All participants are chosen as men whose mind is sexy according to tvN.

Jong Hyun Mu graduated from Yongse University, Actor Ha Sok Jin graduated from the Khaniang University Engineering Faculty.

Kim Ji Sok is an actor who studied in the UK since childhood.

Lee Chan Won, a member of the Peppertones group, is famous for his Ph.D.

KAIST. Tyler Rush, known as a participant in the Abnormal Summit show, is currently a graduate at Seoul National University.

He also gets into 1 of gifted students on the basis of national test exams in high school.

His IQ is 156, is a member of Mensah (the most famous organization for people with high IQ).

Variability in anticoagulant response also results from inaccuracies in laboratory testing, patient noncompliance, and miscommunication between the patient and physician.

Vitamin K is a cofactor for the carboxylation of glutamate residues to -carboxyglutamates (Gla) on the N-terminal regions of vitamin K-dependent proteins (Figure 1) 16.

These proteins, which include the coagulation factors II, VII, IX, and X, require -carboxylation by vitamin K for biological activity.

By inhibiting the vitamin K conversion cycle, warfarin induces hepatic production of partially decarboxylated proteins with reduced coagulant activity 7,8.

The vitamin K cycle and its link to carboxylation of glutamic acid residues on vitamin K-dependent coagulation proteins.

Vitamin K 1 obtained from food sources is reduced to vitamin KH 2 by a warfarin-resistant vitamin K reductase.

This carboxylation step renders the coagulation factors II, VII, IX, and X and the anticoagulant factors protein C and protein S functionally active.

Vit KO is then reduced to Vit K 1 in a reaction catalyzed by vitamin KO reductase.

By inhibiting vitamin KO reductase, warfarin blocks the formation of vitamin K 1 and vitamin KH 2, thereby removing the substrate (vitamin KH 2 ) for the carboxylation of glutamic acids.

Vitamin K 1, either given therapeutically or derived from food sources, can overcome the effect of warfarin by bypassing the warfarin-sensitive vitamin KO reductase step in the formation of vitamin KH 2.

Carboxylation promotes binding of the vitamin K-dependent coagulation factors to phospholipid surfaces, thereby accelerating blood coagulation 911.

Carboxylation requires the reduced form of vitamin K (vitamin KH 2 ).

Coumarins block the formation of vitamin KH 2 by inhibiting the enzyme vitamin K epoxide reductase, thereby limiting the -carboxylation of the vitamin K-dependent coagulant proteins.

In addition, the vitamin K antagonists inhibit carboxylation of the regulatory anticoagulant proteins C and S.

The anticoagulant effect of coumarins can be overcome by low doses of vitamin K 1 (phytonadione) because vitamin K 1 bypasses vitamin K epoxide reductase (Figure 1).

Patients treated with large doses of vitamin K 1 (usually 5 mg) can become resistant to warfarin for up to a week because vitamin K 1 accumulating in the liver is available to bypass vitamin K epoxide reductase.

Warfarin also interferes with the carboxylation of Gla proteins synthesized in bone 1215.

Although these effects contribute to fetal bone abnormalities when mothers are treated with warfarin during pregnancy 16,17, there is no evidence that warfarin directly affects bone metabolism when administered to children or adults.

Pharmacokinetics and pharmacodynamics of warfarin Warfarin is a racemic mixture of 2 optically active isomers, the R and S forms, in roughly equal proportion.

It is rapidly absorbed from the gastrointestinal tract, has high bioavailability 18,19, and reaches maximal blood concentrations in healthy volunteers 90 minutes after oral administration 18,20.

The relationship between the dose of warfarin and the response is influenced by genetic and environmental factors, including common mutations in the gene coding for cytochrome P450, the hepatic enzyme responsible for oxidative metabolism of the warfarin S-isomer 18,19.

Several genetic polymorphisms in this enzyme have been described that are associated with lower dose requirements and higher bleeding complication rates compared with the wild-type enzyme CYP2C9 2224.

In addition to known and unknown genetic factors, drugs, diet, and various disease states can interfere with the response to warfarin.

The anticoagulant response to warfarin is influenced both by pharmacokinetic factors, including drug interactions that affect its absorption or metabolic clearance, and by pharmacodynamic factors, which alter the hemostatic response to given concentrations of the drug.

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