Some things are just too important to leave to biologists or chemists. Like science, for example, which requires a physicist if yer wanna solve anything decent. There ain’t nothing physicists can’t help with, if they got some spit ‘n’ elbow grease. This week its protein condensation.
When proteins condense within the body they form plaques which seriously screw up ordinary function. They lie at the heart of diseases as diverse as Alzheimers, sickle cell disease and type II diabetes. Not to mention cataracts, a clouding of the lens in the eye which is a leading cause of blindness. This is the focus (geddit!) of Anna “Auburn” Stradner at the University of Fribourg in Switzerland and her buddies.
There are three kindsa proteins in lenses. Cataracts occur when these proteins condense. What Auburn Stradner and co have done is simulate the forces between these groups of proteins and watched what happens. Turns out that if yer assume that groups of proteins mutually repel each other but at short range also attract, then they disperse nicely and form a stable mixture in which the proteins stay at arms length, like nuns in a biker bar.
But switch off the short range attraction something interestin happens: the proteins condense, just as they do in cataracts.
Of course, the model is a lil simplistic–the proteins are hard spheres, for example. But ain’t it remarkable how a toy model like this can provide some important insight?
So with a lil speculatin, yer might imagine that protein condensation diseases might be caused by a chemical change that switches off (or cancels out) the mutual short range attraction between proteins. And that a-spottin’ and a-preventin’ that change could stop cataracts developin.
Zat help any a you biologists out there?
Ref: arxiv.org/abs/0708.3370: New Insight into Cataract Formation — Enhanced Stability through Mutual Attraction
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