Influence of different processing technology on sialic acid content of edible bird's nest products

本文以毛燕为原料,研究浸泡、挑拣、高温灭菌等工艺流程处理后燕窝唾液酸含量的变化。采用LC-MS/MS检测分析燕窝中唾液酸种类,此外,测定了不同加; 工条件下燕窝产品唾液酸含量并分析加工条件对唾液酸含量的影响,进一步分析了唾液酸热稳定性。结果表明:燕窝中唾液酸仅由N-乙酰基神经氨酸(Neu5A; c)组成,经不同工艺条件处理后,Neu5Ac保留率均可高达95%以上,且Neu5Ac热稳定性好,不同情况下Neu5Ac含量无明显差异。说明燕窝经; 过上述加工处理后不会造成燕窝酸的大量流失,并且其受工艺条件变化影响小,燕窝加工产品可以很好地保存燕窝的营养价值,从而稳定发挥其营养功效,具有很高; 的消费价值。In this paper,raw edible bird's nest was used as raw material to study; the change of sialic acid content in edible bird's nest after processed; by technology such as soaking,picking and choosing and high temperature; sterilization. LC-MS/MS was used to detect and analyze the type of; sialic acid in edible bird's nest. Besides,sialic acid content in edible; bird's nest products was measured under different condition,and the; influence of process condition on sialic acid content was; analyzed.Furthermore,thermostability of sialic acid was analyzed.; Results showed that sialic acid in edible bird's nest was only consist; by N-acetylneuraminic acid(Neu5Ac),retention rates of Neu5Ac all; exceeded 95% when edible bird's nest was processed by different; technology,and thermostability of Neu5Ac was excellent,there was no; obvious difference in Neu5Ac content under different conditions. These; illustrated that above mentioned technology wouldn't lead to a massive; loss of sialic acid in edible bird's nest and sialic acid was influenced; slightly by the change of technology condition,nutritional value of; edible bird's nest could be kept well,thus,its nutritional efficacy; could be exerted stably,so edible bird's nest products have a very high; consumption value

MiR-127-3p靶向MAPK4对葡萄膜黑色素瘤细胞增殖、凋亡、迁移和侵袭的影响

【目的】探讨miR-127-3p对葡萄膜黑色素瘤细胞增殖、凋亡、迁移和侵袭的作用。【方法】通过RT-qPCR检测人葡萄膜黑色素瘤组织及细胞、正常组织及细胞中miR-127-3p与MAPK4mRNA的表达；通过Lipofectamine2000说明书将mimic-NC、miR-127-3pmimic、pc-MAPK4质粒分别或联合转染进入SP6.5或OM431细胞；通过双荧光素酶报告检测miR-127-3p与MAPK4复染靶向关系；通过CCK-8法检测细胞增殖，流式细胞术检测细胞凋亡，划痕实验检测细胞迁移能力，Transwell法检测细胞侵袭能力，蛋白印迹法检测AKT/mTOR通路蛋白相对表达水平。【结果】在葡萄膜黑色素瘤组织和细胞系中，miR-127-3p表达明显下调（P<0.01），而MAPK4表达明显上调（P<0.01）；miR-127-3p与MAPK43′UTR区存在结合位点，miR-127-3p高表达明显抑制了含有野生型MAPK4质粒的荧光素酶活性（P<0.01），但对突变型MAPK4质粒的荧光素酶活性无影响；与Control组相比，miR-127-3pmimic组SP6.5细胞和OM431细胞增殖均明显下降（P<0.01），凋亡率均明显增加（P<0.01），划痕闭合率均明显降低（P<0.01），每视野侵袭细胞数目均明显减少（P<0.01），p-AKT（T308）/AKT、p-mTORr（S473）/mTOR蛋白表达均明显下调（P<0.01），共转染pc-MAPK4逆转上述变化。【结论】MiR-127-3p通过靶向下调MAPK4来抑制葡萄膜黑色素瘤细胞增殖、迁移和侵袭，诱导细胞凋亡，这可能与抑制AKT/mTOR通路激活有关

基于变分模态分解和符号熵的齿轮故障诊断方法

为提高齿轮的故障诊断效果，提出了基于变分模态分解（Variational Modal Decomposition，VMD）和符号熵（Symbol Entropy， SE）的齿轮故障诊断方法。首先，利用VMD对齿轮故障振动信号进行分解，得到若干个本征模态分量（Intrinsic Mode Function，IMF）；然后，计算IMF分量的符号熵，并将IMF符号熵组成齿轮故障特征向量；最后，将特征向量输入SVM进行故障诊断。齿轮故障诊断实测结果验证了该方法的有效性和优势