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In this paper, 75 concrete prisms were tested under different temperatures (20, 200, 400, 600 and 800 °C) and molybdenum tailings replacement ratio (0, 25, 50, 75, and 100 %). The axial compression failure modes and mechanical properties of molybdenum tailings concrete were studied. The results show that the increase in temperature will aggravate the failure of concrete under axial compression, instead of molybdenum tailing replacement ratio. With the increase of temperature (20–800 °C), the surface color of the concrete becomes lighter, and obvious cracks began to appear from 400 °C, the mass loss ratio and peak strain of molybdenum tailings concrete show an increasing trend, and reach the maximum growth ratio (6.58 % and 34 %) at 800 °C. The peak stress and elastic modulus of molybdenum tailings concrete show a decreasing trend, and reach the maximum reduction at 800 °C (52 % and 71 %). With the increase of replacement ratio, the mass loss ratio of molybdenum tailings concrete increases linearly. The peak stress, peak strain and elastic modulus of molybdenum tailings concrete at all temperatures increase first and then decrease. The 25 % molybdenum tailings content can improve the deterioration of molybdenum tailings concrete after exposure to high temperature. Based on the experimental data, the prediction formulas of peak stress/strain and elastic modulus of molybdenum tailings under different temperature-molybdenum tailings replacement ratio coupling conditions are fitted respectively. The experimental and calculated values of the formula are in good agreement.

Abstract Retinoblastoma is a rare, intraocular paediatric cancer that originates in the neural retina and is most frequently caused by bi-allelic loss of RB1 gene function. Other oncogenic mutations, such as amplification and increased expression of the MYCN gene, have been found even with proficient RB1 function. In this study, we investigated whether MYCN over-expression can drive carcinogenesis independently of RB1 loss-of-function mutations. The aim was to elucidate the events that result in carcinogenesis and identify the cancer cell-of-origin. We used the chicken retina, a well-established model for studying retinal neurogenesis, and established human embryonic stem cell-derived retinal organoids as model systems. We over-expressed MYCN by electroporation of piggyBac genome-integrating expression vectors. We found that over-expression of MYCN induced tumorigenic growth with high frequency in RB1-proficient chicken retinas and human organoids. In both systems, the tumorigenic cells expressed markers for undifferentiated cone photoreceptor/horizontal cell progenitors. The over-expression resulted in metastatic retinoblastoma within 7–9 weeks in chicken. Cells expressing MYCN could be grown in vitro and, when orthotopically injected, formed tumours that infiltrated the sclera and optic nerve and expressed markers for cone progenitors. Investigation of the tumour cell phenotype determined that the potential for neoplastic growth was embryonic stage-dependent and featured a cell-specific resistance to apoptosis in the cone/horizontal cell lineage, but not in ganglion or amacrine cells. We conclude that MYCN over-expression is sufficient to drive tumorigenesis and that a cell-specific resistance to apoptosis in the cone/horizontal cell lineage mediates the cancer phenotype.