Pulmonary Embolism Support Group
By far the most common form of pulmonary embolism is a thromboembolism, which occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs. Symptoms may include difficulty breathing, pain during breathing, and more rarely circulatory instability and death.
Shaken or stirred?
But I won't talk about the officiating of that game either...
http://www.youtube.com/watch?v=kQFKtI6gn9Y
Officiating, Schmofficiating... REFS GOTTA LET 'EM PLAY
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2007/ucm108967.htm
"FDA Approves Updated Warfarin (Coumadin) Prescribing Information
New Genetic Information May Help Providers Improve Initial Dosing Estimates of the Anticoagulant for Individual Patients"
"FDA spokespeople, however, point out that this is the first time that a widely used agent has included these types of genetic details; currently warfarin is taken by an estimated two million people in the US and, after insulin, is the second most likely drug to send people to the emergency room with drug-related side effects."
Since that distant year not much has changed. Still looking for just CYP2C9 and VKORC1!
CYP2C9 is an important cytochrome P450 enzyme with a major role in the oxidation of both xenobiotic and endogenous compounds. CYP2C9 makes up about 18% of the cytochrome P450 protein in liver microsomes. Some 100 therapeutic drugs are metabolized by CYP2C9, including drugs with a narrow therapeutic index such as warfarin and phenytoin and other routinely prescribed drugs such as acenocoumarol, tolbutamide, losartan, glipizide, and some nonsteroidal anti-inflammatory drugs. By contrast, the known extrahepatic CYP2C9 often metabolizes important endogenous compound such as arachidonic acid, 5-hydroxytryptamine, and linoleic acid.[3]
http://en.wikipedia.org/wiki/CYP2C9
and
Vitamin K epoxide reductase complex subunit 1 is an enzyme that in humans is encoded by the VKORC1 gene.[1]
Vitamin K is essential for blood clotting but must be enzymatically activated. This enzymatically activated form of vitamin K is a reduced form required for the carboxylation of glutamic acid residues in some blood-clotting proteins. The product of this gene encodes the enzyme that is responsible for reducing vitamin K 2,3-epoxide to the enzymatically activated form. Fatal bleeding can be caused by vitamin K deficiency and by the vitamin K antagonist warfarin, and it is the product of this gene that is sensitive to warfarin. In humans, mutations in this gene can be associated with deficiencies in vitamin-K-dependent clotting factors. In humans and rats it has also been associated with warfarin resistance - but these mutations are rare except in Ethiopian and certain Jewish populations. Two pseudogenes have been identified on chromosome 1 and the X chromosome. Two alternatively spliced transcripts encoding different isoforms have been described.[1]
http://en.wikipedia.org/wiki/VKORC1
This does not suprise me at all. Many things have not changed since 1955 when warfarin was first used.
Many scientific journal can be found from the 1990s and are still the up to date data being used in this year of 2013.