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，维蛋白则不会结块。

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，这是维蛋白降解产物，当维蛋白血凝块崩解时产生。

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.

这强化以维蛋白线的形式出现，维蛋白线连接在起形成网，可以捕获血小板和血细胞。

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名为维蛋白的蛋白质合作，通过产生凝块来阻止伤口的血液流动。

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

的维蛋白在关节外围形成了坚韧的维带，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，当血凝块通过溶崩解时，维蛋白降解产物释放入血液循环，干扰血小板聚集和血凝块形成，导致凝血更加困难。

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.

在被称为血友病的疾病家族中，病人通常可以很好地完成止血的前两个步骤，但是他们不能制造有效的维蛋白凝块。

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，而成维细胞会用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.

通常情况下血栓会开始溶解，比如维蛋白溶解酶可将维蛋白溶解成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.

凝固酶阳性细菌（如金黄色葡萄球菌）能将可溶性维蛋白原转化为粘性维蛋白，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、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，胶原被损毁并被维蛋白取代，最终化，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，因为维蛋白溶解产物水平在血栓存在时往往更高。

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血时防止过度凝血（即维蛋白形成过多）。

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。

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.

之后凝血酶将可溶的因子I（维蛋白原）转变为因子Ia（维蛋白原），维蛋白不可溶，便在损伤部位从血液中析出。

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

最后步是维蛋白原活化为维蛋白，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与维蛋白通过交叉连接形成稳固的血凝块。