Silica-based ceramic cores play key roles in the casting of aeroengine blades, but they are highly limited by the poor high-temperature mechanical property. Here, fused mullite (FM) and sintered mullite (SM) powders were modified in silica-based ceramic cores, and the microstructure evolution and crystallization kinetics of ceramic cores depending on mullite types were studied. The ceramic cores with FM showed a dense microstructure and superior mechanical properties compared to those with SM. The ceramic cores with 10 wt.% of FM showed a crystallization activation energy of 1119.5 kJ/mol and a crystallization exponent of 1.74, and the values of 938.4 kJ/mol and 1.86 as SM were employed; the decreased crystallization activation energy and the elevated crystallization exponent by SM suggested that the excess impurities of alkali oxides and alkaline-earth oxides significantly promoted the crystallization of cristobalite. Even though the ceramic cores with mullite powders decreased slightly in the room-temperature mechanical property, their high-temperature flexure strength and creep deformation resistance were enhanced. The ceramic cores with 10 wt.% of FM showed excellent comprehensive performance, with linear shrinkage of 0.69%, room-temperature strength of 18.9 MPa, and high-temperature strength of 15.5 MPa, which satisfied the demands for hollow-blade casting.
Context
Acute promyelocytic leukaemia (APL) is a malignant hematological tumour characterized by the presence of promyelocytic leukaemia–retinoic acid receptor A (PML-RARA) fusion protein. Cinobufagin (CBG) is one of the main effective components of toad venom with antitumor properties. However, only a few reports regarding the CBG treatment of APL are available.
Objective
We explored the effect and mechanism of action of CBG on NB4 and NB4-R1 cells.
Materials and methods
We evaluated the viability of NB4 and NB4-R1 cells treated with 0, 20, 40, and 60 nM CBG for 12, 24, and 48 h. After treatment with CBG for 24 h, Bcl-2 associated X (Bax), B-cell lymphoma 2 (Bcl-2), β-catenin, cyclin D1, and c-myc expression was detected using western blotting and real-time polymerase chain reaction. Caspase-3 and PML-RARA expression levels were detected using western blotting.
Results
CBG inhibited the viability of NB4 and NB4-R1 cells. The IC
50
values of NB4 and NB4-R1 cells treated with CBG for 24 h were 45.2 nM and 37.9 nM, respectively. CBG induced NB4 and NB4-R1 cell apoptosis and PML-RARA degradation in a caspase-dependent manner and inhibited the β-catenin signalling pathway.
Discussion and conclusion
CBG induced NB4 and NB4-R1 cell apoptosis and PML-RARA degradation in a caspase-dependent manner by inhibiting the β-catenin signalling pathway. This study proposes a novel treatment strategy for patients with APL, particularly those with ATRA-resistant APL.
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