In a vacuum, electrons travel at the speed of light. Even though the speed of an electron in tissues would be expected to be drastically reduced, the electron-oxygen transactions must still take place at amazingly fast speeds. Such free radicals oxidize proteins of coagulation cascades, thus triggering oxidative coagulopathy, which further fans the fires of AA oxidopathy. However, our high-resolution microscopic observations described in this article lead us to conclude that accelerated oxidative stress on components of circulating blood is neither confined to oxidative injury of coagulation pathways nor, indeed, are the coagulative phenomena the initial events. We return to this essential issue later in this paper.
Human cells regulate themselves, just as unicellular organisms do.
In medical literature, the discussions of cellular growth and regulation are generally limited to how cells maintain their structure and function by affecting key transcription factors. One commonly used mechanism by which cells turn key proteins on and off is adding or removing phosphate groups. The prevailing notions of human cell biology hold that greater the oxygen supply to cells, the more efficient their growth and the better their structural integrity and functional stability. Such simplification, however, ignores the diverse roles oxygen plays under different conditions. We cite here the example of cytotrophoblastic growth and differentiation to illustrate this important point.