10 research outputs found


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    金沢大学理工研究域電子情報学系Electromagnetic devices such as superconducting magnets, magnetically levitated vehicles and magnetic resonance imaging(MRI) create strong magnetic fields within their immediate vicinity. This has generated some concerns over the effects that these fields may have on the outside environment and in particular on living organisms. 50/60Hz magnetic fields are of special concern because living organisms are exposed to them on a continuing basis.We investigate the influence of a strong 60Hz AC magnetic field of 1.2T on organisms. The high AC magnetic field is generated by using a multilayer eddy-current type AC magnetic generator developed in our laboratory. In this paper, in vitro experiments were performed with biochemical reactions, enzyme and restriction endonuclese activities.As a result, the magnetic field inhibited catalase activity slightly only in biochemical reactions. Other reactions such as β-galactosidase activity and restriction endonuclese activity were not influenced at all. The results suggest that high 60Hz AC magnetic fields may influence biological functions in some organisms

    On Freudenburg's counterexample to the Fourteenth Problem of Hilbert

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    The Histone Methyltransferase SETD8 Regulates the Expression of Tumor Suppressor Genes via H4K20 Methylation and the p53 Signaling Pathway in Endometrial Cancer Cells

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    The histone methyltransferase SET domain-containing protein 8 (SETD8), which methylates histone H4 lysine 20 (H4K20) and non-histone proteins such as p53, plays key roles in human carcinogenesis. Our aim was to determine the involvement of SETD8 in endometrial cancer and its therapeutic potential and identify the downstream genes regulated by SETD8 via H4K20 methylation and the p53 signaling pathway. We examined the expression profile of SETD8 and evaluated whether SETD8 plays a critical role in the proliferation of endometrial cancer cells using small interfering RNAs (siRNAs). We identified the prognostically important genes regulated by SETD8 via H4K20 methylation and p53 signaling using chromatin immunoprecipitation sequencing, RNA sequencing, and machine learning. We confirmed that SETD8 expression was elevated in endometrial cancer tissues. Our in vitro results suggest that the suppression of SETD8 using siRNA or a selective inhibitor attenuated cell proliferation and promoted the apoptosis of endometrial cancer cells. In these cells, SETD8 regulates genes via H4K20 methylation and the p53 signaling pathway. We also identified the prognostically important genes related to apoptosis, such as those encoding KIAA1324 and TP73, in endometrial cancer. SETD8 is an important gene for carcinogenesis and progression of endometrial cancer via H4K20 methylation