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Objective: This study aimed to optimize the extraction process of visceral fish oil from grass carp. Methods: Using grass carp viscera as raw material, fish oil was extracted by using ultrasonic assisted enzyme method. The effects of enzyme type, enzyme addition amount, enzymatic hydrolysis time, enzymatic hydrolysis temperature, ultrasonic treatment time, and ultrasonic treatment power on the extraction rate of fish oil were investigated. Results: The optimal process conditions for ultrasonic assisted enzymatic extraction of fish oil were neutral protease hydrolysis, enzyme addition of 2.5%, enzymatic hydrolysis time of 2 hours, enzymatic hydrolysis temperature of 45 ℃, ultrasonic treatment power of 50 W, and ultrasonic treatment time of 30 minutes. At this time, the extraction rate of fish oil was 68.4%. A total of 27 fatty acids were detected by GC-MS, including 10 saturated fatty acids, accounting for 21.12% of the total fatty acid content, mainly palmitic acid and stearic acid; There were 7 kinds of monounsaturated fatty acids, accounting for 54.68% of the total fatty acids, mainly oleic acid, palmitoleic acid and eicosanoic acid; There were 10 kinds of polyunsaturated fatty acids, accounting for 24.20% of the total fatty acids, mainly linoleic acid. Conclusion: Compared with individual enzymatic extraction, ultrasonic assisted enzymatic extraction of grass carp visceral fish oil significantly improved the yield of fish oil extraction.

Abstract Developing effective therapy to inhibit postoperative recurrence and metastasis of colorectal cancer (CRC) is challenging and significant to reduce mortality and morbidity. Here, a granular hydrogel, assembled from gelatin microgels by dialdehyde starch and interpenetrated with in situ polymerized poly(sulfobetaine methacrylate‐co‐N‐isopropylacrylamide) (P(SBMA‐co‐NIPAM)), is prepared to load and lock Food and Drug Administration (FDA)‐approved indocyanine green (ICG) with definite photothermal function and biosafety for photothermal therapy (PTT) combining with checkpoint inhibitor. The presence of P(SBMA‐co‐NIPAM) endows granular hydrogel with high retention to water‐soluble ICG, preventing easy diffusion and rapid scavenging of ICG. The ICG‐locking granular hydrogel can be spread and adhered onto the surgery site at wet state in vivo, exerting a persistent and stable PTT effect. Combined with αPD‐L1 treatment, ICG‐locking granular hydrogel‐mediated PTT can eradicate postsurgery residual and metastatic tumors, and prevent long‐term tumor recurrence. Further mechanistic studies indicate that combination treatment effectively promotes dendritic cells maturation in lymph nodes, enhances the number and infiltration of CD8+ T and CD4+ T cells in tumor tissue, and improves memory T cell number in spleen, thus activating the antitumor immune response. Overall, ICG‐locking gel‐mediated PTT is expected to exhibit broad clinical applications in postoperative treatment of cancers, like CRC.

The poor-reactivity anthracite urgently needs more ways for large-scale and high-quality utilization. Due to the advantage of good fuel adaptability, the circulating fluidized bed (CFB) gasification technology has the potential of high-quality utilization of anthracite. In this paper, one kind of anthracite from Shanxi province, China, was employed to be gasified in a pilot-scale CFB gasifier. It is found that at the operating temperature of 1049°C and oxygen concentration of 60.75%, the gas with a concentration of combustibles of 66% and a low heating value of 7.93 MJ/m3 (at about 25°C and 101.325 kPa) was produced in the CFB gasification process. However, the overall gasification efficiency was not desired because a large amount of gasification fly ash (GFA) escaped and its yield was up to 22%. In this case, the cold gas efficiency was below 48% and the carbon conversion ratio was only 62%. Further analysis reveals that the GFA was featured with a developed pore structure and the specific surface area (SBET) reached 277 m2/g. This indicates such GFA has a potential to use as activated carbon (AC) or AC precursor. Basis on this, steam activation experiments of the GFA produced were conducted to investigate the activation characteristics of GFA and thereby to determine its activation potential. Experimental results indicate that increasing temperature sharply accelerated the activation process, while did not impair the maximum activation effect. After activation, the SBET of GFA maximumly increased by 63%, reaching 452 m2/g. With the progress of activation, the pore structure of GFA presents a three-stage evolution process: development, dynamic balance, and collapse. Such a process can be divided and quantified according to the carbon loss. In order to achieve an optimal activation of GFA, the carbon loss shall be controlled at ~15%. This work provides a new scheme for high-quality utilization of anthracite. [ABSTRACT FROM AUTHOR]

MyD88 was reported to be associated with paclitaxel sensitivity in lung cancer; however, its roles in breast cancer remain unclear. The objective of this study is to investigate the expression and function of MyD88 in breast cancer. Immunohistochemistry (IHC) was used to analyze the expression of MyD88 in both breast cancer tissues and adjacent normal tissues. Real-time PCR and Western blots were further used to measure the messenger RNA (mRNA) and protein expression. The proliferation was assessed by WST-1. Flow cytometry was used to measure the cell cycle and apoptosis. The transwell assay was used to observe the change of migration and invasion of transfected cells. In breast cancer tissues, the expression of MyD88 was significantly higher than that in tumor-adjacent normal tissues ( P < 0.001). MyD88 expression was found to be associated with the differentiation stages ( P = 0.019). Kaplan-Meier survival curves showed statistically significant difference on survival in patients with high expression of MyD88 compared with those with normal expression of MyD88 ( P = 0.018). Knockdown of MyD88 reduced the proliferation, migration, and invasion of MCF-7 cells and increased the sensitivity of MCF-7 cells to paclitaxel treatment through the inhibition of activation of NF-κB via PI3K/Akt. Our data indicate that MyD88 may be a potential target molecule to be used in diagnosis and treatment of breast cancer. [ABSTRACT FROM AUTHOR]

Limited healthcare capacity highlights the needs of integrated sensing systems for personalized health-monitoring. However, only limited sensors can be employed for point-of-care applications, emphasizing the lack of a generalizable sensing platform. Here, we report a metal organic framework (MOF) ZIF-90-ZnO-MoS 2 nanohybrid-based integrated electrochemical liquid biopsy (ELB) platform capable of direct profiling cancer exosomes from blood. Using a bottom-up approach for sensor design, a series of critical sensing functions is considered and encoded into the MOF material interface by programming the material with different chemical and structural features. The MOF-based ELB platform is able to achieve one-step sensor fabrication, target isolation, nonfouling and high-sensitivity sensing, direct signal transduction, and multiplexed detection. We demonstrated the capability of the designed sensing system on differentiating cancerous groups from healthy controls by analyzing clinical samples from lung cancer patients, providing a generalizable sensing platform.

MyD88 was reported to be associated with paclitaxel sensitivity in lung cancer; however, its roles in breast cancer remain unclear. The objective of this study is to investigate the expression and function of MyD88 in breast cancer. Immunohistochemistry (IHC) was used to analyze the expression of MyD88 in both breast cancer tissues and adjacent normal tissues. Real-time PCR and Western blots were further used to measure the messenger RNA (mRNA) and protein expression. The proliferation was assessed by WST-1. Flow cytometry was used to measure the cell cycle and apoptosis. The transwell assay was used to observe the change of migration and invasion of transfected cells. In breast cancer tissues, the expression of MyD88 was significantly higher than that in tumor-adjacent normal tissues (P < 0.001). MyD88 expression was found to be associated with the differentiation stages (P = 0.019). Kaplan-Meier survival curves showed statistically significant difference on survival in patients with high expression of MyD88 compared with those with normal expression of MyD88 (P = 0.018). Knockdown of MyD88 reduced the proliferation, migration, and invasion of MCF-7 cells and increased the sensitivity of MCF-7 cells to paclitaxel treatment through the inhibition of activation of NF-κB via PI3K/Akt. Our data indicate that MyD88 may be a potential target molecule to be used in diagnosis and treatment of breast cancer.

Ursolic acid (UA), a potential chemotherapeutic agent, has the properties of inhibition of the growth of many human cancer cell lines. Whether UA can inhibit the growth and metastasis of human gastric cancer cells remains unknown. In this study, it was found that UA inhibited the growth and metastasis of human gastric cancer cells in vitro. Our results showed the increase of the percent of apoptotic cells and G1 phase, the inhibition of cell migrations well as the decrease of the expression of Bax, caspase 3 and Bcl-2 in BGC-823 cells after the treatment with UA. Real-time quantitative PCR analysis showed that UA treatment upregulated the level of miR-133a in BGC-823 cells. Overexpression of miR-133a increased the G1 phase of cell cycle and decreased Akt1 expression in BGC-823 cells. These outcomes might be secondary to the increased expression of miR-133a after the treatment with UA.