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与蛋白通过交叉连接形成稳固的血凝块。

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

对凝固酶阴性的细菌，例如腐生葡萄球菌或表皮葡萄球菌，蛋白则不会结块。

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，蛋白产生减少，凝血速度大大减慢。

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）能将可溶性蛋白原转化为粘性蛋白，从而出现肉眼可见的团聚现象。

And this process produces fibrin degradation products.

这个过程产生了蛋白的降解产物。

Chronic pericarditis typically results from fibrin deposition in the serous pericardium and it prevents the heart from fully relaxing.

慢性心包炎源蛋白在浆膜心包沉积，影响心肌的舒张充盈功能。

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溶解，比如蛋白溶解酶可将蛋白溶解成D二聚体的片段。

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血时防止过度凝血（即蛋白形成过多）。

This slows down blood flow, allowing platelets, clotting factors, and fibrin to stick together.

这会减慢血流速度，使血小板、凝血因子和蛋白粘在一起。

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、中性粒细胞和蛋白，开始填满气腔，使肺实变。

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蛋白的蛋白质合作，通过产生凝块来阻止伤口的血流动。

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

一层层的蛋白在关节外围形成了坚韧的带，限制了关节的活动范围。

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

最后一步是蛋白原活化为蛋白，聚集成网包绕着血小板。

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，因为蛋白溶解产物水平在血栓存在时往往更高。

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，胶原被损毁并被蛋白取代，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.

最后一步是蛋白原（因子I）激活转变为蛋白，蛋白沉积在血小板上，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.

最后的反应是将蛋白原转化为蛋白，捕获血细胞和血浆以产生凝块。

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.

高浓度尿素刺激浆膜心包，使其分泌富含蛋白和白细胞的浓稠渗出。

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，而成细胞会用蛋白取代被破坏的关节组织。

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、蛋白沉积，导致破坏性肺炎，使气腔消失，损害呼吸功能。