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1)  cold denaturation
冷变性
2)  frozen denaturation
冷冻变性
1.
Research status on the fish protein frozen denaturation;
鱼肉蛋白质冷冻变性研究进展
2.
The mechanisms and the progresses of fish protein frozen denaturation and cryoprotective effects of fish protein by sugars,salts,dairy ingredients and protein or chitin hydrolysates are reviewed.
简述了鱼肉蛋白冷冻变性机理的研究现状,综述了糖类、盐类、乳蛋白、不同水解物等添加物的抗冷冻变性机理,介绍了鱼肉蛋白冷冻变性的评价指标及其测定方法,展望了抗鱼肉蛋白冷冻变性的新途径及应用前景。
3.
The deterioration of muscle is mainly attributed to the frozen denaturation of myofibirillar protein.
测定结果表明,蔗糖、山梨醇混合物和海藻糖都抑制了冻藏过程中肌原纤维蛋白盐溶性、Ca2+-ATPase活性、巯基含量的降低和表面疏水性的升高,延缓了鳙肌原纤维蛋白的冷冻变性。
3)  cold heading ability
冷变形性
1.
The alloy design of high strength steel for bolts was discussed from the point of strength and toughness in combination, delayed fracture resistance and cold heading ability.
从强韧性、耐延迟断裂性和冷变形性三个方面介绍了高强度螺栓钢的设计思路和前期研究结果,并在此基础上设计出一种1500MPa级的高强度螺栓钢。
4)  freeze denaturation
冷冻变性
1.
The thermostability and freeze denaturation of ATPase activity, total-SH and actomyosin(AM) from Charybdis japonica were studied.
冷冻变性后,肌动球蛋白ATPase活性和总巯基数随冷藏时间而明显下降,冷藏温度越低,ATPase活性下降越慢。
5)  freezing denaturation
冷冻变性
1.
This review discussed the mechanism of protein denaturation during frozen storage or ice storage,summarized common methods that were applied in study of fish protein freezing denaturation and then introduced several fish protein cryoprotectants and their effect and mechanism.
低温贮藏是保存鱼蛋白的重要方法,然而鱼蛋白在低温下仍会发生冷冻变性并导致其功能特性的下降。
6)  cold plastic deformation
冷塑性变形
1.
The effect of cold plastic deformation on pack chrome-RE-boronizing of steel 45 was studied by OM,SEM and Micro-hardometer.
利用金相显微镜和扫描电镜观察及显微硬度测试,研究了冷塑性变形对45钢硼铬稀土共渗的影响。
2.
The boronizing speed increases obviously after cold plastic deformation (CPD)under two processes,and the depth of the layer increases with the increase .
结果表明,低温共渗层的组织比高温共渗层的致密,疏松、孔洞少;冷塑性变形在两种工艺条件下都明显促进了渗硼的进行,且都随着变形量的增加渗层深度增加;高温共渗得到FeB和Fe2B双相硼化物,低温共渗得到单一Fe2B相;冷塑性变形对渗层的硬度基本没有影响。
补充资料:变性
变性
degeneration
    在致病因素的作用下 , 组织和细胞发生物质代谢障碍,在细胞内和间质中出现各种异常物质或原有的某些物质堆积过多的现象。细胞受到致病因子的作用后,细胞的功能和结构可在适应能力范围内改变。如果致病因子作用过强,上述改变超过该细胞的适应能力则出现变性 。 致病因子除去后,该细胞可能恢复正常,但严重的变性可能发展为坏死。变性一般分为 :蛋白质代谢障碍 、脂肪代谢障碍、糖代谢障碍、矿物质代谢障碍和病理性色素沉着等 。 常见的变性有肿胀、水性变 、脂肪变 、玻璃样变、淀粉样变、病理性色素沉着、钙化、粘液变和纤维样变。
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