With coagulase negative species, like Staph saprophyticus or Staph epidermidis, the fibrin doesn't clump up.

对于固酶阴性的细菌，例如腐葡萄球菌或表皮葡萄球菌，纤维蛋白则不会结。

In addition to lower levels of specific clotting factors, there are elevated levels of D-dimer, which is a fibrin degradation product that is produced when fibrin clots are broken down.

除了低水平的特定因子外，尚有较高水平的D-二聚体，这是一种纤维蛋白降解物，当纤维蛋白崩解时。

This reinforcement comes in the form of fibrin threads, protein strands that join together to make a sort of mesh that traps the platelets and blood cells.

这种强化以纤维蛋白线的形式出现，纤维蛋白线连接在一起形成一种网，可以捕获小板和细胞。

The high levels of urea irritate the serous pericardium, making it secrete a thick pericardial fluid that's full of fibrin strands and white blood cells.

高浓度素刺激浆膜心包，使其分泌富含纤维蛋白和白细胞的浓稠渗出液。

Their main job, in collaboration with a protein called fibrin, is to stem the flow of blood from wounds by causing clots.

他们的主要工作是与一种名为纤维蛋白的蛋白质合作，通过来阻止伤口的液流动。

Layers and layers of fibrin form a tough fibrous band around the outside of the joints, which limits their range of motion.

一层层的纤维蛋白在关节外围形成了坚韧的纤维带，限制了关节的活动范围。

This is where exudate, which contains red blood cells, neutrophils, and fibrin starts filling the airspaces and makes them more solid.

渗出物含有红细胞、中性粒细胞和纤维蛋白，开始填满气腔，使肺实变。

To make things worse, as the clots are broken down through fibrinolysis, fibrin degradation products are released into the circulation and these interfere with platelet aggregation and clot formation, making hemostasis even more difficult.

更糟的是，当通过纤溶崩解时，纤维蛋白降解物释放入液循环，干扰小板聚集和形成，导致更加困难。

In the family of disorders known as hemophilia, a patient can usually complete the first two steps of hemostasis just fine, but they can't make an effective fibrin clot.

在被称为友病的疾病家族中，病人通常可以很好地完成止的前两个步骤，但是他们不能制造有效的纤维蛋白。

Over time, the inflammation destroys the intervertebral joints, as well as the facet joints, and the sacroiliac joints, and fibroblasts replace the destroyed joint with fibrin.

随着时间推移，炎症会破坏椎间盘、关节突关节和骶髂关节，而成纤维细胞会用纤维蛋白取代被破坏的关节组织。

Usually the clot might start naturally breaking down, for example, enzymes like plasmin break down fibrin into fragments called D-dimers.

通常情况下栓会开始溶解，比如纤维蛋白溶解酶可将纤维蛋白溶解成D二聚体的片段。

Coagulase-positive bacteria, like Staph aureus, convert the soluble fibrinogen into sticky fibrin, which then visibly clumps up.

固酶阳性细菌（如金黄色葡萄球菌）能将可溶性纤维蛋白原转化为粘性纤维蛋白，从而出现肉眼可见的团聚现象。

This leads to fluid exudation and deposition of fibrin in the alveoli, resulting in a destructive pneumonia that obliterates the air spaces and compromise respiratory function.

这会引起肺泡中液体渗出、纤维蛋白沉积，导致破坏性肺炎，使气腔消失，损害呼吸功能。

In this process, collagen gets destroyed and replaced by fibrin, and ultimately ossification sets in, forming a " bamboo spine" on Xray or CT-scan.

在该病中，胶原被损毁并被纤维蛋白取代，最终骨化，在X线摄片或CT中脊椎呈“竹节样”改变。

Also, a D-dimer blood test can be helpful, because fibrin break-down product levels are usually higher in presence of a clot.

另外，D-二聚体的检测也很有帮助，因为纤维蛋白溶解物水平在栓存在时往往更高。

The main role of protein C and protein S is to prevent excess coagulation, or fibrin formation, during secondary hemostasis.

蛋白C和蛋白S的主要作用是在二期止时防止过度（即纤维蛋白形成过多）。

So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury.

这一加强小板栓强度的过程即为二期止，最终使得伤口上的栓很牢固。

Thrombin then turns factor I or fibrinogen, which is soluble, into factor Ia or fibrin, which is insoluble and precipitates out of the blood at the site of injury.

之后酶将可溶的因子I（纤维蛋白原）转变为因子Ia（纤维蛋白原），纤维蛋白不可溶，便在损伤部位从液中析出。

The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets.

最后一步是纤维蛋白原活化为纤维蛋白，聚集成网包绕着小板。

Thrombin also turns factor XIII into factor XIIIa which cross links the fibrin to form a stable clot.

酶也能使因子XIII转变为因子XIIIa；因子XIIIa与纤维蛋白通过交叉连接形成稳固的。