Trypsin is a pancreatic digestive enzyme that is produced as the zymogen trypsinogen.

白酶是一种消化酶，以白酶原形式产生。

They added a couple enzymes, trypsin and chimotrypsin that break down proteins.

他们添加了几种酶，白酶和壳构白酶，它们可以分解白质。

There's also pancreatic amylase which breaks down carbohydrates into shorter oligosaccharides, and proteases, like trypsin, which cleaves proteins down into smaller peptides.

另外还有淀粉酶，可将碳水化合物分解为小分子的寡糖；再者还有白酶，如白酶，可将白质分解成小分子肽链。

You've got trypsin and peptidase in there, which break proteins down into amino acids, and you have lipases that turn triglycerides into fatty acids and glycerol.

你有白酶和肽酶，它们将白质分解成氨基酸，还有肪酶将甘油三酯转化为肪酸和甘油。

Misfolded alpha-1 antitrypsin can aggregate and get stuck in the endoplasmic reticulum of the liver hepatocytes where it's made, causing some of those cells to die.

错误折叠的α-1白酶可聚集并阻塞于肝细胞内质网中，即α-1白酶产生的地方，导致其中一部分肝细胞死亡。

Contemporary, 'normal' flu viruses require the presence of the enzyme trypsin in their human host, in order to replicate.

在当代，“正常”流感病毒需要在其人类宿主中有白酶才能复制。

Zymogen granules might fuse with lysosomes bringing trypsinogen into contact with lysosomal digestive enzymes.

酶原颗粒可能会和溶酶体融合，使白酶原与溶酶体消化酶接触。

Trypsins are a type of protease, which is an enzyme that can break down other proteins.

白酶是一类白酶，能够水解多种白质。

The 1918 virus instead could proliferate even in the absence of trypsin, making it more pathogenic than other viruses.

1918年的病毒甚至在没有白酶的情况下也能增殖，这使得它比其他病毒更具致病性。

Fortunately, the liver makes alpha-1 antitrypsin which gets released into the blood and sent to the lungs, where it inhibits neutrophil elastase just like it inhibits trypsin, inactivating it before it can break down the protein elastin.

幸运的是，肝产生α-1白酶，释放入血进肺，在肺中像抑制白酶一样，抑制中性粒细胞弹性白酶，使弹性白酶在水解弹性纤维之前失活。

Trypsinogen might then be turned into activated trypsin which begins the cascade of digestive enzyme activation and autodigestion of the pancreas—which is acute pancreatitis.

于是白酶原可能被转化为活化的白酶，开启消化酶激活的级联反应，导致腺自溶——这就是急性腺炎。

So alpha-1 antitrypsin deficiency can lead to both emphysema and chronic bronchitis, the two types of chronic obstructive pulmonary disease, or COPD.

因此α-1白酶缺乏症可导致肺气肿和慢支，而肺气肿和慢支是慢阻肺（COPD）中的2种类型。

Normally, trypsinogen isn't activated until it is cleaved by protease enteropeptidase which is found in the duodenum.

通常情况下，白酶原在被十二指肠中的肠肽酶切割之后才会被激活。

To digest a meal, these zymogens are released into the pancreatic duct, and delivered to the small intestine where they are activated by the protease trypsin.

当消化食物时，这些酶原被释放入管，然后进入小肠，在那里它们被白酶激活。

Diagnosis of alpha-1 antitrypsin deficiency often begins with a chest X-ray or Chest CT to look for hyperinflated lungs or evidence of damaged lung tissue.

α-1白酶缺乏症的诊断常通过X线胸片或胸部CT寻找肺过度膨胀或肺组织受损的证据。

This test stains glycoproteins like alpha-1 antitrypsin a pink color.

这个检测将如α-1白酶等糖白染成粉红色。

Since you need both mutant copies for the disease, this makes alpha-1 antitrypsin deficiency a recessive disease.

由于罹患α-1白酶缺陷必须有2个突变基因拷贝，α-1白酶缺乏症是一种隐形遗传病。

Another, more common cause of COPD is smoking, and if someone with alpha-1 antitrypsin deficiency also smokes, they tend to get an earlier onset of COPD than they have otherwise, an example of a gene-environment interaction.

另外，COPD更常见的病因是吸烟，如果有人患有α-1白酶缺乏症且同时吸烟，那他们患上COPD的时间会比其他人要早，这就是基因-环境相互作用的一个例子。

We're then going to have trypsin and chymotrypsin working in the small intestine.

接下来，白酶和糜白酶将在小肠中发挥作用。

Without alpha-1 antitrypsin, the opposite happens - neutrophil elastase goes unchecked, and it damages the walls of the alveoli, and without that elastin, the alveoli loses its elasticity and structural integrity.

如果没有α-1白酶，情况就会背道而驰：中性粒细胞弹力白酶不受抑制，将会损伤肺泡壁，没有了那层弹性纤维，肺泡壁便失去弹性和结构完整性。