the girl next door

right now i am sitting at borders across from a beautiful, demure korean girl who is sifting through a massive pile of novels. i have decided that i love her. and so this entry, my first official post of the year, is dedicated to the lovely agashi across the way.

the coagulation cascade is a remarkable piece of biological machinery that keeps our blood flowing when it should and clots it when it shouldn't. in fact, it is so remarkable that it is a commonly cited example, like the eye, of how evolution may fail to explain all the complexities of the human body. the coagulation cascade, in other words, is a kind of "all or nothing" system, i.e. take away any one of its many parts and the whole things breaks. evolution is about incremental change, yet it is difficult to imagine the simpler precursor mechanism to coagulation that should have come before the present clotting system.

anyway, last year we learned about the basics of coagulation--the names of all the different factors, the intrinsic vs. extrinsic pathways, and a couple disorders resulting from disruptions to the cascade. this year we're learning all about what goes wrong in the body, and our first unit is hematology/oncology. a friend of mine from college used to wear a silver bracelet that indicated his having von Willebrand's disease. von Willebrand's factor (VWF) is one of the many coagulation cascade factors that mediate blood clotting. VWF in particular mediates platelet adhesion to the inner lining of blood vessels... ok hold on, the girl just talked to me! and she smiled at me! anyway, so VWF helps platelets adhere to blood vessel endothelium, so-called "primary hemostasis." in order to activate platelets so that they become sticky, VWF binds to the platelet receptor GP1b. this binding then activates a second binding site, GPIIb/IIIa, which allows for tight adhesion of platelets to one another. incidentally, GPIIb/IIIa inhibitors are now crucial drugs in the treatment of heart disease, and their use was made popular by my awesome boss, dr. topol.

so yeah, von Willebrand's disease is the result of some abnormality of VWF, either quantitative or qualitative. quantitative disorders are the most common, such as the partial deficiency of VWF known as type 1 VWD, and this is what i suspect my friend had, although now we'll never know because he lost his bracelet. there are other qualitative variations of the disease where the VWF binds too well to GP1b, or it binds poorly, or it is completely absent (this is quantitative but whatever).

ok i'm much too distracted to continue. go evolution, boo intelligent design.