In order to improve the usability of mealworm and the nutritional quality of acorn Mook mostly composed of carbohydrates, we prepared acorn Mook using with different levels of mealworm powder, and the physico-chemical and sensory evaluation were investigated. In the content of proximate chemical composition, moisture content did not show any significant difference. But crude protein, crude ash, and crude fat contents were increased with increasing mealworm content. Carbohydrate content was reduced as mealworm content increased. Lightness showed no significant difference among treatments, redness was increased, and yellowness was decreased as the amount of mealworm powder increased. In physiological properties, hardness, gumminess, chewiness, and springiness were significantly increased as the amount of mealworm powder decreased. However, adhesiveness and cohesiveness were not significantly different. Ascorbic acid content, activities of DPPH and ABTS radical scavenging activities were decreased with increasing amount of mealworm in acorn Mook. In sensory evaluation, acorn Mook containing 0.75% of mealworm powder showed highly preference compared with the control.

Few studies have evaluated the apoptosis-inducing efficacy of NaF on cancer cells in vitro but there has been no previous investigation of the apoptotic effects of NaF on human oral squamous cell carcinoma cells. In this study, we have investigated the mechanisms underlying the apoptotic response to NaF treatment in the YD9 human squamous cell carcinoma cell line. The viability of YD9 cells and their growth inhibition were assessed by MTT and clonogenic assays, respectively. Hoechst staining, DNA electrophoresis and TUNEL staining were conducted to detect apoptosis. YD9 cells were treated with NaF, and western blotting, immunocytochemistry, confocal microscopy, FACScan flow cytometry, and MMP and proteasome activity assays were performed sequentially. The NaF treatment resulted in a time- and dose-dependent decrease in YD9 cell viability, a dose-dependent inhibition of cell growth, and the induction of apoptotic cell death. The apoptotic response of these cells was manifested by nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, a decreased DNA content, the release of cytochrome c into the cytosol, the translocation of AIF and DFF40 (CAD) into the nucleus, a significant shift of the Bax/Bcl-2 ratio, and the activation of caspase-9, caspase-3, PARP, Lamin A/C and DFF45 (ICAD). Furthermore, NaF treatment resulted in the downregulation of G1 cell cyclerelated proteins, and upregulation of p53 and the Cdk inhibitor p27KIP1. Taken collectively, our present findings demonstrate that NaF strongly inhibits YD9 cell proliferation by modulating the expression of G1 cell cycle-related proteins and inducing apoptosis via mitochondrial and caspase pathways.