Impact of the first-forbidden β\beta decay on the production of A∼195A \sim 195 r-process peak

We investigated the effects of first-forbidden transitions in $\beta$ decays on the production of the r-process $A \sim 195$ peak. The theoretical calculated $\beta$-decay rates with $\beta$-delayed neutron emission were examined using several astrophysical conditions. As the first-borbidden decay is dominant in $N \sim 126$ neutron-rich nuclei, their inclusion shortens $\beta$-decay lifetimes and shifts the abundance peak towards higher masses. Additionally, the inclusion of the $\beta$-delayed neutron emission results in a wider abundance peak, and smoothens the mass distribution by removing the odd-even mass staggering. The effects are commonly seen in the results of all adopted astrophysical models. Nevertheless there are quantitative differences, indicating that remaining uncertainty in the determination of half-lives for $N=126$ nuclei is still significant in order to determine the production of the r-process peak.Comment: 6 pages, 4 figures, 1 table, Phys. Lett. B, in pres

Impact of New beta-decay Half-lives on r-process Nucleosynthesis

We investigate the effects of newly measured beta-decay half-lives on r-process nucleosynthesis. These new rates were determined by recent experiments at the radioactive isotope beam factory facility in the RIKEN Nishina Center. We adopt an r-process nucleosynthesis environment based on a magnetohydrodynamic supernova explosion model that includes strong magnetic fields and rapid rotation of the progenitor. A number of the new beta-decay rates are for nuclei on or near the r-process path, and hence they affect the nucleosynthesis yields and time scale of the r-process. The main effect of the newly measured beta-decay half-lives is an enhancement in the calculated abundance of isotopes with mass number A = 110 -- 120 relative to calculated abundances based upon beta-decay rates estimated with the finite-range droplet mass model. This effect slightly alleviates, but does not fully explain, the tendency of r-process models to underproduce isotopes with A = 110 -- 120 compared to the solar-system r-process abundances.Comment: 9 pages, 3 figures, 1 table, published in PR

The effect of molecular target drug, erlotinib, against endometrial cancer express ing high levels of epidermal growth factor receptor

学位記番号:医博甲152

太陽光中のUVA/UVBの比率の季節差がDNA損傷（6-４）型光産物のDewar型光産物への光異性化の効率に影響を及ぼす

The UVA and UVB components of sunlight can produce three classes of bipyrimidine DNA photolesions [cyclobutane pyrimidine dimers (CPDs), pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) and related Dewar valence isomers (DewarPPs)]. The UVA/UVB ratio of sunlight is high in winter and low in summer in the Northern Hemisphere. Since UVB radiation produces 6-4PPs and UVA radiation converts them into DewarPPs through photoisomerization, it is expected that there may be differences in the photoisomerization of 6-4PPs between summer and winter, although that has never been documented. To determine that, isolated DNA was exposed to natural sunlight for 8 h in late summer and in winter, and absolute levels of the three classes of photolesions were quantified using calibrated ELISAs. It was found that sunlight produces CPDs and 6-4PPs in DNA at a ratio of about 9:1 and converts approximately 80% of 6-4PPs into DewarPPs within 3 h. Moreover, photoisomerization is more efficient in winter than in late summer after sunlight irradiation for the same duration, at similar solar UV doses and with the same induction level of CPDs. These results demonstrate that seasonal differences in the UVA/UVB ratio influence the efficiency of the photoisomerization of 6-4PPs into DewarPPs.博士（医学）・甲第775号・令和3年3月15日© 2020 The Authors. Photochemistry and Photobiology published by Wiley Periodicals LLC on behalf of American Society for Photobiology. This is an open access article under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited

Diet-induced obesity in zebrafish shares common pathophysiological pathways with mammalian obesity

<p>Abstract</p> <p>Background</p> <p>Obesity is a multifactorial disorder influenced by genetic and environmental factors. Animal models of obesity are required to help us understand the signaling pathways underlying this condition. Zebrafish possess many structural and functional similarities with humans and have been used to model various human diseases, including a genetic model of obesity. The purpose of this study was to establish a zebrafish model of diet-induced obesity (DIO).</p> <p>Results</p> <p>Zebrafish were assigned into two dietary groups. One group of zebrafish was overfed with <it>Artemia </it>(60 mg dry weight/day/fish), a living prey consisting of a relatively high amount of fat. The other group of zebrafish was fed with <it>Artemia </it>sufficient to meet their energy requirements (5 mg dry weight/day/fish). Zebrafish were fed under these dietary protocols for 8 weeks. The zebrafish overfed with <it>Artemia </it>exhibited increased body mass index, which was calculated by dividing the body weight by the square of the body length, hypertriglyceridemia and hepatosteatosis, unlike the control zebrafish. Calorie restriction for 2 weeks was applied to zebrafish after the 8-week overfeeding period. The increased body weight and plasma triglyceride level were improved by calorie restriction. We also performed comparative transcriptome analysis of visceral adipose tissue from DIO zebrafish, DIO rats, DIO mice and obese humans. This analysis revealed that obese zebrafish and mammals share common pathophysiological pathways related to the coagulation cascade and lipid metabolism. Furthermore, several regulators were identified in zebrafish and mammals, including APOH, IL-6 and IL-1β in the coagulation cascade, and SREBF1, PPARα/γ, NR1H3 and LEP in lipid metabolism.</p> <p>Conclusion</p> <p>We established a zebrafish model of DIO that shared common pathophysiological pathways with mammalian obesity. The DIO zebrafish can be used to identify putative pharmacological targets and to test novel drugs for the treatment of human obesity.</p