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        Heavy concrete shielding properties for carbon therapy

        Jin-Long Wang,Jiade J Lu,Da-Jun Ding,Wen-Hua Jiang,Ya-Dong Li,Rui Qiu,Hui Zhang,Xiao-Zhong Wang,Huo-Sheng Ruan,Yan-Bing Teng,Xiao-Guang Wu,Yun Zheng,Zi-Hao Zhao,Kai-Zhong Liao,Huan-Cheng Mai,Xiao-Dong Korean Nuclear Society 2023 Nuclear Engineering and Technology Vol.55 No.6

        As medical facilities are usually built at urban areas, special concrete aggregates and evaluation methods are needed to optimize the design of concrete walls by balancing density, thickness, material composition, cost, and other factors. Carbon treatment rooms require a high radiation shielding requirement, as the neutron yield from carbon therapy is much higher than the neutron yield of protons. In this case study, the maximum carbon energy is 430 MeV/u and the maximum current is 0.27 nA from a hybrid particle therapy system. Hospital or facility construction should consider this requirement to design a special heavy concrete. In this work, magnetite is adopted as the major aggregate. Density is determined mainly by the major aggregate content of magnetite, and a heavy concrete test block was constructed for structural tests. The compressive strength is 35.7 MPa. The density ranges from 3.65 g/cm<sup>3</sup> to 4.14 g/cm<sup>3</sup>, and the iron mass content ranges from 53.78% to 60.38% from the 12 cored sample measurements. It was found that there is a linear relationship between density and iron content, and mixing impurities should be the major reason leading to the nonuniform element and density distribution. The effect of this nonuniformity on radiation shielding properties for a carbon treatment room is investigated by three groups of Monte Carlo simulations. Higher density dominates to reduce shielding thickness. However, a higher content of high-Z elements will weaken the shielding strength, especially at a lower dose rate threshold and vice versa. The weakened side effect of a high iron content on the shielding property is obvious at 2.5 µSv=h. Therefore, we should not blindly pursue high Z content in engineering. If the thickness is constrained to 2 m, then the density can be reduced to 3.3 g/cm<sup>3</sup>, which will save cost by reducing the magnetite composition with 50.44% iron content. If a higher density of 3.9 g/cm<sup>3</sup> with 57.65% iron content is selected for construction, then the thickness of the wall can be reduced to 174.2 cm, which will save space for equipment installation.

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        MicroRNA-375 is a therapeutic target for castration-resistant prostate cancer through the PTPN4/STAT3 axis

        Gan Junqing,Liu Shan,Zhang Yu,He Liangzi,Bai Lu,Liao Ran,Zhao Juan,Guo Madi,Jiang Wei,Li Jiade,Li Qi,Mu Guannan,Wu Yangjiazi,Wang Xinling,Zhang Xingli,Zhou Dan,Lv Huimin,Wang Zhengfeng,Zhang Yanqiao,Q 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

        The functional role of microRNA-375 (miR-375) in the development of prostate cancer (PCa) remains controversial. Previously, we found that plasma exosomal miR-375 is significantly elevated in castration-resistant PCa (CRPC) patients compared with castration-sensitive PCa patients. Here, we aimed to determine how miR-375 modulates CRPC progression and thereafter to evaluate the therapeutic potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes loaded with miR-375 antisense oligonucleotides (e-375i). We used miRNA in situ hybridization technique to evaluate miR-375 expression in PCa tissues, gain- and loss-of-function experiments to determine miR-375 function, and bioinformatic methods, dual-luciferase reporter assay, qPCR, IHC and western blotting to determine and validate the target as well as the effects of miR-375 at the molecular level. Then, e-375i complexes were assessed for their antagonizing effects against miR-375. We found that the expression of miR-375 was elevated in PCa tissues and cancer exosomes, correlating with the Gleason score. Forced expression of miR-375 enhanced the expression of EMT markers and AR but suppressed apoptosis markers, leading to enhanced proliferation, migration, invasion, and enzalutamide resistance and decreased apoptosis of PCa cells. These effects could be reversed by miR-375 silencing. Mechanistically, miR-375 directly interfered with the expression of phosphatase nonreceptor type 4 (PTPN4), which in turn stabilized phosphorylated STAT3. Application of e-375i could inhibit miR-375, upregulate PTPN4 and downregulate p-STAT3, eventually repressing the growth of PCa. Collectively, we identified a novel miR-375 target, PTPN4, that functions upstream of STAT3, and targeting miR-375 may be an alternative therapeutic for PCa, especially for CRPC with high AR levels.

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