bada bing!
made again famous by the sopranos, sonny corleone uttered these famous words after his little brother delivered the monologue that i consider to be the turning point of michael corleone in the godfather. some people point to michael's tender moment at his father's bedside in the hospital; others say it's when he pulled the trigger on sollozzo and mccluskey in louis' restaurant; a strong case can also be made for apollonia's death by car bomb, which presumably sealed michael's fate to a life of violence.
but no, my favorite scene is when michael is sitting in a chair, one leg crossed over the other, simultaneously thinking through and explaining his plan to prevent sollozzo and mccluskey from ever harming his father again. that, i think, was when he irreversibly committed himself to the family, and his monologue--with the slow zoom in on his busted jaw and his droopy eyes--marks the first of his many calculated, cruel masterstrokes of vengeance. it is the beginning of his end.
that's how i like to think of heart disease. the beginning of the end. research shows that coronary arteries start narrowing not at 30 or 40 but at childhood. everyone, it appears, has some baseline degree of heart "disease." but what is it that causes heart disease--specifically, disease of the coronary arteries (CAD), the arteries that supply the heart with blood? is it the infamous things--high blood pressure, high cholesterol, obesity, smoking? how about family history, or IV drug use? or is it something else? my summer research has to do with how heart attacks are inherited, strange as it may sound. after AP bio and bs50 and bs52 and bs57 and the first-year genetics committee, i have a decent handle on how genetics works and the molecular machinery that results in a heart attack gene moving from one generation to the next. what i don't really understand, though, is how CAD works, i.e. its pathogenesis.
it turns out no one else really knows how it works either. as recently as the early 1990s, many physicians and researchers still believed that, if they could eliminate high blood pressure and high cholesterol, the elimination of CAD would follow. unfortunately, CAD isn't so simple, and its pathogenesis is now largely understood to be a complicated inflammatory process. allow me to be a shameless dork here and say that i think inflammation is fascinating. inflammation can be good, can be bad, can be seen and felt, can be invisible and silent, can be acute, can be chronic... it can do pretty much anything, anywhere (think of all the -itis diseases you've heard of. arthritis, gastritis, conjunctivitis, etc. even elephantitis, although not glorified like eminem would have you believe). now it seems it can even result in CAD and heart attacks.
all this brings me back to two of my least favorite subjects--basic cell physiology and immunology. these are the two biology fields that absolutely and obscenely adore using senseless numbers and letters to name things. unsurprisingly, these were the two subjects with which i struggled most last year. and, also unsurprisingly, cell phys and immunology are the cornerstones to the heart disease inflammatory process.
therefore, tomorrow i'll begin with a review of cell phys, using my beloved costanzo review book as my guide. i'll then move through the different organ systems, although slightly out of order so that i can do heart and vasculature first and thereby provide at least some semblance of narrative continuity throughout this summer's posts.
"it's not personal, sonny. it's strictly business."
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