This is what unexposed cells look like:


Now all of this is exciting, but here's what really caught my eye, and unfortunately, is left unexplained in the full article. After the field is removed, the blood needs about 2 - 3 hours to fully recover it's normal viscosity.
Why?
Why such a long relaxation time for such a low viscosity material? I am really at a loss to explain this, and somewhat strangely, the article doesn't even really seem to think that there is anything unusual about it as they make no mention of this hysteresis. Does it really take that long for the magnetization of the iron to relax at body temperature, or in the same vein (heh, heh), does it take that long for the thermal energy to drive the cells apart and negate the magnetic attraction? Is there now some stickiness between the cells that keeps them together that wasn't there before? Is the magnetic field interacting with more than just the iron in the blood? I am greatly puzzled about this "thixotropic" behavior, and if anyone has any ideas, please add your comments.
And of course, the devious retired-bicycle-racer-who-now-gets-fat-in-the-winter in me wonders if how long before such a device is used to improve athletic performances. It won't help you win a long event such as the Tour de France, but for a short track event (200m sprints for instance), it could give you an edge. Get your blood all magnetized before your event, go onto the track and let the low viscosity fluid run all through your veins while you pump out a sub-10.5 record. By the time the lab could even look at your blood, the viscosity would have return to normal. How is anybody ever go to catch that short of quarantining the athletes before a competition (and that approach would never fly).
4 comments:
From the image, it looks like the persistence of the RBC chains would be due to cell-cell adhesion and/or membrane fusion. A few hours seems reasonable for those effects.
Interesting.
Somehow I would have thought that blood cells would be immune to such junctures due to the potential for clotting.
Clotting is caused by a cascade. Factor X/XV/XVII proteins(?) signal changes I think. It's not just a physical agglomeration of cells.
I would be interested to see if all the tissues were still sufficiently vascularized. I wonder if the affinity between the RBC's would effect the ability to interact with the cells.
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