diet (HFD)-induced obesity. Six-week-old male and female C57BL/6 gpt delta mice were fed HFD or standard diet (STD) for 13 or 26 weeks. At the end of the experiments, reporter gene mutation assays of liver, kidney, and colon were performed. Final body weights and serum leptin levels of male and female mice fed HFD for 13 or 26 weeks were significantly increased compared with corresponding STD-fed groups. Reporter gene mutation assays of liver, kidney, and colon revealed that there were no significant differences in gpt or $Spi^-$ mutant frequencies between STD- and HFD-fed mice in either the 13-week or 26-week groups. These results indicate that HFD treatment and consequent obesity does not appear to influence the spontaneous occurrence of somatic gene mutations.
Tonna Ryutaro,Sasaki Takayuki,Kodama Yuji,Kobayashi Taishi,Akiyama Daisuke,Kirishima Akira,Sato Nobuaki,Kumagai Yuta,Kusaka Ryoji,Watanabe Masayuki 한국원자력학회 2023 Nuclear Engineering and Technology Vol.55 No.4
Simulated debris was synthesized using UO2, Zr, and stainless steel and a heat treatment method under inert or oxidizing conditions. The primary U solid phase of the debris synthesized at 1473 K under inert conditions was UO2, whereas a (U, Zr)O2 solid solution formed at 1873 K. Under oxidizing conditions, a mixture of U3O8 and (Fe, Cr)UO4 phases formed at 1473 K, whereas a (U, Zr)O2+x solid solution formed at 1873 K. The leaching behavior of the fission products from the simulated debris was evaluated using two methods: the irradiation method, for which fission products were produced via neutron irradiation, and the doping method, for which trace amounts of non-radioactive elements were doped into the debris. The dissolution behavior of U depended on the properties of the debris and aqueous solution for immersion. Cs, Sr, and Ba leached out regardless of the primary solid phases. The leaching of high-valence Eu and Ru ions was suppressed, possibly owing to their solid-solution reaction with or incorporation into the uranium compounds of the simulated debris.
Pleiotrophin exhibits a trophic effect on survival of dopaminergic neurons in vitro
Hida, Hideki,Jung, Cha-Gyun,Wu, Chen-Zhen,Kim, Hye-Jung,Kodama, Yuji,Masuda, Tadashi,Nishino, Hitoo 한림대학교 환경·생명과학연구소 2003 [일송 국제심포지엄] 노화와 만성퇴행성 신경질환 Vol.- No.5
To understand what kind of trophic factors are up-regulated in dopamine(DA)-depleted striatum, we first analysed the up-regulation of mRNAs using a DNA microarray in DA-depleted striatum where DAergic inputs were denervated by 6-OHDA. We then investigated whether or not such trophic factors had an effect on cultured dopaminergic neurons. The microarray analysis revealed that pleiotrophin (PTN), glial-derived neurotopic factor(GDNF) and others were up-regulated in DA-depleted striatum. As PTN has been reported to have a wide range of trophic effects on neurons, we focused on the functional role of PTN in the present study. The increase in PTN mRNA was confirmed by Northern blotting at 1-3 weeks after the lesion, reaching a peak at 1 week. In embryonic day 15 mesencephalic neuron culture, PTN increased the number of tyrosine hydroxylase (TH)-positive neurons in a dose-dependent manner (125.2±2.0% of the control at 50ng/mL), while a family protein, midkine(10ng/mL) did not show any trophic effect (99.3±0.7%). In addition, the PTN effect on DAergic neurons was additive to the GDNF effect. As PTN did not increase the number of microtubule-associated protein-2(MAP 2)-positive neurons or promote the proliferation of dopaminergic progenitors in a bromodeoxyuridine(BrdU) labelling study, the effect appeared to enhance the specific survival of dopaminergic neurons. Expression of PTN receptors (syndecan-3, PTP-ζ) was detected on the cultured mesencephalic neurons, and also up-regulated in DA-depleted striatum. The data indicate that PTN is up-regulated in DA-depleted striatum and exhibits a trophic effect specifically on the survival of cultured dopaminergic neurons.