Friday, December 12, 2008

Tunneling Nanotubes .

Tunneling Nanotubes .
Andre Willers
12 Dec 2008

Synopsis :
Nanotube tunnels in animal tissue have been observed between cells transferring proteins (ie information and material) directly from cell to cell , bypassing the cellular wall and the inter-cellular medium .
Source : New Scientist 15 nov 2008 ,p42 .

Discussion :
This is a hot new subject , especially in immunology , AIDS , embryology , etc .

Why has it not been noticed before ?
Sigh . It has . Many times . By students , usually . The scientific dogma did not allow for it , so the poor student had to redo the experiment until he got the desired result .

The "correct" methodology of microscopy would not show these fragile structures , either . The theory was also ignorant of fullerene tubes , so nanotubes were deemed impossible . The Dogma would not allow it .
Only a combination of flukes allowed this to come to general notice .

Of course , now they pop up all over the place .

Evolutionary History .
Free bacteria formed (and still forms) colonies and plaques that interchange materials.
The materials include genetic information (plasmids , etc)

The mechanism seems to be an adaptation of the cellular reticulation system developed originally for dragging components around during cell-division . The development of sex forced further change , as did the incorporation of mitochondria .
(See http://andreswhy.blogspot.com "ATP and Catalytic Motors")

We would thus expect transport tubes inside the cell .
Where are they ? Right where you would expect them , but called something else, usually vacuoles , sacs , garbage disposal , reticular system , etc .

Some evacuation vacuole got stuck in the open position due to mutation , but in a pulsed fashion . This would have major advantages in a colony .

Macro-receptor sites .
Think of a tube passing through the cell-wall as a semi-permanently open portal (macro-receptor site) . To avoid trouble , it connects only to another cell (or tube) which is similar . How does it recognize similarity ? The handshake is simplest with budded offspring of the cell (ie during growth or replacement) . The mother-cell keeps on sending material , even mitochondria(this has been observed) via the nano-tubes . This includes information on how the new cell is to develop . Which genes has to switched on and in which order and how long . Hence the importance to embryology or organ maintenance .

Weaning .
Every multicellular organism develops from one cell .
At some stage the mother-cell has to terminate the tubes to the daughter-cell , as new daughter-cells take up resources and space for the tubes on the cell-wall .

But it would have a definite advantage if it maintained the capability of recognizing a handshake of any daughter-cell . Reconnecting with daughter-cells if the mother-cell is under stress forms a mini-colony (read organ or organism) to smooth troubles .
This evolved into the immune system .

The Handshake .
There is no organism . There is the original mother-cell (ovum) and all the others are daughter-cells in various stages of development , forming a traveling wave down the river of time. An iterative , fractal system with whirlpools of attractor basins interacting via a secure handshake . Expand this to the whole stream of life .

But who watches the watchers?
What is secure enough , but with a small error percentage to allow evolution ?
In a situation like this (complex , long term and conflicting goals) we can haul out our trusty Infinite Probe (see http://andreswhy.blogspot.com "Infinite Probes" et al) .

We can immediately say there is a reserve mechanism (ie nil error allowed) at about 33% level . A mechanism that fits the bill is Quantum Entanglement . A set of molecules in the original cell can be entangled with a set in every daughter-cell (this can be done – there is experimental proof) . Every nanotube formed will use up some of these molecules both on the mother and daughter side to do the handshake .

The question is then whether the cell has the ability to manufacture new entangled molecules outside of the budding-mechanism .

There are three possibilities :
1.If it cannot , eventually it runs out of handshakes and is forced into apoptosis . This gives rise to something like the Hayflick limit .

2. If it can without limit , the organism will not have an ageing mechanism , but be prone to cancers . Remember , a micro-tumor can be thought of as bio-hazard laboratory that needs handshakes to exist . (See previous posts.) The other 2/3 of the immune mechanism is supposed to keep it in check . If this fails , the entangled molecules have to be dis-entangled .
Physics has a number of these methods , since with them the problem is the opposite .

The easiest is to take a measurement . Since a biological mechanism has probably evolved a buffered meta-material (see previous posts) , some ingenuity might be required .

The easiest would be to flash-switch a very bright delineated light (like a laser) alternatively between the affected volume and surrounding volumes of healthy tissue .
The variation in measurements should decohere the entanglements . The cancerous cells will have no more handshakes and can then be mopped up by the immune system . This is part of what happens in radiation therapy .

Many other delineated , varying measurements using electrical fields , magnetic fields , pH values , sound , etc , etc can be used . Consult physics and chemistry colleagues .

3. It can manufacture new entangled molecules outside of the budding-mechanism , but there are limitations . The limitations are under the control of the organism (ie a top-down control) . This is what is evolving at the moment .

The brain is a good example . A lot of interconnectivity is not via neurons or even glial or fluid systems . Direct nanotube interaction between various cells adds a new layer of complexity . Note that the handshake entanglement mechanism is evolving into something rich and strange .

Nanotubes can backfire in Shock or metastasis .
Shock messengers bypass the bloodplasma and go directly from cell-to-cell , especially if given a bit of time .
But emergency reconnect probably means that some new daughter-cells are prematurely disconnected , leading to apoptosis in many cases .

Hibernation anti-shock therapy .
Do an emergency disconnect on immature daughter-cells and hibernate them with H2S .
Feed and stimulate the healthy , mature daughter cells surrounding the trauma .
Once the shock-cytokines have been mopped up , restore immature daughter-cells under mild stress to promote re-establishment of nanotubes .

Immune System .
Dendritic cells of the immune system use this mechanism to share information about new pathogens . (Hence Immunology's interest)
Some pathogens have evolved to hide in the nanotubes . Hence the interest of AIDS researchers .

Mitochondria Transfer .
As mentioned above , some nanotubes are large enough to transfer mitochondria . This has been observed . Now , why would cells do this ? Fair enough if the mother-cell is helping out the daughter-cell . But , as discussed before ,
(See http://andreswhy.blogspot.com "ATP and Catalytic Motors") ,
the problem is usually too much energy , not too little .

This process might not be under the cell's control . The mitochondria are partners , not slaves . They have their own requirements . Some might just feel like moving up to a more fashionable , hip environment . They still have motility capability (remember the flagellae) .
Like moving from a cold-water second-storey walk-up apartment in the CBD to the suburbs .

They also do not have access to the handshake system .
This would be a disaster to the host . But the mitochondria has been stripped of any capability to use it (stripped genome:see below).

But why has the cell not taken over the ATP generation function ?
It would have if it was a purely chemical process . But it involves a physical process .

The Catalytic Motor .
The original mitochondria evolved inhibitors to competitors which also took out the ur-host's motor-capacity , forcing the cell to become multicellular to achieve higher survival potential via organism locomotion .

Beautiful !

But this would mean they would have some sort of quorum-system to prevent over-population in the cell . Hence the migration . From their viewpoint , they are the masters .
Which is why their genome is stripped to the bone .
"As for THAT , our servants do it!"

Which also means that they do not have the equivalent of the handshake . You could transplant mitochondria without rejection by other mitochondria . But would the host accept them ?

Weaning again .
The mother cell keeps on pumping ATP and mitochondria through nanotubes into daughter-cell until they cannot take any more . The nanotubes are severed from the daughter-cell side .

Ageing
From the above , the problem seems to be overpopulation by mitochondria turning cells into the equivalent of slums , leading to apoptosis . It is the markers of mitochondria that are important . Note the correlation between carbohydrate (non-alcohol) starvation and longevity .

Anti-agathics :
1.Fool nanotubes into sending mitochondria into the bloodstream instead of into another cell . This compound is probably already known . A variant of some growth factor . Since the mitochondrium lacks a handshake , the immune system will polish it
off . Effective if used from ages 24-35 . The organism will be more sensitive to shock

2. Pulse the system .
This is a very complex feedback system , not possible to keep under steady-state except with Beth(2+) systems . But it can be kept at an acceptable average by controlled pulsing around the attractor-basins with Beth(1) technology . Para(1) above is a variant of this method .


3. Fine-tune the sulfur system .
Mitochondria treat chemicals with sulfur in them differently . The catalytic motor marks them by some process analogous to epigenetic marking as not to be stored.

Since the H2S mechanism of hibernation brings the whole metabolism to an immediate halt at specific concentrations , the system evolved not to store certain sulfur compounds . There is not much point in storing sulfur fats that stutters finely tuned metabolic processes . Storing involves concentration . The results can be catastrophic in an emergency downdraw . This is sufficient for evolution to nix it .

Hence the Atkins system .
Proteins all have sulfur .
This marks them for immediate use , not storage .
The glucose from protein gets methylated and enters the cell by a completely different, metered pathway . The metering is done by the mitochondria , not the cell .
The system has a method of regulating excess , but only for molecules marked as originating from sulfur-bearing compounds .

Sulfur Salts .
Dousing carbohydrates with a very dilute hydrosulfuric acid should give the same effect as vinegar sauces as far as acidity is concerned . (Taste) . The sulfur should trigger the effects described above .

The only way to try it is by experiment .
I will keep you posted .
This obviously has major implications for diabetics and dieters .
The effects of sulfur in normally non-sulfur foods like sugar is unknown .
But diabetics can measure it quickly by blood-sugar measurements .
The long-term effects are unknown .
But we have an evolutionary history of these effects: see below .

Chixilub impact :
This was on top of a massive deposit of sulfur-bearing rocks . The fallout rendered the oceans acidic for decades . But it was sulfuric acid . The sulfur prevented build-up of fat reserves as discussed above . This rendered many large sea-going (and land-going) species extinct , as their pulse-feeding habits could not be sustained in an environment where fat-storage did not take place . Their reserve mechanism vanished .
(See http://andreswhy.blogspot.com "The Flower , the Dinosaur and Puff")

This helps to explain why sea-going dinosaurs also could not survive . Without an energy storage mechanism like fat , large animals simply could not survive from meal-to-meal in an energy-poor environment .

This begs the question : why have mitochondria not evolved a coping mechanism for sulfur ?
The answer is that they cannot . They are in an mutual dependency with multi-cellular organisms . Both have genetic machinery that halts all cellular activity in the presence of a certain concentration of H2S . The probability of both changing fundamental metabolic processes and genetic switches by ordinary chance (Beth(0) ) evolutionary processes are far less than the probability of going extinct .

Of course , we can design them that way (Beth(1) process) . But these processes are so deeply rooted , that it is not recommended without access to a Beth(2) processor

Sulfur shortage .
I have discussed this at nauseam in previous posts .
Our present planetary ecosystem has a net shortage of biologically available sulfur .
This is clear from the fact that furriers and leather merchants have to feed their source animals MSM to get usable products .

Cell walls (animals and plants) , reticulation systems , nanotubes , etc all need sulfur as a vital part of their structures .

Eutrophication of rivers , lakes and oceans can be vastly decreased by limiting their intake of sulfur . (Mostly human sewerage) .

Experimental protocol :
The above can be easily tested .
Dimension one:
Angiosperms:
Sugar , bread , barley , rice .
Non-Angiosperms :
Mushrooms , leaf veggies , potatoes , acorns

Dimension two :
Douse with dilute hydrosulfuric acid to give resultant mixture a pH of
4 (about CocaCola) , 5,
7 (neutral)
9 (alkaline)

Monitor fasting and non-fasting Glucose levels with and without diabetic persons .

This will give a 4x9x4 matrix .

A quick and dirty test would be sugar plus pH 4 hydrosulfuric acid for a person on Atkins diet .


And they sneered that the impudent little wine might be a wee bit sulphurous .

Andre

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