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

对于凝固酶阴性的细菌，例如腐生葡萄球菌或表皮葡萄球菌，纤维蛋则不会。

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

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

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

通常情况下血栓会开始，比如纤维蛋酶可将纤维蛋成D二聚体的片段。

By inhibiting both the intrinsic and common pathway, less fibrin is produced and coagulation slows down dramatically.

通过抑制内源性和共同凝血途径，纤维蛋产生减少，凝血速度大大减慢。

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

蛋C和蛋S的主要作用是在二期止血时防止过度凝血（即纤维蛋形成过多）。

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，因为纤维蛋产物水平在血栓存在时往往更高。

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

最后一步是纤维蛋原活化为纤维蛋，聚集成网包绕着血小板。

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

凝血酶也能使因子XIII转变为因子XIIIa；因子XIIIa与纤维蛋通过交叉连接形成稳固的血凝。

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取代，最终骨化，在X线摄片或CT中脊椎呈“竹节样”改变。

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

最后一步是纤维蛋原（因子I）激活转变为纤维蛋，纤维蛋沉积在血小板上，并聚合形成网状。

The final reaction is the conversion of fibrinogen to threads of fibrin that trap blood cells and plasma to produce the clot.

最后的反应是将纤维蛋原转化为纤维蛋，捕获血细胞和血浆以产生凝。

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.

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

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取代被破坏的关节组织。

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.

除了低水平的特定凝血因子外，尚有较高水平的D-二聚体，这是一种纤维蛋降产物，当纤维蛋血凝崩时产生。

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.

之后凝血酶将可的因子I（纤维蛋原）转变为因子Ia（纤维蛋原），纤维蛋不可，便在损伤部位从血中析出。

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.

这一加强血小板血栓强度的过程即为二期止血，最终使得伤口上的血栓很牢固。

That's involved in the clotting mechanism and it probably explains why virtually 100% of babies who die of SIDS have a liquid unclotted blood. Now, you can get raised fibrin degradation products in very severe bacterial infection.

这涉及到凝血机制，它可能释了为什么几乎100%死于SIDS的婴儿有未凝的血。现在，你可以在非常严重的细菌感染中得到纤维蛋降产物。