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The emergence of TKX-50, an energetic ionic salt with a high enthalpy of formation and low sensitivity, has opened a new path for the development of high-energetic, insensitive composite explosives. However, due to the poor interfacial binding properties of TKX-50 with conventional binders, there is a lack of effective guidance for the design of TKX-50 based composite explosives. To address the above issues, the interactions between carboxymethyl cellulose acetate butyrate (CMCAB) and other binders with explosives TKX-50/HMX were compared using the molecular dynamics method. Based on the simulations, TKX-50/HMX/CMCAB-based polymer-bonded explosives (PBXs) were prepared with CMCAB as binder, which displays a high binding energy (Ebind) with TKX-50 and high cohesive energy density (CED), and the effect of TKX-50 content on the performance of PBXs was investigated. The physical properties of PBXs, specifically the morphology, mechanical sensitivity, and thermal conductivity, were analyzed by SEM, sensitivity apparatus, and thermal conductivity meter, respectively. The specific heat capacity (Cp) and non-isothermal decomposition temperature of PBXs were tested by DSC, and then the corresponding thermal kinetic parameters were analyzed to evaluate their thermal safety. The adiabatic thermal decomposition processes of PBXs were tested using an ARC instrument. The decomposition mechanism and kinetics were also explored to further analyze their thermal stability and thermal safety under adiabatic conditions. The computer code EXPLO5 was used to predict the detonation parameters of PBXs. The results showed that CMCAB and TKX-50 displayed favorable interfacial bonding properties, and TKX-50 can be bonded with HMX to form a molding powder with a desirable morphology and safety profile. The TKX-50 in PBXs effectively improves the mechanical sensitivity and thermal safety of PBX and has a significant effect on the detonation performance of PBX. This research demonstrates a novel method suitable for screening and investigating high-energetic insensitive explosive systems compatible with TKX-50. [ABSTRACT FROM AUTHOR]

Dysregulated expression of epidermal growth factor receptor (EGFR) has been implicated in many cancer events, while peroxisome proliferator-activated receptor γ (PPARγ) negatively regulates cancer progression. The molecular mechanism of EGFR interaction with PPARγ is still unclear. Here, we found that nuclear EGFR induced phosphorylation of PPARγ at Tyr-74 leading to PPARγ ubiquitination and degradation by mouse double minute 2 (MDM2) ubiquitin ligase. PPARγ degradation by EGFR/MDM2 signaling resulted in accumulation of nuclear factor-kappaB (NF-κB)/p65 protein levels and increasing NF-κB activation. In contrast, PPARγ-Y74A mutant reversed this event. Moreover, PPARγ-Y74A mutant suppressed cell proliferation and increased chemotherapeutic agent-induced cancer cell sensitivity. Importantly, the clinical findings show that the nuclear phosphorylation of PPARγ-Y74 and EGFR expression in colonic cancer tissues was higher than that in control normal tissues. Thus, our study revealed a novel molecular mechanism that nuclear EGFR/NF-κB signaling promoted cell proliferation by destructing PPARγ function, which provides a novel strategy for cancer treatment. [ABSTRACT FROM AUTHOR]