A Fiat shares a lot of physical characteristics with a Lamborgini.
You don't care, I say that there is some difference.
Humans share lots of genes with the mouse. We share ~99% of the genes.
However, religious and ethical believes of many people might tell
them that is not the same to eat rat, pig, human or chicken.

Religious and cultural differences aside, I think having rats
with a complete set of the human immune system running
around in the sewer systems of the world is not a good idea
either. Each organism has it's niche and broadening might not be
a good idea. It might expose us to unknown pathogens.



Jim Webster wrote:

Oz wrote in message
...
writes


would you care if grampa's genes where in your pigs?

No. Why should I?
I wouldn't care if some of my genes were in a pig.
We share lots of genes with pigs anyway.

latest figures was we are 300 genes different from mice, which isn't a
lot in 30,000+ genes.

--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'

Spain does not export oil to America. Today it's coasts are covered with oil.
Who would have thought!
I know about shuch things as continents but corn travels in ships.


Jim Webster wrote:

wrote in message
...


Jim Webster wrote:

wrote in message
They thought the same in USA. The GM corn ended up in México.
Corn can travel across continents, and does so regularly.

just check your map, there didn't use to be a continental land
bridge
between Europe and South America


Corn can travel across continents, and does so regularly.
"The pasture of stupidity is unwholesome to mankind"

as has been pointed out to you, there is no land bridge so it cannot
travel across a continent, and there is also no trade in maize out of
Europe.

--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'



--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'
.

Hi Marcus
You could always follow the recommendations I make in the
http://www.molecularfarming.com/safety.html section of
MolecularFarming.com.
DNA marking with GFP or firefly luciferase, Terminator gene technology,
Chloroplast engineering - or simply use Tobacco, Hemp and non-food plants.
A 'blanket ban' would rob the world of an edible vaccine which could
possibly save 20 million African children a year.

"Marcus Williamson" wrote in message
...

But there need to be much better plans to keep this kind of thing from
being
able to happen.

The only possible solution which will work is to forbid the growing of
pharmaceutical plants completely. Any other approach is guaranteed to
lead to contamination of the food supply, as with StarLink and
Prodigene...

regards
Marcus

writes

A Fiat shares a lot of physical characteristics with a Lamborgini.
You don't care, I say that there is some difference.
Humans share lots of genes with the mouse. We share ~99% of the genes.
However, religious and ethical believes of many people might tell
them that is not the same to eat rat, pig, human or chicken.

OK so just having a whole bunch of genes in common doesn't turn a sheep
into a pig.

Right.

Now what is the simplest solution?
If it looks like a sheep, baaas like a sheep and tastes like a sheep
it's a sheep.

If it looks like a pig, grunts like a pig and tastes like a pig it's a
pig.

Problem solved.

Religious and cultural differences aside,

Ahh, you have figured you have lost that argument then.
OK.

I think having rats
with a complete set of the human immune system running
around in the sewer systems of the world is not a good idea
either.

Even humans don;t have a complete set of human immune systems.
We are all different.

Each organism has it's niche and broadening might not be
a good idea. It might expose us to unknown pathogens.

We are always being exposed to unknown pathogens.
It's what pathogens do.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

Gordon Couger writes

If they put human genes in hogs they
it will take some doing to genetically cripple them so they can't make it in
the wild.

They already have. Organs, transplanting for the (eventual) use of.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

Oz wrote:

writes

A Fiat shares a lot of physical characteristics with a Lamborgini.
You don't care, I say that there is some difference.
Humans share lots of genes with the mouse. We share ~99% of the genes.
However, religious and ethical believes of many people might tell
them that is not the same to eat rat, pig, human or chicken.

OK so just having a whole bunch of genes in common doesn't turn a sheep
into a pig.

Right.

Now what is the simplest solution?
If it looks like a sheep, baaas like a sheep and tastes like a sheep
it's a sheep.

If a certain percentage of the population is deadly allergic to ei. peanuts
and if someone puts the allergenic genes into corn. It will still be corn,
but now how can the allergic people tell? It looks like corn, it might
taste like corn, but now they can die from it.

http://www.aboutpeanuts.com/win98pg5.htm
Profile of Peanut Allergy
With Increased Exposure Comes Increased Risk

If you are religious and you don't eat human meat and somebody puts all the
human genes that encode for the human inmune system into a cow or pig
(Ok, Ok, put just those genes that make human's immune system different
from the pig's or cow's).
You will still be eating cow or pig, but are they? Now the pig has been
exposed and has had similar reactions to the pathogens that we humans are
susceptible to. Hepatitis anybody? I mean, that is why religion has some
taboos about consuming some foods or preparing them in certain ways, isn't it?
(ok some religious traditions are bogus, but there is a basis for it)


If it looks like a pig, grunts like a pig and tastes like a pig it's a
pig.


I have friends that grunt like a pig and live like a pig. But no thanks.


Problem solved.

Religious and cultural differences aside,

Ahh, you have figured you have lost that argument then.
OK.

No, I put those arguments aside because those are
absolute. You can not argue with someone telling them
that they do not believe in their religious beliefs!


I think having rats
with a complete set of the human immune system running
around in the sewer systems of the world is not a good idea
either.

Even humans don;t have a complete set of human immune systems.
We are all different.


Humans, as a specie, have immune systems different from the pig's.
You are probably talking about alleles of the major histocompatibility
complex (MHC) -our immune system genes.
Bubonic plage affects humans not fish. AIDS affect humans not
fish or even chimps.
Yes, yes there are some pathogens that affect ei. many mammals,
we are different but we share some similitudes with our own
species and with others.
read the sowewhat related article below.


Each organism has it's niche and broadening might not be
a good idea. It might expose us to unknown pathogens.

We are always being exposed to unknown pathogens.
It's what pathogens do.


pathogens interact with their hosts.



--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

*
THE ENEMY WITHIN New Scientist 9 Aug 2000

Trapped among your own genes are those of ancient viral invaders that plagued
our ancestors. Could these fossil viruses be to blame when our immune
system turns traitor? Bryant Furlow investigates

IT'S DARK. As you drift off to sleep, a noise outside yanks you back
into the wakeful world. Instantly alert, your heart pounds against
your ribs. A moment later you hear a snarling bark and a crash as
the intruders beat a hasty retreat. Panic over-good old Fido has seen
them off. But imagine that instead of settling back to sleep, your loyal
watchdog comes bounding into your bedroom, teeth bared, eyes flashing,
and starts attacking you. How do you feel as your flesh is ripped apart?
Now you can begin to understand the shock felt by someone who has been
told that their own immune system-their body's molecular watchdog-has
turned traitor. Autoimmune diseases, including multiple sclerosis, lupus
and rheumatoid arthritis, claim millions of new victims each year. Their
methods vary, but all involve an overzealous immune system attacking the
very body it was designed to defend. Cell by cell, they slowly disable
and ultimately kill many of their victims. Despite decades of research,
few theories have emerged to explain why natural selection would tolerate
such a critical design flaw.
Now a few biologists are starting to point the finger at alien invaders
that have been trapped inside our cells for millions of years. And if
they are right, practices such as gene therapy and xenotransplantation
may be riskier than anyone thought. Researchers agree that the key to
the puzzle of autoimmunity must lie in the major histocompatibility
complex (MHC) -our immune system genes. The MHC is an unusually diverse
region of the genome, which probably reflects our intense and ongoing
co-evolutionary arms race with countless disease organisms. Each MHC
gene in a population can have dozens of versions-or alleles-although
only a couple of these will be present in any given individual. Over
200 MHC genes are packed tightly together in our genome and their job
is to produce proteins that detect and destroy invaders. But some MHC
alleles or haplotypescombinations of alleles-have a major drawback:
people who carry them are more likely to get an autoimmune disease.
For example, nearly every victim of Hirata's disease-in which the body
attacks its insulin-producing cells-carries the MHC allele known as
DR4wl3. Twothirds of those who suffer from rheumatoid arthritis possess
another risky allele called DQBI. The haplotypes dubbed DQ and DR also
confer an increased risk of rheumatoid arthritis and type I diabetes.
And researchers have identified dozens more of these associations.
But strangely, not everybody who carries a risky allele or haplotype
becomes ill. So the simplistic notion that these risky alleles lead
inexorably to autoimmune disease has been abandoned in favour of more
sophisticated explanations.

The widely accepted view is that a risky allele must be switched on
before it turns traitor. The trigger is thought to be bits of foreign
proteins, from food or infectious invaders, that resemble the body's
own proteins. MHC alleles that respond to such "molecular mimics" will
then be primed to attack the body's own proteins as well. Such alleles
could persist through evolutionary time if they help fight off
infectious diseases in early life and do not trigger autoimmune reactions
until middle or late life. So people who carry them are more likely to
survive long enough to reproduce and pass along their double-edged
immunological inheritance. Although this theory doesn't explain
susceptibility to diseases that kick in during childhood, such as
type I diabetes, many find it appealing. Not so Graham Boyd, emeritus
professor of medicine at the University of Tasmania in Hobart. He
doesn't attribute autoimmune diseases to molecular mimics at all.
Instead, Boyd and a growing number of like-minded theorists point
to what at first glance may seem an unlikely culprit: ancient viruses
stuck in the human genome, known as endogenous retroviruses or ERVS.
Outlandish as it sounds, we are the genetic descendants of viruses
as well as primates. The viral ancestors of ERVs invaded the cells
of our forebears during infections millions of years ago and liked
it so much they decided to stay.
Happily integrated into their new home, ERVs have become part of
our own genome, passed down through the generations. In fact,
virologists have spotted ERVs in the genome of every mammal they
have checked. Repeated invasions over more than 30 million years
have left a surprisingly large viral legacy. "Up to 1 per cent of
the human genome is represented by human ERVs and their fragments,"
says Eugene Sverdlov, a geneticist at the Russian Academy of
Sciences, Moscow.

ERVs are relatively simple creatures, genetically speaking. Like
wild retrovir-uses-which include HIV-they have a few genes
codingfor enzymes and structural proteins. These are sandwiched
between long terminal repeat sequences (LTRs), which act like
on-off switches regulating the production of viral genes. They
are called retroviruses because their genes are encoded in RNA
rather than DNA and they infiltrate the host genome by creating
DNA copies of themselves. Infected cells may then be tricked into
duplicating the viral genes as though they were merely instructions
for one of the body's own cellular proteins (see Diagram, p 40).
Sverdlov calls ERVs "the perpetually mobile footprints of ancient
infections". Many of the resident aliens' genes have been broken
up by mutations, but at least:: a few are still intact and able
to make viral proteins. ERVs also have a nasty habit of hopping
around the genome, duplicating as they go. And either behaviour-
jumping or producing viral proteins could explain why certain
MHC alleles are linked to autoimmune disease.
One way ERVs might trigger autoimmune disease is by causing
regulatory problems in the MHC genes, suggests Klaus Badenhoop
from the University of Frankfurt, Germany. Although nobody knows
exactly why, ERVs appear to have a particular affinity for the
MHC region. By some estimates, they are 10 times as common in
the MHC as elsewhere in our genome. When an ERV's regulatory
instructions (its LTR) land near a host regulatory sequence,
the viral on-off switch can be mistaken for the host's own genetic
gadgetry, with disastrous results. The ERV can enhance or modify
the expression of adjacent genes, says Badenhoop. Together with
Ralf Tvnjes from the Paul Ehrlich Institute in Langen, Germany,
and others, Badenhoop is investigating whether risky MHC alleles
might wreak their havoc because they mistake the ERV instructions
for their own, and so are accidentally switched on. If this is
so, you would expect to find more LTRs near risky alleles than
normal MHC alleles. And this is exactly what Badenhoop and
Christian Seidl of the University of Frankfurt discovered when
they looked at the region around the haplotypes DQ and DR that
confer a high risk of type I diabetes and rheumatoid arthritis.
Badenhoop sees promise in the idea that ERVs contribute to
autoimmune disease by causing confusion within the immune system,
but is reluctant to draw firm conclusions yet. "There is sufficient
evidence to regard ERV long terminal repeats in the MHC as genetic
markers for autoimmune disease," he says. But "their function-how
and where they contribute to pathogenesis-still needs to be
elucidated". Boyd also believes that ERVs could play a role in
autoimmune disease.
But instead of seeing people with autoimmune diseases as hapless
victims, he prefers a more co-evolutionary explanation, which he
has dubbed "balanced dynamic polymorphism". Boyd sees viruses and
the hosts they live in as opposing teams in a dynamic co-evolutionary
arms race. Like exotic species settling in new ecosystems-rats on
an island, for example-ERVs can be disruptive when they first
arrive. But like the rats' descendants, the viral lineages tend
eventually to become better adapted to their surroundings. Once
an ERV is integrated into another genome, its survival is hitched
to that of its host. So the longer the association, the more
likely it is that evolution will have quelled an ERV's more
unneighbourly instincts. Boyd likens it to long-running tribal
warfare. "As the years went by," he says, "there would be a sort
of truce whereby the survivors from both sides would generally
agree that all aggression should be curbed." This truce even goes
so far as allowing ERVs to play a major role in our evolution,
by doing away with the need to lay eggs (New Scientist, 12 June
1999, p 26). And recent studies reveal cases where viral genes
have been co-opted by hosts to serve useful functions-ironically,
often helping to fight disease. One such, called P-5, is involved
in producing immune lymph cells. It has "a possible role in
immunity to retrovirus infection", says Jerzy Kulski from the
University of Westem Australia in Nedlands, who made the discovery
with his colleague Roger Dawkins. Such domestication events may
explain why Badenhoop's team found that while many risky genes
are associated with viral LTRs, at least one such haplotype lacks
them. In this case, the viral on-off switches are found near
normal versions of a gene, suggesting that they may provide
some protection against autoimmune disease. ERVs can also help
defend hosts against wild viruses in other ways, according to
Roswitha Lbwer, a geneticist from the Paul Ehrlich Institute
in Langen, Germany. Chickens and mice are protected from infection
by endogenous proteins that stop viruses sticking to host cells,
Lbwer says. And in mice, ERVs interfere with the replication of
wild viruses inside host cells. Normally, then, ERVs pose little
threat to their hosts. But Boyd believes the truce is an uneasy
one. "There would always be renegade rogues on both sides," he
says. Although most ERVs do not normally produce the viral proteins
that provoke attack from the host immune system, many retain the
genetic code for such particles. This unwillingness to disarm,
Boyd believes, may set the stage for autoimmune disease. ERVs
that retain their protein-producing potential are more like
tenuously tamed wolves than loyal puppy dogs. Every once in a
while these ERVs awake from their civilised slumber and begin
pumping out viral proteins. So what makes domesticated ERVs
turn feral? Lower speculates that UV light and bacteria are
possible alarm clocks that wake ERVS. Boyd believes that the
key is repeated damage to cells, either from infection by wild
viruses or from severe psychological stress.
The effects of such stress can affect the sympathetic nerves
controlling arterial blood supply. If the nerves are shut down,
the temporary loss of blood supply can cause cellular damage,
which might contribute to ERV activation, according to Boyd.
Either way, once ERVs start producing molecules that look like
antigens from wild viruses, MHC genes may kick in to fight off
the perceived invasion. The result is an immune attack against
your own cells. The question then is why natural selection hasn't
eliminated those MHC alleles prone to mistake ERV products for
infections. Boyd argues that hosts are in an evolutionary bind,
a Darwinian catch-22. So long as wild relatives of ERVs exist
in nature and pose a threat, there will be a survival advantage
in possessing MHC alleles that can fight them off-even though
individuals carrying such alleles are susceptible to autoimmune
disease. His ideas fit in with today's knowledge of autoimmune
susceptibility alleles and ERVs. He believes that the conflicting
selection pressures for maintaining and eliminating risky MHC
alleles-those that mistake ERV proteins for foreign invaders-result
in some, but not all, individuals possessing dangerous alleles.
If he is right, geneticists will find geographic pattems in the
distribution of risky alleles that reflect varying disease risks.
For the moment, the jury is still out on whether ERVs are an
accessory to autoimmune disease. if they are, the implications
for medicine are wide-ranging. Lower is particularly concemed
about gene therapy and cross-species organ transplantation.
The retroviruses used as vehicles in gene therapy might activate
a patient's ERVSAnd the promise of plentiful supplies of organs
from pigs and baboons for use in xenotransplantation may be
dangerous for similar reasons. The ERVs in pigs and primates,
Lbwer points out, are close relatives of ours. "There is a
risk of uncontrolled human ERV amplifications," she says.
Lbwer's concems seem well founded. Earlier this year, a team
of her colleagues led by Frank Czauderna reported that some
pig ERVs do indeed code for viable viruses. Worse still, the(se
viruses can replicate in human tissues, at least under lab
conditions. Czauderna worries that pig and human ERVs could
hybridise, yielding infectious viruses with new and unfamiliar
properties. But he is hopeful that it will be possible to use
genetic engineering techniques to knock out pig ERVs and create
a cloned lineage of donor animals for xenotransplantations.
And there is a more positive side to all this: it could lead
to ways of fighting off diseases that now seem to strike at
random. If ERVs are activated by repeated stress, as Boyd
suspects, then identifying and avoiding such stress could
one day eliminate the immunological betrayals that lead to
disease. "Autoimmune dis ease is not inevitable," says
Boyd.1-1

wrote in message
...

I have friends that grunt like a pig and live like a pig. But no thanks.


LOL........I think you should find new friends ;-)

M

wrote in message
...
Spain does not export oil to America. Today it's coasts are covered
with oil.
Who would have thought!
I know about shuch things as continents but corn travels in ships.


and how well does maize survive immersion in salt water?

think a little


--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'

writes


Oz wrote:

writes

If a certain percentage of the population is deadly allergic to ei. peanuts
and if someone puts the allergenic genes into corn. It will still be corn,
but now how can the allergic people tell? It looks like corn, it might
taste like corn, but now they can die from it.

See the US regs on this.

If you are religious and you don't eat human meat and somebody puts all the
human genes that encode for the human inmune system into a cow or pig
(Ok, Ok, put just those genes that make human's immune system different
from the pig's or cow's).
You will still be eating cow or pig, but are they? Now the pig has been
exposed and has had similar reactions to the pathogens that we humans are
susceptible to. Hepatitis anybody? I mean, that is why religion has some
taboos about consuming some foods or preparing them in certain ways, isn't it?
(ok some religious traditions are bogus, but there is a basis for it)

No.

If it looks like a pig, grunts like a pig and tastes like a pig it's a
pig.

I have friends that grunt like a pig and live like a pig. But no thanks.

They are still human because they don't look like a pig.
I am not responsible for your friends.

Problem solved.

Religious and cultural differences aside,

Ahh, you have figured you have lost that argument then.
OK.

No, I put those arguments aside because those are
absolute. You can not argue with someone telling them
that they do not believe in their religious beliefs!

You haven't offered any theological argument.

I think having rats
with a complete set of the human immune system running
around in the sewer systems of the world is not a good idea
either.

Even humans don;t have a complete set of human immune systems.
We are all different.


Humans, as a specie, have immune systems different from the pig's.
You are probably talking about alleles of the major histocompatibility
complex (MHC) -our immune system genes.
Bubonic plage affects humans not fish. AIDS affect humans not
fish or even chimps.
Yes, yes there are some pathogens that affect ei. many mammals,
we are different but we share some similitudes with our own
species and with others.

There you go. However pigs with human immune systems are under
development for organ transplants. I would presume in the UK (as in the
UK) this is tightly controlled.

Each organism has it's niche and broadening might not be
a good idea. It might expose us to unknown pathogens.

We are always being exposed to unknown pathogens.
It's what pathogens do.


pathogens interact with their hosts.

Indeed, so?

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

wrote in message
...
A Fiat shares a lot of physical characteristics with a Lamborgini.
You don't care, I say that there is some difference.
Humans share lots of genes with the mouse. We share ~99% of the genes.
However, religious and ethical believes of many people might tell
them that is not the same to eat rat, pig, human or chicken.


ethics are not necessarily rational, and often have no relationship to
the real world.
--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'

Jim Webster wrote:

wrote in message
...
A Fiat shares a lot of physical characteristics with a Lamborgini.
You don't care, I say that there is some difference.
Humans share lots of genes with the mouse. We share ~99% of the genes.
However, religious and ethical believes of many people might tell
them that is not the same to eat rat, pig, human or chicken.

ethics are not necessarily rational, and often have no relationship to
the real world.

In the real world people eat human meat?
Enron, Global Crossing, et al are a rational way to make business?
Child abuse by priests is the way to go in the real world?

I think one thing is people not behaving ethically, another is to make
unethical behavior the accepted norm.


--
Jim Webster

"The pasture of stupidity is unwholesome to mankind"

'Abd-ar-Rahman b. Muhammad b. Khaldun al-Hadrami'

Oz wrote:
...
There you go. However pigs with human immune systems are under
development for organ transplants. I would presume in the UK (as in the
UK) this is tightly controlled.


jajajaja. very funny!
You did not learn anything from the mad cow diseas fiasco didn't you?

Jim Webster wrote:

wrote in message
...
Spain does not export oil to America. Today it's coasts are covered
with oil.
Who would have thought!
I know about shuch things as continents but corn travels in ships.


and how well does maize survive immersion in salt water?

think a little


The original point was that corn can travel over oceans with no problem,
does so regularly. Pollen viability is a small problem compared to
whole shipments of grain from USA to Africa or USA to SouthAmerica.
(Mexican germplasm of maize has already been contaminated with GMO's,
and it was not a cloud of pollen but a shipment of USA 'AID'.
Other sources of germplasm contamination include regular exchanges
between plant breeding programs around the world.
Accidents happen. They happen regularly. GMO's containing
pharmaceutical have been mixed with grain destined for human consumption.
This was reported because of luck. Other accidents have probably not
been reported. Other large scale experiments with humans like those of
mad cow disease in England where denied for years until people started
to suspect something wrong. Before people just died from an unknown disease.
Some of you where arguing that the problem of GMO's are a question of doing
good control and regulation. Well, tell that to the spaniards and their
oiled coasts or tell that to the English and their mad cows, pigs and sheep.
Some problems are much cheaper and easier to fix at the source, not down the
line. That is a basic science and engineering principle.
Now, go ahead take your own advise. Think a little.

writes


Oz wrote:
...
There you go. However pigs with human immune systems are under
development for organ transplants. I would presume in the UK (as in the
UK) this is tightly controlled.


jajajaja. very funny!
You did not learn anything from the mad cow diseas fiasco didn't you?

The world learned more from things like growth hormone and plasma
transmissions of human CJD. It's inconceivable that this will not be
checked for. However if you have a choice aged 70, of dying in six
months or getting a pig heart transplant and dying in 30 years from a
TE, I know which I would choose.

I trust you would choose death in six months.

But I'll bet you wouldn;t.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.

Oz wrote:

writes


Oz wrote:
...
There you go. However pigs with human immune systems are under
development for organ transplants. I would presume in the UK (as in the
UK) this is tightly controlled.


jajajaja. very funny!
You did not learn anything from the mad cow diseas fiasco didn't you?

The world learned more from things like growth hormone and plasma
transmissions of human CJD. It's inconceivable that this will not be
checked for. However if you have a choice aged 70, of dying in six
months or getting a pig heart transplant and dying in 30 years from a
TE, I know which I would choose.

I trust you would choose death in six months.


If there is the strong posibility that the pig organ might carry viruses
that are going to jump the species barrier and infect the human race, and
in exchange I can get a few months of the worse quality of life, what do
you think I can do for my kids? Don't forget, we all die. Learn to live
with that!


But I'll bet you wouldn;t.

--
Oz
This post is worth absolutely nothing and is probably fallacious.
Note: soon (maybe already) only posts via despammed.com will be accepted.