Neocromancy 2012: Reanimate The Dead
    By Hank Campbell | February 11th 2012 05:23 PM | 2 comments | Print | E-mail | Track Comments
    In 1999, a Swedish medical student brought ancient wizardry and horror fiction to life - despite being dead for three hours, Anna Bagenholm was revived and has made a nearly full recovery. 

    It sounds cooler than D&D. Well, science often is - and what was happening in her body on a cellular level during the hours she went without a heartbeat, and what we can learn about how long it takes cells to die, may allow science to really push the boundaries of what it means to be dead.

    As Miracle Max said in "The Princess Bride", there might be a difference between dead and mostly dead. 

    If your cells hunker down in their outer membrane long enough for you to be "reanimated", then you will be - but the most vulnerable cells are those ones in the brain, which could be another mystery for science to pursue.

    Read a terrifically fun piece, Is It Possible to Reanimate the Dead?, by Eli MacKinnon on LiveScience.


    Gerhard Adam
    Actually the most interesting aspect of this piece is that cells deprived of oxygen and nutrients will self-destruct if presented with these missing items too quickly (reperfusion injury).  So it appears that the worst thing one can do, is to respond too quickly to the perceived needs of the cells.
    Mundus vult decipi
    John Hasenkam
    Reperfusion injury is very puzzling. In relation to drownings or death in cold climates a study last year claimed that an important component of this is lack of oxygen as this seems to promote survival of cells. Perhaps and I can only guess, many cells can live for a very long time when we are dead(days) so they must be relying on anaerobic glycolysis. This produces far fewer free radicals than oxphos via mitochondria. There is also the suggestion, some studies on this, that helium and\or xeon are protective against reperfusion injury. Noble gases, make no sense, can only surmise the helium is slowing the rate of O2 uptake. For those so interested, I just found this(The Ca2+ linkage is interesting because mitochondria are important buffers of Ca2+ and its release into the cytostol can induce death signals, neurons appear particularly vulnerable to this. 

    Evidence obtained over the past two decades shows that reactive oxygen species (ROS) are involved in brain lesions, including those due to cerebral ischemia-reperfusion. The mitochondria are the primary intracellular source of ROS, as they generate huge numbers of oxidative-reduction reactions and use massive amounts of oxygen. When anoxia is followed promptly by reperfusion, the resulting increase in oxygen supply leads to overproduction of ROS. In ischemic tissues, numerous studies have established a direct role for ROS in oxidative damage to lipids, proteins, and nucleic acids. Thus, mitochondria are both the initiator and the first target of oxidative stress. Mitochondrial damage can lead to cell death, given the role for mitochondria in energy metabolism and calcium homeostasis, as well as the ability of mitochondria to release pro-apoptotic factors such as cytochrome C and apoptosis-inducing factor (AIF). This review discusses possible mitochondrion-targeted strategies for preventing ROS-induced injury during reperfusion. The sequence of events that follow oxidative damage provides the outline for the review: thus, we will discuss protection of oxidative phosphorylation, mitochondrial membrane integrity and fluidity, and antioxidant or mild-uncoupling strategies for diminishing ROS production. Among mechanisms of action, we will describe the modulation of mitochondrial permeability transition pore (MPTP) opening, which may not only operate as a physiological Ca(2+) release mechanism, but also contribute to mitochondrial deenergization, release of pro-apoptotic proteins, and protection by ischemic preconditioning (IPC). Finally, we will review genetic strategies for controlling apoptotic protein expression, stimulating mitochondrial oxidative defences, and increasing mitochondrial proliferation.

    PMID: 16472163  [PubMed - indexed for MEDLINE]