CryoNet #33150 - #33156

CryoNet - Wed 29 Dec 2010

    #33150: Re: CryoNet #33145 - #33149 [Gerald Monroe]
    #33151: Re: CryoNet #33145 - #33149 [Gerald Monroe]
    #33152: Dr. Death and his loving couple arouses indignation [David Stodolsky]
    #33153: New novel Cryoburn [David Stodolsky]
    #33154: Re: Just a thought [Chris Manning]
    #33155: Scoring Cases [M2darwin]
    #33156: Scoring Cases [M2darwin]

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Message #33150
References: <[email protected]>
From: Gerald Monroe <[email protected]>
Date: Tue, 28 Dec 2010 06:04:06 -0600
Subject: Re: CryoNet #33145 - #33149

--0015175ce0860fa1dc049877414c

Mike Darwin : I'm still stuck on the following.  If we cool the patient down
while preventing hypoxia, and then do not leave them 'liquid' and in a
hypoxic state longer than proven guidelines for possible recovery, freezing
the brain solid and then chilling it to the point that molecular motion
almost ceases, what could go wrong?  What physical structure COULD neurons
store information in that would not be retained in this manner?  The
functional systems of the brain may contain many mysteries, but it's still
an object made of ordinary matter.

Storage at near 0 C during transport might be a big mistake.  You could
easily be correct.

But it we were hypothetically presenting the science of cryonics to an
unbiased review board and we say : step ONE patient's brain is revivable,
therefore it contains the long term memory data.  Step TWO : a short time
after step ONE, we have frozen the brain and the larger molecules are
completely unable to go anywhere.  They have not budged from where they were
located in Step ONE.  Step THREE is of course the brain after a century in
liquid nitrogen...hopefully almost the same as steps 1 and 2.

It seems like it ought to be possible to write equations describing the
information state of the brain in step one followed by step two, and
mathematically PROVE that a negligible amount of information has been lost
in the transition.  We would need to know nothing at all about memory
storage, except that it is performed by large durable molecules above a
certain number of daltons.

This is under ideal circumstances : patient has good standby care by a
competent medical team, and chooses to be suspended a short drive from the
cryonics lab.  One way to ensure this would be to have the patient on an
active life support machine that the patient could order switched off,
causing the patient to legally die when the team is ready.  That would be a
frightening moment, and one that I hope all of us here have a chance to
experience (assuming a method for keeping the brain alive in it's current
form is not developed in the next 50-80 years).

Your clinical examples aren't very illustrative because you're talking about
edema for a period of days killing billions of neurons, and now the patient
cannot retrieve their memories.  Are the memories gone?  Did neurons
involved in the process of searching and retrieving declarative memory data
get destroyed?  Who knows, but the patient has been allowed to fester in a
hospital bed for weeks while the damaged neurons are eaten by macrophages,
and none of the damage has been repaired or the missing cells replaced.  If
I go attack your desktop computer with a soldering iron and short a few
hundred randomly chosen circuits, you would not necessarily conclude that
the data on your computer was destroyed past any method of recovery.
 Especially if your computer stored it's data in hundreds of distributed
storage chips scattered all across the mainboard.

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Message #33151
References: <[email protected]>
From: Gerald Monroe <[email protected]>
Date: Tue, 28 Dec 2010 06:12:54 -0600
Subject: Re: CryoNet #33145 - #33149

--0015175cba0689cf7004987760eb

One quick addendum, Mike : the Arrhenius equation is half the story for the
case of near 0 degree C transport.  What about the rate of diffusion?  In
living cells, diffusion is VERY slow even at body temperature...it is not
possible for protein sized molecules to get from the nucleus of a typical
neuron down the axon to the synapse without help from powered microtubule
transport.  (diffusion is speeds are inversely proportional to the size and
mass of the molecule that is diffusing, hence why ions and water can get
around)

Once the oxygen is gone, and the ATP is all used up, the active transport
mechanisms don't work.  So the nasty lysozomal enzymes that might tear up
the synapses where the memories are stored cannot go anywhere, on top of
being limited in their rate of reaction.  Free radicals can do some damage,
but the pieces of damaged synapses are ALSO going to be inherently limited
by the slow speed of diffusion.  As long as the pieces are close enough to
each other that they can be reassembled like a jigsaw puzzle, we can
probably infer the original state of a synapse.

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Message #33152
From: David Stodolsky <[email protected]>
Subject: Dr. Death and his loving couple arouses indignation
Date: Tue, 28 Dec 2010 19:57:48 +0100

--Apple-Mail-358--424627519

http://ibyen.dk/kunst/ECE1152522/dr-doed-og-hans-samleje-lig-vaekker-forargelse/

Translation:

<http://translate.google.com/translate?hl=en&sl=da&tl=en&u=http%3A%2F%2Fibyen.dk%2Fkunst%2FECE1152522%2Fdr-doed-og-hans-samleje-lig-vaekker-forargelse%2F>


Translation, including my corrections:

--Apple-Mail-358--424627519
Content-Disposition: inline;
	filename=PastedGraphic-1.tiff
	x-unix-mode 66;
	name="PastedGraphic-1.tiff"

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Message #33153
From: David Stodolsky <[email protected]>
Subject: New novel Cryoburn
Date: Tue, 28 Dec 2010 20:02:00 +0100

<http://www.amazon.com/Cryoburn-Vorkosigan-Saga-McMaster-Bujold/dp/1439133948>

>From Publishers Weekly
Fans have been clamoring for Hugo winner Bujold to pen a new Vorkosigan Saga novel since 2002's Diplomatic Immunity, and they will not be disappointed by this thoughtful tale. Only five days after arriving on Kibou-daini for a cryonics conference, interplanetary diplomat Miles Vorkosigan narrowly escapes kidnapping. Drugged, dazed, and alone, he is taken in by Jin Sato, whose mother was the leader of a cryonics reform movement until being declared mentally ill and involuntarily frozen. Now Jin lives in a building full of squatters running an illegal cryonics clinic. Under imperial orders to investigate the shady dealings of the cryo cartels, Miles connects the far-flung pieces and exposes a sneaky plot. Bujold introduces appealing characters to join familiar ones in exploring the ramificat
 ions of a planet-wide culture of postponing death, and her deft and absorbing writing easily corrals the complex plot and softens the blow of a tear-jerking conclusion. (Nov.) (c) 
Copyright C PWxyz, LLC. All rights reserved.




David Stodolsky
[email protected]  Skype: davidstodolsky

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Message #33154
From: "Chris Manning" <[email protected]>
Subject: Re: Just a thought
Date: Wed, 29 Dec 2010 09:10:55 +1100

>From and to David Stodolsky:

chris: There are many possible scenarios in which revival from cryopreservation
will be technically possible but problematic for other reasons, e.g. revival may
be outlawed due to overpopulation.

dss: This is fallacious and considering it would be a concession to our
ideological opponents.

Reply: Our ideological opponents may get into government, where they aren't
already.

chris: I am surprised that these possibilities aren't being canvassed more in
the cryonics community. Anyway, the thought I had is as follows:

dss: (blank)

Reply: I gather you have nothing to say about the thought I had (the main point
of my email).

chris: More generally, I think readers ought to be asking themselves in what
possible future circumstances they do or do not wish to be revived.

dss: This needs to be framed as improved possibilities, however, the uncertainty
involved makes this more of an exercise in fantasy than anything else.

Reply: Let's see if I've understood correctly. It's so difficult to be sure of
anything about the future that we shouldn't bother making statements such as 'I
am willing in principle to live off earth after revival (if that should prove
possible/desirable/necessary).'

How does the likelihood of revival compare with the likelihood of its being
possible to live off earth?

dss: There is a risk that restriction on revival would tie the hands of those
trying to do the best for cryonicists in the future.

Reply: I am trying to make sense of this statement. The only sense I can make of
it is that you thought I meant restriction by the cryonics movement itself. That
possibility had never occurred to me. No, I meant restriction by
repressive/hostile governments.

>From and to John de Rivaz:

John: I was speaking to someone over the holidays who said that he would never
consider cryopreservation on account of the risk of a revival into a hellish
future. I countered that it is easy enough to make people. If your sole purpose
is to enjoy their suffering, why go to the trouble of reviving and rejuvenating
a cryopreserved patient. However this was insufficient in terms of a "sound
byte" to convince him.

chris: I would not be convinced by the above either - because I don't know what
you're talking about. And I've read it several times.

I assume you must mean (in some roundabout way) 'We would not be signed up for
cryonics if we thought the future was going to be unpleasant.'

John: There have been dystopic science fiction novels written about revivals
into less than satisfactory futures, but they usually have "our hero" winning
through in the end.

Reply: I am well aware of that, and could give you a list of my own.

>From and to Eneasz Brodski:

Eneasz: I've always countered that even if the future is crap, it's better than
the alternative. Most people, if forced to choose between living in Dark Ages
Europe or being killed would choose living in the Dark Ages. I doubt the future
can be worse than that.

Reply: And my point, which you also seem to have missed or not seen fit to
comment on, is that we may not have to live in Dark Ages Europe. We may have the
option of living elsewhere.




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Message #33155
From: [email protected]
Date: Tue, 28 Dec 2010 17:12:39 EST
Subject: Scoring Cases

Content-Language: en

 
Gerald, These are very good questions and are  certainly not the kind of 
questions  asked by people who have been recruited into cryonics over the past 
15 years, or  so. Could you tell me more about yourself, either here on 
CryoNet, or via  personal communication? 
References: <[email protected]_ 
(mailto:[email protected]) > 
From: Gerald Monroe <[email protected]_ 
(mailto:[email protected]) > 
Date: Tue, 28 Dec 2010 06:04:06  -0600 
Subject: Re: CryoNet #33145 -  #33149 
--0015175ce0860fa1dc049877414c 
>>I'm still stuck on the following.  If we cool the patient down while  
preventing hypoxia, and then do not leave them 'liquid' and in a hypoxic state  
longer than proven guidelines for possible recovery, freezing the brain 
solid  and then chilling it to the point that molecular motion almost ceases, 
what  could go wrong?  What physical  structure COULD neurons store 
information in that would not be retained in this  manner?  The functional systems of 
 the brain may contain many mysteries, but it's still an object made of 
ordinary  matter.>> 
Yes, the brain is made up of ordinary matter, and for  the record, no, I am 
not a mystic: I think it almost certainly the case that  memory, 
personality and identity can be fully explained on the basis of the  physical 
structure of the brain/body. And if we had a way to render those  structures into a 
solid state, devoid of meaningful biophysical change, then we  would indeed 
be preserving the individual in a viable state - and if we could  reverse 
that process without harm, then we would have suspended animation and  
survival of the treated individual. 
But there's the rub, we do NOT have such a method at  hand. When you write: 
"freezing the brain solid and then chilling it to the  point that molecular 
motion almost ceases, what could go wrong?" you put your  finger on the 
kernel of the problem. Currently, we have two ways to achieve  durable 
(indefinite) biopreservation, and those are freezing and vitrification.  Both of 
these processes cause enormous perturbation of brain structure on both  the 
tissue and the molecular level. Currently, we believe that vitrification  
causes less perturbation to the structures we think are the best candidates for  
encoding memory and personal identity, and so that is why it now considered 
the  "best' treatment. However, there is substantial evidence that most 
patients who  are being "vitrified' are in fact only partially vitrifying and 
in many cases  may be freezing - and freezing under conditions that may be 
far worse than had  they been frozen using conventional methods of 
cryoprotection and slow cooling.  But before I discuss the biophysical changes that 
may attend vitrification, I  want to discuss freezing injury, in part because 
there is some overlap between  it and freezing in terms of the injury 
inflicted. 
WHAT COULD GO WRONG: It is probably no accident that a  large fraction of 
the people recruited to cryonics since its inception have been  engineers, 
mathematicians, computer scientists, programmers, and, in general,  physical 
science types. I believe one reason for this is that there is a  fundamental 
difference in the way biological machines and electromechanical  machines 
are structured and operate. Almost all electromechanical systems may be  
fairly described as solid state - even those in existence before the advent of  
electronics, and before the advent of the transistor. By solid state I mean 
that  virtually all their components are, literally, solid at their normal 
operating  temperatures.  
A consequence of this is that I can take a  21st Century Android phone or a 
17th century clock, and  whack them with a sledgehammer and the end result 
would broadly be the same: I'd  have a bunch of solid pieces of varying 
sizes and shapes that just sat there -  and of course, neither the phone nor the 
clock would work any longer. But, all  the pieces would still be there and 
they would retain their individuality and  unique identity. And such will be 
the case indefinitely, as long as they are  protected from the elements. 
Biological systems are NOT solid state devices, and  they operate in very 
different ways. The core of biological systems is the  membrane; and 
membranes in living systems are not just passive walls or  "compartment makers': 
they are the engines of chemistry and action in living  systems. They have 
enormous complexity and they derive a great deal of their  unique ability to 
function as living systems from their liquidity and  plasticity. If I were to 
reach for a meaningful physical analogy in the everyday  macro-world, the 
analogy would be that of soap bubbles. Cell membranes are very  much like soap 
bubbles, and they behave in broadly similar ways when stressed.  If you 
osmotically stress a cell by shrinking or swelling it too much, it does  not 
behave like a glass sphere and shatter into discrete pieces which can be  
collected and reassembled. Rather it buds and blebs and behaves like what it is, 
 a liquid. And if you stress it enough, it simply comes apart into little  
droplets and into smaller "cells,' vesicles that have formed from the 
original  membrane.  
Before such dramatic changes occur, the structure of  the membrane can 
undergo reorganization in many ways, and the proteins embedded  in the membrane 
may be rearranged as well. This is true not just for the plasma  membrane 
that encases the cell, but also for the membranes that comprise the  cellular 
organelles. In fact, it is rearrangement of mitochondrial membrane  
structure that underlies some of the damage that occurs in ischemia. Freezing  
causes enormous mechanical stress to the plasma membrane, and to organelle  
membranes, and some of the response to this stress is to radically alter  
membrane structure. In the worst case, the cell membrane(s) disappear as the  
structures they were, and reappear as new structures; droplets of membrane  
material, brand new micro-cells and so on. And they shed structures that were  
embedded or enclosed in them; thus the debris fields seen in frozen thawed  
tissues.  
Biological systems are NOT solid state devices and if  you damage them 
badly enough they do not sit around as discrete, broken pieces  waiting to have 
their pre-injury, functioning structure inferred from the broken  pieces. 
And it is important to understand that some of this "remorphing' goes on  
during the freezing process as a consequence of the enormous osmotic and  
mechanical stresses imposed by ice formation. Further, there are significant  
changes to membrane structure, such crystallization of the lipids that occur  
solely as a result of cooling, and completely independent of freezing. To 
return  to the Android phone analogy, it would be as if the Android were made 
up of  liquids encased in soap bubbles and you squashed it.   
Imagine a soap bubble with an exquisitely detailed  painting embedded into 
its surface. A painting made up of millions of tiny  pixels comprised of 
colored nanoparticles. If you burst the bubble, some of the  bubble wall 
material will return to a simpler, all-fluid state, and some of it  may reform 
into new bubbles. But in any event, the painting is gone and what's  more, it 
is not obvious that it can be inferred from the puddle of particles in  
liquid and the new bubbles that result. So that is one thing that can go wrong.   
I think it likely that procedural memory is encoded in  hard connections 
between neurons. But it is possible that declarative memory  relies on a 
different mechanism; perhaps changes in the character of the  synapses, neuronal 
cell membranes, number or distribution of vesicles or other  membrane-based 
structures, or discrete changes in the chemistry of the neuronal  membranes. 
BOTH freezing and vitrification have the potential to disrupt those  kinds 
of structures in ways that would leave them uninferrable. Vitrification  may 
do this by the expedient of altering membrane structure irreversibly by  
dehydration, or by changing the molecular structure of the membranes or 
membrane  components by directly perturbing their structure. Vitrification 
solution is NOT  water, and water is critical to the structure of many of the 
molecules inside  cells. Indeed, a good part of the science behind designing 
tolerable  vitrification solutions is to make them behave as much like water as 
possible -  while at the same time behaving as good glass forming agents 
when  cooled. 
As I said before, we simply don't how memories are  encoded in the brain 
and far more profoundly, we do not have a solid proven  theory of what 
comprises human identity - leaving particular structures out of  it. This is one of 
many reasons why we should be striving mightily to achieve  fully 
reversible suspended animation; because we JUST DON'T KNOW ENOUGH  YET. 
>>Storage at near 0 C during transport might be  a big mistake.  You  could 
easily be  correct.>> 
>>But it we were hypothetically presenting the  science of cryonics to an 
unbiased review board and we say : step ONE patient's  brain is 
revivable,therefore it contains the long term memory data.  Step TWO : a short time after 
step ONE,  we have frozen the brain and the larger molecules are completely 
unable to go  anywhere.  They have not budged from  where they were located 
in Step ONE.  Step THREE is of course the brain after a century in liquid  
nitrogen...hopefully almost the same as steps 1 and  2.>> 
This is all fine and dandy as long as you can posit  that the molecules 
have not budged from where they were whist in a fully  functional state. But 
you cannot do that, and neither can anyone  else. 
>>It seems like it ought to be possible to write  equations describing the 
information state of the brain in step one followed by  step two, and 
mathematically PROVE that a negligible amount of information has  been lost in the 
transition.  We  would need to know nothing at all about memory storage, 
except that it is  performed by large durable molecules above a certain number 
of  daltons.>> 
Yes, that is correct: now, define "negligible' and  prove that the 
molecular structure is essentially unperturbed. Do that, and your  statement stands 
as correct. 
>>This is under ideal circumstances: patient has  good standby care by a 
competent medical team, and chooses to be suspended a  short drive from the 
cryonics lab.  One way to ensure this would be to have the patient on an 
active life  support machine that the patient could order switched off, causing 
the patient  to legally die when the team is ready.  That would be a 
frightening moment, and one that I hope all of us here  have a chance to experience 
(assuming a method for keeping the brain alive in  it's current form is not 
developed in the next 50-80  years).>> 
Well, it might be frightening to you, but having seen  countless dying 
patients in this condition, and knowing the distress and  hopelessness they feel 
(after all, many know they are DYING), I would not find  the "switch off' 
of "life support' frightening at all - indeed it would be the  prospect of 
CONTINUED life support that might render my brain into an  unrecoverable 
state that I would find - not frightening - but  terrifying. 
>>Your clinical examples aren't very  illustrative because you're talking 
about edema for a period of days killing  billions of neurons, and now the 
patient cannot retrieve their memories.  Are the memories gone?  Did neurons 
involved in the process of  searching and retrieving declarative memory data 
get destroyed?  Who knows, but the patient has been  allowed to fester in a 
hospital bed for weeks while the damaged neurons are  eaten by macrophages, 
and none of the damage has been repaired or the missing  cells replaced.  If 
I go attack your  desktop computer with a soldering iron and short a few 
hundred randomly chosen  circuits, you would not necessarily conclude that the 
data on your computer was  destroyed past any method of recovery.  
Especially if your computer stored it's  data in hundreds of distributed storage 
chips scattered all across the  mainboard.>> 
I think my clinical example of cerebral edema and  declarative memoery loss 
is very much on point because it COULD imply that it is  NOT the death of 
brain cells that cause's memory loss, but rather some  alteration in membrane 
structure as a result of edema. In fact, we can be sure  that neuronal cell 
death, either from apoptosis or necrosis is NOT the cause of  such memory 
loss. These patient do not experience global loss of neurons and the  areas 
where they suffer the most neuron loss, the prefrontal cortex, is not  
generally associated with memory storage or retrieval. Nor are there visible  
losses in the white matter connections in the inflow/outflow tracts to the  
hippocampus - nor is the hippocampus catastrophically injured (e.g. by MRI  
imaging).  
Certainly it is possible that they have lost access to  their memories, 
rather than the memories themselves. But this hypothesis fails  to explain why, 
after they make a recovery from the acute injury, they can form,  store and 
retrieve new declarative memories, but still not access the ones  create 
prior to the trauma? Thus, there is much we don't know.   
And again, BRAINS ARE NOT COMPUTER CHIPS ON A  MAINBOARD ;-). And neurons 
are not like transistors in a microchip; that analogy  holds only where they 
do non-unique tasks. It might be better to think of them  as microscopic 
flash drives written on soap  bubbles. 
Finally, the quality of cryopreservation most patients  are now receiving 
is dismal and has, on average, deteriorated since 1990.  Optimal pretty much 
is a thing of the past in cryonics anywhere in the world  today. 
Mike  Darwin


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Message #33156
From: [email protected]
Date: Tue, 28 Dec 2010 19:31:02 EST
Subject: Scoring Cases

Content-Language: en

From: Gerald Monroe <[email protected]_ 
(mailto:[email protected]) >
Date:  Tue, 28 Dec 2010 06:12:54 -0600
Subject: Re: CryoNet #33145 - #33149
 
--0015175cba0689cf7004987760eb
 
>>One quick addendum, Mike : the Arrhenius equation is half the story  for 
the case of near 0 degree C transport.  What about the rate of  diffusion?  
In living cells, diffusion is VERY slow even at body  temperature...it is not
possible for protein sized molecules to get from the  nucleus of a typical 
neuron down the axon to the synapse without help from  powered microtubule 
transport.  (diffusion is speeds are inversely  proportional to the size and 
mass of the molecule that is diffusing, hence why  ions and water can get 
around)>>
 
Gerald, the example of the diffusion of skeletal proteins through the  
axoplasm to the synapses is not a good one, in that it is not representative of  
diffusion in the cytoplasm, and in the extracellular spaces. It's rather 
like a  US general projecting the speed of movement of a Chinese mechanized 
division  (equipped with all terrain vehicles) towards LA from San Diego based 
on the  speed they could travel up the 5 Freeway at rush hour. Regular 
traffic is slowed  to a crawl because it is constrained by the "tube' of the 
freeway, the  requirement to obey certain traffic rules, and so on. Diffusion 
time for the  lytic proteins is faster than you might expect, because many 
of them are small,  and they are not constrained by the narrow tunnel of the 
axon. Take a look at  the MW ranges for the small serine proteases, for 
example (90 kd). The matrix  metalloproteinases (MMPs) are also quite mobile, 
and they are *widely  distributed, but inactive.*
 
But, apart from diffusional mobility, you must also consider the fact that  
many of the most destructive proteases and lipases are NOT confined to the  
lysosomes. In fact, they are distributed all over the cells and in the  
extracellular spaces but are INACTIVE. For instance, the MMPs are activated by  
sequential proteolysis of the propeptide blocking their active site, and 
this is  brought about by cell-associated plasmin generation by urokinase-like 
 plasminogen activator: both of which are produced in abundance in 
ischemia, and  both of which are sufficiently active in hypothermia to cause injury; 
 principally degradation of the basement membrane of the capillaries 
leading to  increased edema during subsequent perfusion. In turn, the MMPs appear 
to be  involved in the initiation of cascades of activation of gelatinase A, 
 collagenase 3 and gelatinase B which are also implicated in basement 
membrane  destruction. This just one example that comes to mind, there are many, 
many more  and anyone who has actually perfused cold ischemic cryopatients - 
even ones  stabilized ideally, but then transported on ice for 24 hours 
(and sometime less)  will report that the amount of edema is dramatically 
different between such  patients and those who arrested locally and were promptly 
perfused and subjected  to deep cooling.
 
The brain is one of the most sensitive (and dramatic) indicators of this  
cold ischemic injury. In a patient with very little or no cold ischemia the  
brain will shrink (dehydrate) dramatically during cryoprotective perfusion 
and  it will STAY shrunken. In cold ischemic patients the initial volume 
reduction is  followed by a rebound to normal volume and then swelling. This 
rebound is NOT  equilibration of the cryoprotectants, rather it is EDEMA. 
 
You must also realize that white blood cells, particularly the neutrophils  
(PMNLs) will have been activated during the agonal period and/or by the 
disease  process killing the patient - and if not then, then during ischemia - 
even very  brief periods of ischemia of 10 or 15 minutes. These cells 
contain enormous  reservoirs of hypohalous acids - principally sodium 
hypochlorite (household  bleach). The MW of NaOCL- is ~74, and it diffuses quite 
rapidly at 0 deg C and  is quite chemically reactive at that temperature, as well. 
What's more, the PMNL  chlorinated oxidants destroy I 1- proteinases 
inhibitor activating the proteases.  In effect, chlorinated oxidants create a zone 
of oxidized I 1-proteinase  inhibitor that allows released elastase to 
attack and degrade endothelial cell  membranes and cell-cell junctions. PMNL 
activation and degranulation are  operational on a large scale in most slowly 
dying patients, and in patients who  are not cooled very rapidly to ~5 deg C 
there will be continuing neutrophil  degranulation with associated release of 
chlorinated (and, in the case of the  eosinophils, brominated oxidantants). 
These highly destructive molecules are  small, mobile and can directly 
degrade proteins into indistinguishable small  "chunks' of amino acids. 
 

>>Once the oxygen is gone, and the ATP is all used up, the active  
transport mechanisms don't work.  So the nasty lysozomal enzymes that might  tear up 
the synapses where the memories are stored cannot go anywhere, on top of  
being limited in their rate of reaction.  Free radicals can do some damage,  
but the pieces of damaged synapses are ALSO going to be inherently limited 
by  the slow speed of diffusion.  As long as the pieces are close enough to  
each other that they can be reassembled like a jigsaw puzzle, we can 
probably  infer the original state of a synapse.>>
 
This clearly does not happen, and the cold ischemic state is a dynamic  
place, in terms of both protease and lipase activity. Diffusion is slowed, but  
it is by no means halted, or reduced to biologically insignificant rates. 
And  what's more, phase change in the membranes may open up pores large 
enough to  allow the movement of small, lytic enzymes from the lysosomes...
 
Mike Darwin
 
 
 
 
 


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