Hot air-assisted radio frequency drying of corn kernels: the effect on structure and functionality properties of corn starch.

Hot air (HA) drying caused quality damage of grains with long treatment time. Radio frequency (RF) heating as an emerging technology was applied to improve drying quality of cereals effectively. The effects of HA-RF drying (50 °C, 70 °C, 90 °C) of corn kernels on the morphology, structure, and physicochemical properties of starch were investigated and compared with HA drying. The surface of treated starch became rough, along with fragments and pores. Drying treatments increased the amylose content from 10.59 % to 23.88 % and the residual protein content of starch from 0.58 % to 1.23 %, and reduced the crystallinity from 31.95 % to 17.15 % and short-range order structures of starch from 0.918 to 0.868. The change of structures in turn resulted in the increase of pasting viscosity, gelatinization temperature, storage modulus and loss modulus. Furthermore, the HA-RF dried starch displayed stronger thermal stability, higher gelatinization degree and better gelation properties than the HA-treated starch at the same temperature. The data proved that the synergistic effects of HA and RF were more effective in modulating the starch structure and improving the functional characteristics of corn starch. This paper would like to provide potential reference for better application of HA-RF technologies to corn.

Long non-coding RNA X-Inactive Specific Transcript (XIST) interacting with USF2 promotes osteogenic differentiation of periodontal ligament stem cells through regulation of WDR72 transcription.

BACKGROUND: Periodontal ligament stem cells (PDLSCs) are the most potential cells in periodontal tissue regeneration and bone tissue regeneration. Our prior work had revealed that WD repeat-containing protein 72 (WDR72) was crucial for osteogenic differentiation of PDLSCs. Here, we further elucidated its underlying mechanism in PDLSC osteogenic differentiation. METHODS: Human PDLSCs, isolated and identified by flow cytometry, were prepared for osteogenic differentiation induction. Levels of WDR72, long non-coding RNA X-Inactive Specific Transcript (XIST), upstream stimulatory factor 2 (USF2), and osteogenic marker genes (Runx2, Osteocalcin, and Collagen I) in human PDLSCs and clinical specimens were detected by RT-qPCR. Protein expressions of WDR72, Runx2, Osteocalcin, and Colla1 were tested by Western blot. The interactions among the molecules were verified by RIP, RNA pull-down, ChIP, and luciferase reporter assays. Osteogenic differentiation was evaluated by alkaline phosphatase (ALP) and alizarin red staining (ARS). RESULTS: WDR72 was decreased in periodontal tissues of periodontitis patients, and overexpression reversed TNF-α-mediated suppressive effects on PDLSC osteogenic differentiation. Mechanically, XIST recruited the enrichment of USF2 to the WDR72 promoter region, thereby positively regulating WDR72. WDR72 silencing overturned XIST-mediated biological effects in PDLSCs. CONCLUSION: WDR72, regulated by the XIST/USF2 axis, enhances osteogenic differentiation of PDLSCs, implying a novel strategy for alleviating periodontitis.

Hsa_circ_0049396 inhibited oral squamous cell carcinoma progression by regulating the miR-663b/ENDOU axis.

BACKGROUND: Circular RNA (circRNAs) play an important role in oral squamous cell carcinoma (OSCC) progression and has been widely reported. In this study, we aimed to investigate the role of a novel circRNA, circ_0049396, and its underlying mechanism in OSCC. METHODS: The expression levels of circ_0049396, miR-663b, and theuridylate-specific endoribonuclease (ENDOU) were assessed by quantitative reverse transcription PCR (qRT-PCR). Cell proliferation and migration were evaluated using CCK-8 and Transwell assays, respectively. Western blotting was performed to measure the levels of the apoptosis-associated proteins (Bcl-2 and Bax). The functional role of circ _0049396 was further validated in a xenograft experiment in vivo. The interactions of miR-663b with circ_0049396/ENDOU were verified using the dual luciferase reporter, RNA pull-down, and RNA immunoprecipitation (RIP) assays. RESULTS: The expression of circ_0049396 and ENDOU was downregulated in OSCC tissues and cells, whereas miR-663b was upregulated. Circ_0049396 overexpression weakened OSCC cell proliferation and migration but enhanced their apoptosis. Circ_0049396 overexpression suppresses tumorigenesis in vivo. The circ_0049396/miR-663b/ENDOU regulatory network predicted through bioinformatic analysis was validated using RNA pull-down, luciferase reporter, and RIP experiments. MiR-663b mimic enhanced the migratory and proliferative abilities of OSCC cells, but suppressed apoptosis. Furthermore, circ_0049396 or ENDOU overexpression partially reversed the malignant behavior of miR-663b-overexpressing OSCC cells. CONCLUSIONS: Our study illustrated that circ_0049396 overexpression inhibited the malignant behavior of OSCC cells by regulating the miR-663b/ENDOU axis. Based on our findings, circ_0049396 can be used as a potential therapeutic agent for OSCC.

Stability of low density lipoprotein particles affect the formation of off-flavor in thermal egg yolk.

This study aimed to investigate the role of stability of low density lipoprotein (LDL) spherical particles as well as oxidation of lipids and proteins on formation of off-odor in heated egg yolk (EY). Off-odor attributes and volatile components of EY with different thermal temperature (25 °C-90 °C) were investigated by sensory evaluation, gas chromatography-mass spectrometry (GC-MS) and GC-ion mobility spectrometry (IMS). The off-flavor and volatile compounds increased significantly when EY were heated at 60 °C-65 °C. Destruction of LDL particle structure was presented by confocal laser scanning microscopy with thermal treatment at 60 °C. A positive correlation (r = 0.899, p < 0.05) was shown between oil exudation and off-odor of heated EY. Moreover, oxidation of lipids and proteins, protein aggregation, and changes of protein secondary structure (increased ß-sheets and decreased α-helices) in LDL particles were all found when heating temperature rose to 65 °C. It was speculated that unstability of LDL particles resulted in the leakage of lipids; then oxidative products of lipids took part in the formation of off-odor volatiles in heated EY.

The anti-tumor effects of evodiamine on oral squamous cell carcinoma (OSCC) through regulating advanced glycation end products (AGE) / receptor for advanced glycation end products (RAGE) pathway.

Evodiamine (EVO) is emerging as a novel anti-tumor drug, which is involved in the inhibition of cell proliferation and apoptosis. High-Mobility Group Box 1 (HMGB1)/RAGE is involved in invasive behavior of OSCC cells and angiogenesis. In this study, we evaluated the potential of EVO in OSCC in vitro and in vivo. We found that RAGE silencing suppressed HSC-4 cell proliferation and invasion, and tube formation of HUVEC. EVO showed marked inhibitory effects on the malignant behaviors of HSC-4 cells in a dose-dependent manner. Further experiments revealed that the RAGE overexpression was able to markedly block the effects of EVO on cell proliferation and invasion, and tube formation. By analyzing the expression of High-Mobility Group Box 1 (HMGB1) and RAGE in HSC-4 cells, the result showed that EVO slightly reduced HMBG1 levels and dramatically decreased RAGE levels, while RAGE overexpression did have no marked influences on HMBG1 levels. The anti-tumor effects of EVO were further confirmed in mouse oral squamous cell carcinoma xenograft models. Remarkable anti-tumor effects of EVO were also demonstrated, as presented by reduced tumor size and levels of HMBG1 and RAGE in tumor tissue of mouse oral squamous cell carcinoma xenograft models. The results demonstrated that EVO has a direct binding effect on HMGB1, but it may be involved in degrading the protein. More importantly, it can reduce the activity of RAGE pathway by affecting the binding between HMBG1 and RAGE. To conclude, EVO inhibited proliferation, invasion and angiogenesis of OSCC through affecting the downstream signal transduction system of AGE/RAGE by targeting RAGE.