Wuyi University

This study is based on 2,276 real transaction data from the Xianyu platform and uses a three-stage regression model to systematically analyze the moderating effect of blind box brand value on scarcity premium. The research first reveals the overall premium level of the market through descriptive statistics, then builds a basic model to verify the scarcity effect, and then introduces the brand fixed effect to control the inherent value differences of brands. Finally, it tests the interaction between brand value and scarcity through the moderating effect model. The empirical results show that the average premium rate of the hidden model reaches 164.9%, significantly higher than 7.2% of the regular model. Brand value has a significant moderating effect on the scarcity effect. The scarcity effect coefficient of SKULLPANDA (2.230) is 2.6 times that of MOLLY (0.862). The research conclusion provides important empirical evidence for the pricing mechanism of the blind box market, consumers' investment decisions, and brand IP operations.

Glioblastoma (GBM), a highly aggressive primary brain tumor, presents substantial treatment challenges due to its resistance to genotoxic therapies and frequent recurrence. Oncogenic alterations significantly impact lipid metabolism in GBM cells. G Protein-Coupled Receptor 40 (GPR40), a receptor for polyunsaturated fatty acids (PUFAs), plays a key role in neural development and neurogenesis. Additionally, ferroptosis induction in GBM relies on PUFA peroxidation within cell membranes. Considering the persistent oxidative stress in the central nervous system, aberrant GPR40 activation in glioma lipid metabolism might suppress ferroptosis, thus contributing to chemotherapy resistance. Transcriptomic analysis of TCGA data revealed upregulated GPR40 expression in malignant gliomas, alongside alterations in ferroptosis-related and drug resistance pathways. To model GBM temozolomide (TMZ) resistance, a TMZ-resistant GL261 cell line was established. Additionally, key ferroptosis markers, including iron metabolism, lipid peroxidation, and glutathione levels, as well as TMZ treatment sensitivity, were assessed. Our findings confirm that GPR40 reduces glioma sensitivity to TMZ chemotherapy by inhibiting ferroptosis. These results highlight the GPR40-ferroptosis regulatory axis as a potential therapeutic target to enhance ferroptosis-induced treatment and overcome TMZ chemotherapy resistance in GBM.