Page 152 - The Miracle of the Blood and Heart

THE MIRACLE OF THE
BLOOD AND HEART

the fibrinogen chain. This protein is now converted to fibrin,
and is now in an active state. The severed fibrin surfaces pos-
sess adhesive sections, which cause other fibrins to approach
and bind to them. This mass brought into being by fibrins
sticking to one another is the primary clot produced to halt the
bleeding. In the first phase, the first clot forms without too
much detailed work. The objective here is to halt the blood,
and also to perform first aid using as little protein as possi-
ble—in other words, to economize on protein.
Thrombin, which goes into action straightaway with the
opening of a wound in the body, begins cutting all the fib-
rinogen links it finds. However, thrombin must not do this
constantly or in any other location than that of the wound. If
it acted independently in that way, then all the fibrins it sev-
ered would stick to one another, and uncontrolled clotting
would take place in the bloodstream, leading to the veins
becoming blocked. That being so, the thrombin has to be kept
under tight control and instructed to act in the right place and
at the right time.
At this stage, another connection proving the mechanism's
irreducible complexity appears: another protein that sets
thrombin in motion, known as Stuart factor. It severs the pro-
thrombin in the blood plasma and turns it into active throm-
bin. However, if the Stuart factor were to turn every pro-
thrombin it encountered into thrombin aimlessly, then the
result would again be uncontrolled activity and the likelihood
of clotting in the bloodstream. Therefore, Stuart factor must
not be in a constantly active state in the bloodstream, but
must await an order to go into action.
The command for Stuart factor to begin work-
Harun
Yahya

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