#coagulation

Me: “Just a second, let me check…OK, yep-that specimen is only about 8 hours old. It should be fine to run a PT.”

So, my sibling and I are working through the original xbox halo 2 campaign but on our xbox 360 (RIP 360 support). And every time we go to split-screen it's set for slayer on ivory tower. Well, the other day we decided to see what that was about so we hit play instead of switching to co-op campaign like we usually do. There is a special kind of fun about killing your sibling over and over again in a videogame.

And today we decided to explore the other game modes and maps. Slayer is the only mode you can do with 2 people, so that was a slight bummer. But, then we saw it. That beloved map introduced to us by Red vs Blue. It was called Coagulation, but the terrain was unmistakable. We spawned in, I as red, my sibling as blue. And we decided to explore a bit of that glorious map ourselves for the first time ever. We will definitely be returning.

I found Sheila. She wasn't very useful with the banshee in the sky. May she rest in peace... I couldn't manage to find Grif's screaming cave, but I am pretty sure I found where Church died that first time. Getting to explore such a historical site ourselves was a very cool and exciting experience. It was almost like we were walking through history itself. Next time we will explore more of Blood gulch and see what the other maps hold as well.

Blood Gulch. Amazing place to explore. Lots of things to do and see. 5 stars.

The seventh and final phase of alchemy is known as coagulation, in which the alchemist completes the Great Work and creates the Philosopher’s stone.  In laboratory alchemy, this is thought to occur after the process of distillation is completed and the matter congeals into a solid substance.  In personal alchemy, it signifies the completion of the process of solve et coagula, or dissolve and…

Book of the Day – Alchemy: Science of the Cosmos, Science of the Soul

Today’s Book of the Day is Alchemy: Science of the Cosmos, Science of the Soul written by Titus Burckhardt and published in 1997 by Fons Vitae (the book was originally published in 1960, in German, under the title Alchemie, Sinn- und Weltbild). Eminent Swiss metaphysician and scholar Dr. Titus Burckhardt (1908 – 1984) was an expert and a leading member of the Perennialist or Traditionalist…

On the left is a depiction of anahata chakra with hanuman sitting in meditation experiencing omnipresent omniscient vibrations. On the right is what I beleive is an alchemical/goetic manuscript with the omniscient/omnipresent eye of creation in the heart of the six point star. Around the Star is an alchemical glyph the serpent eating its tail, which corresponds with the infinite waves of energy surrounding the anahata chakra.

3 key components of the coagulation cascade:

Calcium ions, which are required for several key reaction steps.

Coagulation factors, which are the driving forces of the cascade; they comprise proenzyme factors are transformed to active enzymes, and are signified by the lower case "a." Many coagulation factors are synthesized by the liver; thus, coagulation disorders are associated with liver disease.

Co-factors are reaction accelerators; they form complexes with activated coagulation factors and calcium ions.

2 Pathways:

Traditionally, these pathways have been categorized as "intrinsic" and "extrinsic," but modern models emphasize their cooperation in thrombin formation.

Endothelial rupture exposes tissue factor to the blood; because tissue factor is exogenous to the blood, it is the start of the so-called "extrinsic" pathway(tissue factor is also known as thromboplastin or CD142).

Tissue factor activates coagulation factor VII, and, with calcium, forms a complex that activates factor IX (this complex is sometimes called extrinsic tenase).

Activated factor IX, with calcium and co-factor VIIIa, activates factor X.

Activated factor X combines with calcium and co-factor Va to form prothrombinase, which is the complex that transforms prothrombin (aka, factor II) to thrombin (factor IIa).

Thrombin converts fibrinogen to fibrin, which forms a meshwork that surrounds the aggregated platelets and traps other materials, including red and white blood cells and serum.

Return to the aggregated platelets to show how they influence thrombin production; because all the elements in this pathway are inherent to the blood, this is traditionally called the "intrinsic" pathway.

The negative surface of activated platelets activates Factor XII (aka, Hageman factor).

Factor XI Ia activates factor XI.

Factor XIa activates factor IX, which, as we've seen, forms a complex that ultimately leads to the production of thrombin and conversion of fibrinogen to fibrin.

Thrombin has other, indirect ways of promoting clotting:

It activates co-factors VIII and V, and factor XI; thus, it promotes its own production.

Thrombin also ensures the stability of the clot: show that it activates factor XIII, aka, fibrin stabilizing factor, which, as its name implies, strengthens the bonds of the fibrin mesh of the clot.

Retraction

Soon after the clot is formed, retraction occurs: the platelets contract and expel serum.

Serum lacks fibrinogen and clotting factors, so it cannot coagulate.

Thrombin also acts outside of the coagulation cascade via protease activation receptors (PARs):

Thrombin promotes platelet activation and release of thromboxane A2 for platelet plug formation.

It triggers endothelial activation and release of anticoagulants.

Thrombin also up-regulates pro-inflammatory mediators, such as cytokines and chemokines, implicating it in inflammatory conditions.

Endogenous anti-coagulation mechanisms:

Fibrin fibers absorb thrombin, which prevents excessive clotting.

Unabsorbed thrombin combines with anti-thrombin III, which neutralizes it.

Heparin, which is normally circulating in small concentrations but can be administered in higher doses, increases the effectiveness of anti-thrombin III and removes factors IX, X, XI, XII. Thus, it is prescribed to prevent thrombosis.

Healthy, intact endothelial cells produce nitric oxide, prostacyclin, and tissue plasminogen activator (t-PA) to prevent platelet adhesion and clot formation.

Fibrinolysis

Once the vessel wall heals, the clot must be removed via fibrinolysis, the breakdown of the fibrin mesh.

To illustrate, redraw the vessel, and show a platelet trapped by fibrin fibers.

Plasminogen binds to the fibrin; plasminogen is a proenzyme produced by the liver.

Endothelial cells release tissue plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), which bind to fibrin and cleave plasminogen to form active plasmin. Recall that thrombin itself is a stimulus for t-PA release.

Plasmin breaks down fibrin, fibrinogen, and some coagulation factors to dissolve the clot.

Fibrinolysis produces fibrin degradation products (FDPs), most notably D-dimer, which is measured to assess thrombotic states (an elevated result may indicate excessive thrombotic states).

When not bound to fibrin, plasminogen and plasmin activity is inhibited:

In a positive feedback cycle, plasmin also converts t-PA and u-PA into their more active forms, which promotes further fibrinolysis.

Unbound t-PA and u-PA are inhibited by plasminogen activator inhibitor 1 (PAI-1).

Alpha-2 antiplasmin inhibits unbound plasmin.

Vitamin K

Vitamin K is critical to hepatic synthesis of prothrombin and factors VII, IX, and X.