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Archive for April, 2012

Mick Farren steals my idea for an article

[I’d been sketching out a piece about how Dan Brown should share some
of his dough w/RAW, using passages from _The Widow’s Son_ in an
exegetical style that falls somewhere between Eco and my own
narcissism, and under heady infl. of Lawrence Lessig. But now why
bother? – rmjon23]


The ‘Da Vinci’ Plagiarism
Where does ownership of an idea really begin?


 "Art is either plagiarism or revolution."
-Paul Gauguin

"What’s talent but the ability to get away with something?"
-Tennessee Williams

A lawsuit currently being decided by Justice Peter Smith in the British
High Court in London puts much of our most cherished nonsense in
jeopardy. Michael Baigent and Richard Leigh, two of the three authors
of the 1982 book Holy Blood, Holy Grail, are suing Random House, the
publisher of Dan Brown’s 2003 best-seller The Da Vinci Code
(ironically, also their book’s publisher), claiming that what had
been referred to in court as the architecture and central theme of the
novel were stolen in part from their earlier, supposedly nonfiction
work. Millions of dollars in royalties hang in the balance, and a
potential movie blockbuster is on temporary hold. But, on a deeper and
more profound level, the question has been raised. In a world where
sports announcer Michael Buffer can trademark the phrase "let’s get
ready to rumble!" and Paris Hilton considers ownership of "that’s
hot," can individuals lay sole claim to whole segments of
contemporary pop folklore simply because they have written a book about

As most reading this will already know, the core of The Da Vinci Code
is a 2,000-year-old conspiracy theory that Jesus Christ had children by
Mary Magdalene, and founded a bloodline protected by secret societies
like the Knights Templar and the Priory of Sion against the patriarchy
of the Catholic church and its supposed gestapos, the Inquisition and
Opus Dei. The theory certainly wasn’t formulated by Brown, but
neither was it invented by Baigent and Leigh. It’s been a heresy for
centuries, received a massive boost from the late Victorian fascination
with alternative history, paganism, and the occult, and now looms large
in the paranoid quadrants of the Internet somewhere between crop
circles and the bar code of Satan. But, right when The Da Vinci Code
movie is being readied for release, and cash settlements would be
optimum, Baigent and Leigh have decided to lay copyright claim to the
whole deal. By that reasoning, half of contemporary conspiracy
theorizing, from JFK to Freemasonry, would be the property of Robert
Shea and Robert Anton Wilson, whose 1975 Illuminatus! trilogy was a
grand compendium of every paranoid fantasy of those highly paranoid

Even the honest author’s every work and every outlandish theory is
based on all that went before, and most of us draw the line by
instinct. While it would be both criminal and patently absurd to steal
(say) the James Bond character and canon and pass it off as your own
invention, it would be equally insane for Ian Fleming’s estate to
maintain that it owned the entire secret-agent genre. I learned all
this while writing four neo-goth vampire novels over the last few
years. Our modern pop-myth vampire was created from Eastern European
folklore as Dracula by Bram Stoker in the 1890s. It was refined and
expanded by the Universal monster movies of the 1940s, Hammer horror
films of the 1950s and 1960s, Anne Rice and countless others, all the
way to Joss Whedon and Buffy the Vampire Slayer, with some heavy
cross-cultural borrowing from Freud and H.P. Lovecraft.

Stoker’s widow did sue film director F.W. Murnau over the movie
Nosferatu in 1922, but, since then, it’s been a matter of having the
artistic integrity to bring something more to the collective folklore
than you take out.

With their litigious greed, Baigent and Leigh have risked replacing
creative ethics and previous good sense with yet another snarling
lawyer-frenzy over "intellectual property," in which the attorneys
get fat and art, to put it indelicately, yet again gets the shaft.


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the great work

work is great. what a marvelous thing work is. find a labor of love.
Next monday I have to solve a problem with the general ledger. that’s
what they are paying me for. Find the missing 20k. Well, it’s probably
somewhere. anyway

I ordered Angel Tech and it’s en route. It should be a great read. I
have read P.R. and I wish I still had a copy. I can buy one.. but it
doesn’t teach me how to make money, it only teaches one how to use
one’s brain and open one’s mind, much like the Rich Dad books. It
teaches one how to expand one’s Context- aka Reality Tunnel, sound

I already know what the so called "philosopher’s stone" is that turns
lead into gold. It is none other than the human brain, which creates
our perceptions and emotions. So yes, well, I know what it is, but that
doesn’t mean I have won, just yet. I know it’s the brain that turns
lead into gold (liability into asset) but that doesn’t mean I know
exactly specifically how at this moment and point in time, what my
first deal will be. I still maybe have some path to walk.

I have fallen in love with the questions, and not even the answers. the
answers are just the realizations, and the realizations are good, but
there will always be more questions, as you strive to that great goal.
I have fallen in love with planning, because a plan is a brige over a
river to a dream. A plan requires people, requires paper work, requires

I am using my philosopher’s stone for personal advantage and gain. But
also to serve others. when you know what the philosopher’s stone is,
you can use it any way you see fit. Once you know a secret or a truth
you can do as you will with it. If you weren’t qualified to receive or
have it, you would not have gotten it.

That’s all, but I also want to say that I hate the concept of the
weekend. Who defines time, who makes the calandar. I know in minnesota
people go into differnet modes based on the calandar and time. I feel
different when I know weekend is coming, or just when my shift ends at
4:30, but I try not to make myself too happy, because that is a bad
pattern. You need work that you enjoy FULL TIME. I don’t change my
neurons just because I am on the job. Earn mode and spend mode, is most
people. Ahh well. I spend as fast as I can, on good expenses and
investments, as often as I can find them, and gain leverage.

may the word become flesh and reality become fresh.

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i love freedom – panera

I love it’s the age and era of "authorization" and who has it. I go
online at panera bread and try to go to
http://www.hermetic.com/crowley/ and they say

The SonicWALL Content Filter Has Blocked this site.
If you feel this site has been blocked in error,
Please submit a URL Rating Review at:

URL: http://www.hermetic.com/crowley/

Reason for restriction: Forbidden Category "Cult/Occult"

I also did the same at www.nomarriage.com another time.

they are very restrictive, anal retentive. I don’t know. it’s their
culture, that’s ok. I have never been to a panera and had their
wireless down or not working, and I’ve been at other coffeeshops where
it was down sometimes, so that is a good thing, an advantage. also, I
don’t really have a sense of entitlement.. it is just funny, they try
decide, they make a rule. Actually it’s the software algorithm,
probably, but they decide what that software decision matrix is. words.
those sites don’t even have any "bad" pictures. just "bad" words.
hahaa. I’ll tell you

It’s not even what I believe. It’s the ability to read that which
expands your empire of the mind. It’s the thought policy. Also with
dealerships and deals, my car, everything seems thenardieran. whatever.
the journey’s longer than it seems.

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RMJon23 steals my idea for posting

Speaking of plagiarism RMJon23 steals my idea for posting "The ‘Da
Vinci’ Plagiarism" article on this group. Arguments are as follows
(Sorry for the E-prime!):

a) I read the article in the paper (Los Angeles City Beat) before
she/he posted it on the group.

b) The fact that he/she posted it twice (2 times) proves that she/he
wanted to make sure he/she nails me and beats me in this artistic race.

c) Since I live in LA (And HE or SHE does not!) I fall closer to Los
Angeles City Beat epicenter which allows me more intellectual property

d) In closing and in general, people who live in a different city and
quote articles published in OUR city exercise the act of pure

If this begins to sound like nonsense, that is inevitable on this level
(rings the bell?).

"If we steal thoughts from the moderns, it will be cried down as
plagiarism; if from the ancients, it will be cried up as erudition." –
Charles Caleb Colton

"The more absurd life is, the more insupportable death is." – Jean Paul

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SMI2LE: Unlocking The Secrets Of Longevity Genes


Scientific American
February 20, 2006

Unlocking the Secrets of Longevity Genes

A handful of genes that control the body’s defenses during hard times
can also dramatically improve health and prolong life in diverse
organisms. Understanding how they work may reveal the keys to extending
human life span while banishing diseases of old age

By David A. Sinclair and Lenny Guarente

You can assume quite a bit about the state of a used car just from its
mileage and model year. The wear and tear of heavy driving and the
passage of time will have taken an inevitable toll. The same appears to
be true of aging in people, but the analogy is flawed because of a
crucial difference between inanimate machines and living creatures:
deterioration is not inexorable in biological systems, which can
respond to their environments and use their own energy to defend and
repair themselves.
At one time, scientists believed aging to be not just deterioration but
an active continuation of an organism’s genetically programmed
development. Once an individual achieved maturity, "aging genes" began
to direct its progress toward the grave. This idea has been
discredited, and conventional wisdom now holds that aging really is
just wearing out over time because the body’s normal maintenance and
repair mechanisms simply wane. Evolutionary natural selection, the
logic goes, has no reason to keep them working once an organism has
passed its reproductive age.

Yet we and other researchers have found that a family of genes involved
in an organism’s ability to withstand a stressful environment, such as
excessive heat or scarcity of food or water, have the power to keep its
natural defense and repair activities going strong regardless of age.
By optimizing the body’s functioning for survival, these genes maximize
the individual’s chances of getting through the crisis. And if they
remain activated long enough, they can also dramatically enhance the
organism’s health and extend its life span. In essence, they represent
the opposite of aging genes–longevity genes.

We began investigating this idea nearly 15 years ago by imagining that
evolution would have favored a universal regulatory system to
coordinate this well-known response to environmental stress. If we
could identify the gene or genes that serve as its master controllers
and thereby act as master regulators of an organism’s life span, these
natural defense mechanisms might be turned into weapons against the
diseases and decline that are now apparently synonymous with human

Many recently discovered genes, known by such cryptic names as daf-2,
pit-1, amp-1, clk-1 and p66Shc, have been found to affect stress
resistance and life span in laboratory organisms, suggesting that they
could be part of a fundamental mechanism for surviving adversity. But
our own two laboratories have focused on a gene called SIR2, variants
of which are present in all organisms studied so far, from yeast to
humans. Extra copies of the gene increase longevity in creatures as
diverse as yeast, roundworms and fruit flies, and we are working to
determine whether it does the same for larger animals, such as mice.

As one of the first longevity genes to have been identified, SIR2 is
the best characterized, so we will focus here on its workings. They
illustrate how a genetically regulated survival mechanism can extend
life and improve health, and growing evidence suggests that SIR2 may be
the key regulator of that mechanism.

Silence Is Golden
We first discovered that SIR2 is a longevity gene by asking what causes
individual baker’s yeast cells to grow old and whether a single gene
might control aging in this simple organism. The notion that an
understanding of yeast life span would tell us anything about human
aging was deemed preposterous by many. Aging in yeast is measured by
counting how many times mother cells divide to produce daughters before
dying. A typical yeast cell’s life span is about 20 divisions.

One of us (Guarente) began by screening yeast colonies for unusually
long-lived cells in the hope of finding genes responsible for their
longevity. This screen yielded a single mutation in a gene called SIR4,
which encodes part of a complex of proteins containing the Sir2 enzyme.
The mutation in SIR4 caused the Sir2 protein to gather at the most
highly repetitive region of the yeast genome, a stretch containing the
genes that encode the protein factories of the cell, known as ribosomal
DNA (rDNA). More than 100 of these rDNA repeats exist in the average
yeast cell’s genome, and they are difficult to maintain in a stable
state. Repetitive sequences are prone to "recombining" with one
another, a process that in humans can lead to numerous illnesses, such
as cancer and Huntington’s disease. Our yeast findings suggested that
aging in mother cells was caused by some form of rDNA instability that
was mitigated by the Sir proteins.

In fact, we found a surprising kind of rDNA instability. After dividing
several times, yeast mother cells spin off extra copies of the rDNA as
circular rings that pop out of the genome. These extrachromosomal rDNA
circles (ERCs) are copied along with the mother cell’s chromosomes
prior to cell division but remain in the mother cell’s nucleus
afterward. Thus, a mother cell accumulates an ever increasing number of
circles that eventually spell her doom, possibly because copying the
ERCs consumes so many resources that she can no longer manage to
replicate her own genome.

When an extra copy of the SIR2 gene was added to the yeast cell,
however, formation of the rDNA circles was repressed and the cell’s
life span was extended by 30 percent. That finding explained how sir2
could act as a longevity gene in yeast, but amazingly, we soon
discovered that extra copies of the sir2 gene also extended the life
span of roundworms by as much as 50 percent. We were surprised not only
by this commonality in organisms separated by a vast evolutionary
distance but by the fact that the adult worm body contains only
nondividing cells–thus, the replicative aging mechanism in yeast could
not apply to worms. We wanted to know exactly what the SIR2 gene does.

As we soon discovered, the gene encodes an enzyme with a completely
novel activity. Cellular DNA is wrapped around a complex of packaging
proteins called histones. These bear chemical tags, such as acetyl
groups, that determine how snugly the histones package DNA. Removing
acetyl groups from histones tightens the packaging further and renders
the DNA inaccessible to the enzymes responsible for popping the rDNA
circles out of the chromosome. This deacetylated form of DNA is said to
be silent because any genes in these regions of the genome are rendered
inaccessible to being activated.

Sir proteins were already known to be involved in gene
silencing–indeed, SIR stands for silent information regulator. Sir2 is
one of several enzymes that remove acetyl tags from the histones, but
we discovered that it is unique in that its enzymatic activity
absolutely requires a ubiquitous small molecule called NAD, which has
long been known as a conduit of many metabolic reactions in cells. This
association between Sir2 and NAD was exciting because it linked Sir2
activity to metabolism and thus potentially to the relation between
diet and aging observed in calorie restriction.

The Calorie Connection
Restricting an animal’s calorie intake is the most famous intervention
known to extend life span. Discovered more than 70 years ago, it is
still the only one absolutely proven to work. The restricted regime
typically involves reducing an individual’s food consumption by 30 to
40 percent compared with what is considered normal for its species.
Animals ranging from rats and mice to dogs and possibly primates that
remain on this diet not only live longer but are far healthier during
their prolonged lives. Most diseases, including cancer, diabetes and
even neurodegenerative illnesses, are forestalled. The organism seems
to be supercharged for survival. The only apparent trade-off in some
creatures is a loss of fertility.

Understanding the mechanisms by which calorie restriction works and
developing medicines that reproduce its health benefits have been
tantalizing goals for decades [see "The Serious Search for an Antiaging
Pill," by Mark A. Lane, Donald K. Ingram and George S. Roth; Scientific
American: The Science of Staying Young, 2004]. The phenomenon was long
attributed to a simple slowing down of metabolism–cells’ production of
energy from fuel molecules–and therefore reduction of its toxic
by-products in response to less food.

But this view now appears to be incorrect. Calorie restriction does not
slow metabolism in mammals, and in yeast and worms, metabolism is both
sped up and altered by the diet. We believe, therefore, that calorie
restriction is a biological stressor like natural food scarcity that
induces a defensive response to boost the organism’s chances of
survival. In mammals, its effects include changes in cellular defenses,
repair, energy production and activation of programmed cell death known
as apoptosis. We were eager to know what part Sir2 might play in such
changes, so we looked first at its role during calorie restriction in
simple organisms.

In yeast, we have found that restricting food availability affects two
pathways that increase Sir2 enzymatic activity in the cells. On one
hand, calorie restriction turns on a gene called PNC1, which produces
an enzyme that rids cells of nicotinamide, a small molecule similar to
vitamin B3 that normally represses Sir2. Consistent with the idea that
calorie restriction is a stressor that activates a survival response,
PNC1 is also stimulated by other mild stressors known to extend yeast
life span, such as increased temperature or excessive amounts of salt.

A second pathway induced in yeast by restricted calories is
respiration, a mode of energy production that creates NAD as a
by-product while lowering levels of its counterpart, NADH. It turns out
that not only does NAD activate Sir2, but NADH is an inhibitor of the
enzyme, so altering the cell’s NAD/NADH ratio profoundly influences
Sir2 activity.

Having seen how life-extending biological stress increases Sir2
activity, the question became, Is Sir2 necessary to produce the
longevity? The answer appears to be a resounding "yes." One way to test
whether Sir2 is essential to this process is to remove its gene and
determine whether the effect remains. In organisms as complex as fruit
flies, calorie restriction does require SIR2 to extend life span. And
because the body of an adult fruit fly contains numerous tissues that
are analogous to mammalian organs, we suspect that calorie restriction
in mammals is also likely to require SIR2.

Yet if humans are ever to reap the health benefits of calorie
restriction, radical dieting is not a reasonable option. Drugs that can
modulate the activity of Sir2 and its siblings (collectively referred
to as Sirtuins) in a similar manner will be needed. Just such a
Sirtuin-activating compound, or STAC, called resveratrol has proven
particularly interesting. Resveratrol is a small molecule present in
red wine and manufactured by a variety of plants when they are
stressed. At least 18 other compounds produced by plants in response to
stress have also been found to modulate Sirtuins, suggest?-ing that the
plants may use such mole?-cules to control their own Sir2 enzymes.

Feeding resveratrol to yeast, worms or flies or placing them on a
calorie-restricted diet extends their life spans about 30 percent, but
only if they possess the SIR2 gene. Moreover, a fly that overproduces
Sir2 has an increased life span that cannot be further extended by
resveratrol or calorie restriction. The simplest interpretation is that
calorie restriction and resveratrol each prolong the lives of fruit
flies by activating Sir2.

Resveratrol-fed flies not only live longer, despite eating as much as
they want, but they do not suffer from the reduced fertility often
caused by calorie restriction. This is welcome news for those of us
hoping to treat human diseases with molecules that target Sir2 enzymes.
But first we want a better understanding of the role of Sir2 in

Leader of the Band
The mammalian version of the yeast SIR2 gene is known as SIRT1 ("SIR2
homolog 1"). It encodes a protein, Sirt1, that has the same enzymatic
activity as Sir2 but that also deacetylates a wider variety of proteins
both inside the cell nucleus and out in the cellular cytoplasm. Several
of these proteins targeted by Sirt1 have been identified and are known
to control critical processes, including apoptosis, cell defenses and
metabolism. The potential longevity-enhancing role of the SIR2 gene
family seems, therefore, to be preserved in mammals. But not
surprisingly in larger and more complex organisms, the pathways by
which Sirtuins achieve their effect have grown considerably more
complicated as well.

Increased Sirt1 in mice and rats, for example, allows some of the
animals’ cells to survive in the face of stress that would normally
trigger their programmed suicide. Sirt1 does this by regulating the
activity of several other key cellular proteins, such as p53, FoxO and
Ku70, that are involved either in setting a threshold for apoptosis or
in prompting cell repair. Sirt1 thus enhances cellular repair
mechanisms while buying time for them to work.

Over the course of a lifetime, cell loss from apoptosis may be an
important factor in aging, particularly in nonrenewable tissues such as
the heart and brain, and slowing cell death may be one way Sirtuins
promote health and longevity. A striking example of Sirt1′s ability to
foster survival in mammalian cells can be seen in the Wallerian mutant
strain of mouse. In these mice, a single gene is duplicated, and the
mutation renders their neurons highly resistant to stress, which
protects them against stroke, chemotherapy-induced toxicity and
neurodegenerative diseases.

In 2004 Jeffrey D. Milbrandt of Washington University in St. Louis and
his colleagues showed that the Wallerian gene mutation in these mice
increases the activity of an enzyme that makes NAD, and the additional
NAD appears to protect the neurons by activating Sirt1. Moreover,
Milbrandt’s group found that STACs such as resveratrol conferred a
protective effect on the neurons of normal mice similar to the
Wallerian mutation.

In a more recent study by Christian N鲩 of the French National
Institute of Health and Medical Research, resveratrol and another STAC,
fisetin, were shown to prevent nerve cells from dying in two different
animal models (worm and mouse) of human Huntington’s disease. In both
cases, the protection by STACs required Sirtuin gene activity.

The protective effect of Sirtuins in individual cells is becoming
increasingly clear. But if these genes are the mediators of calorie
restriction’s benefits, an unsolved puzzle remains how diet can
regulate their activities and thus the rate of aging in an entire
animal. Recent research by Pere Puigserver of the Johns Hopkins
University School of Medicine and his colleagues has shown that NAD
levels rise in liver cells under fasting conditions, prompting
increased Sirt1 activity. Among the proteins Sirt1 acts on is an
important regulator of gene transcription called PGC-1, which then
causes changes in the cell’s glucose metabolism. Thus, Sirt1 was found
to act both as a sensor of nutrient availability and a regulator of the
liver’s response.

Similar data have given rise to the idea that Sirt1 is a central
metabolic regulator in liver, muscle and fat cells because it senses
dietary variations via changes in the NAD/NADH ratio within cells and
then exerts far-reaching effects on the pattern of gene transcription
in those tissues. This model would explain how Sirt1 may integrate many
of the genes and pathways that affect longevity described on page 54.

More than one mechanism may mediate Sirt1′s bodywide activities,
however. Another appealing hypothesis is that mammals register their
food availability by the amount of energy they have stored in the form
of body fat. Fat cells secrete hormones that convey signals to the
other tissues in the body, but their message depends on the levels of
fat stored. By reducing fat stores, calorie restriction may establish a
pattern of hormone signals that communicates "scarcity," which
activates cell defenses. Consistent with this idea is the fact that
mice genetically engineered to be extra lean regardless of their food
intake tend to live longer.

This possibility led us to wonder whether Sirt1, in turn, also
regulates fat storage in response to diet. Indeed, Sirt1 activity is
increased in fat cells after food limitation, causing fat stores to
move from the cells into the bloodstream for conversion to energy in
other tissues. We surmise that Sirt1 senses the diet, then dictates the
level of fat storage and thus the pattern of hormones produced by fat
cells. This effect on fat and the signals it sends would, in turn, set
the pace of aging in the entire organism and make Sirt1 a key regulator
of the longevity conferred by calorie restriction in mammals. It would
also closely link aging and metabolic diseases, including type 2
diabetes, associated with excess fat. Intervening pharmacologically in
the Sirt1 pathway in fat cells might therefore forestall not only aging
but also specific ailments.

Another critical process modified by Sirt1 is inflammation, which is
involved in a number of disorders, including cancer, arthritis, asthma,
heart disease and neurodegeneration. Recent work by Martin W. Mayo and
his colleagues at the University of Virginia has shown that Sirt1
inhibits NF-B, a protein complex that promotes the inflammatory
response. The Sirt1-activating compound resveratrol has the same
effect. This finding is particularly encouraging, both because the
search for molecules that inhibit NF-B is a highly active area of drug
development and because another well-known effect of calorie
restriction is its ability to suppress excessive inflammation.

If SIR2 is thus the master controller of a regulatory system for aging
that is activated by stress, it may function by acting as the conductor
of an orchestra of players that includes hormonal networks,
intracellular regulatory proteins and other genes associated with
longevity. One of the more notable discoveries in recent years was that
Sirt1 regulates production of insulin and insulinlike growth factor 1
(IGF-1) and that those two powerful signaling molecules, in turn, seem
to regulate Sirt1 production as part of a complex feedback loop. The
relation between Sirt1, IGF-1 and insulin is intriguing because it
explains how Sirt1 activity in one tissue might be communicated to
other cells in the body. Moreover, circulating levels of insulin and
IGF-1 are known to dictate life span in various organisms–worms,
flies, mice, possibly ourselves.

>From Defense to Advance

Because people have sought to slow aging for tens of thousands of years
without success, some may find it hard to accept that human aging might
be controlled by tweaking a handful of genes. Yet we know it is
possible to forestall aging in mammals with a simple dietary change:
calorie restriction works. And we have shown that Sirtuin genes control
many of the same molecular pathways as calorie restriction. Without
actually knowing the precise, and potentially myriad, causes of aging,
we have already demonstrated in a variety of life-forms that it can be
delayed by manipulating a few regulators and letting them take care of
the organisms’ health.

We also know that the SIR2 family of genes evolved far back in time
because today they are found in organisms ranging from baker’s yeast,
Leishmania parasites and roundworms to flies and humans. In all these
organisms but the last, which has not yet been tested, Sirtuins dictate
length of life. This fact alone convinces us that human Sirtuin genes
probably hold the key to our health and longevity as well.

Both our labs are running carefully controlled mouse experiments that
should soon tell us whether the SIRT1 gene controls health and life
span in a mammal. We will not know definitively how Sirtuin genes
affect human longevity for decades. Those who are hoping to pop a pill
and live to 130 may have therefore been born a bit too early.
Nevertheless, those of us already alive could live to see medications
that modulate the activity of Sirtuin enzymes employed to treat
specific conditions such as Alzheimer’s, cancer, diabetes and heart
disease. In fact, several such drugs have begun clinical trials for
treatment of diabetes, herpes and neurodegenerative diseases.

And in the longer term, we expect that unlocking the secrets of
longevity genes will allow society to go beyond treating illnesses
associated with aging and prevent them from arising in the first place.
It may seem hard to imagine what life will be like when people are able
to feel youthful and live relatively free of today’s diseases well into
their 90s. Some may wonder whether tinkering with human life span is
even a good idea. But at the beginning of the 20th century, life
expectancy at birth was around 45 years. It has risen to about 75
thanks to the advent of antibiotics and public health measures that
allow people to survive or avoid infectious diseases. Society adapted
to that dramatic change in average longevity, and few people would want
to return to life without those advances. No doubt, future generations
accustomed to living past 100 will also look back at our current
approaches to improving health as primitive relics of a bygone era.

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Stanislaw Lem dies

Author of ‘Solaris’ Dies at 84
By RYAN LUCAS, Associated Press Writer
Mon Mar 27, 4:26 PM ET

Stanislaw Lem, a science fiction writer whose novel "Solaris" was made
into a movie starring George Clooney, died Monday in his native Poland,
his secretary said. He was 84.

Lem died in a Krakow hospital from heart failure "connected to his old
age," Wojciech Zemek told The Associated Press. He gave no other

Lem was one of the most popular science fiction authors of recent
decades to write in a language other than English, and his works were
translated from Polish into more than 40 other languages. His books
have sold 27 million copies.

"A great artist has died, a man with the hallmarks of a genius,"
renowned Polish film director Andrzej Wajda told the country’s PAP news

His best-known work, "Solaris," was adapted into films by director
Andrei Tarkovsky in 1972 and by Steven Soderbergh in 2002. That version
starred George Clooney and Natascha McElhone.

Set on a spaceship above a fictional planet, a psychologist meets the
likeness of a long-dead lover as he and the crew grapple with
suppressed memories of lost loves.

Lem’s first important novel, "Hospital of the Transfiguration," was
censored by communist authorities for eight years before its release in
1956 amid a thaw following the death of Soviet dictator Josef Stalin.

Other works include "The Invincible," "The Cyberiad," "His Master’s
Voice," "The Star Diaries," "The Futurological Congress" and "Tales of
Prix the Pilot."

"He was an amazingly talented man, and Polish literature never had
anyone like him before," said Tomasz Fialkowski, co-author of a book of
interviews with Lem and the deputy editor of the weekly Tygodnik

While Lem was widely known as a writer of science fiction, his works
were never simple tales of spaceships and light sabers.

Instead, he wrote about new scientific discoveries and the evolution of
man and technology, Fialkowski said. Lem also foresaw many new
technologies, including virtual reality, Fialkowski said.

While his novels often took place in space in the undetermined future,
Lem "connected it all with his interest in what is going on in the here
and now, with politics," Fialkowski said.

Lem was born into a Polish Jewish family on Sept. 21, 1921, in Lviv,
then a Polish city but now part of Ukraine.

His father was a doctor and he initially appeared set to follow in that
path, taking up medical studies in Lviv before World War II.

After surviving the Nazi occupation, in part thanks to forged documents
that concealed his Jewish background, Lem continued his medical studies
in Krakow. Soon afterward, however, he took up writing science fiction.

Lem addressed his multiple talents with a touch of modesty and humor.

"If I was a child prodigy, it could only have been in the eyes of
doting aunts," Lem once said. "In my fourth year, I learned to write,
but had nothing of great importance to communicate by that means."

Lem is survived by his wife and a son, Zemek said. Funeral arrangements
were not disclosed.

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Chinese and Croatia acquire Complete Collection

The Chinese and the Croatians have acquired the Complete Collection of
a very rare American occult resource.

This Resource is available for a limited time on E-Bay but there are
less than five days left…

This is a very exclusive offer of one of those collections you just
don’t hear aout being around.

Check it out…



Chris Titan

P.S. There is some info by T Allen Greenfield in his re-relase of his
classic "Cypher of the UFOnauts" that can help deepen the mystery here

One has to wonder it there cyphers are not being worked on by foriegn
governements who are less hampered by christianity, judaism, or
Islam…mostly former communist governments who are fresh to these
ideas and not saturated in dogma. Not to offened anyone…just trying
to make a tough point.

It might be high time we start funding "weird science" again to keep up
with what were once called "Psychic Discoveries Behind the Iron
Curtain." Now these countries are our hard fought friends but we must
keep abreast to what they may discover from our own ignored past.

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It's Howdy Dubai Time!

Say, kids, what time is it?
It’s Howdy Dubai Time!

It’s Howdy Dubai Time,
It’s Howdy Dubai Time.

John Snow and Bushie too
Say Howdy Do to you.
Let’s give a rousing cheer,
Cause Howdy Dubai’s here,
It’s time to start the show,
So kids let’s go!

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rawilsonfans.com has new look


LQQKS hot, bandito…


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Why not polytheism and perhaps more architecture of pleasure instead of architecture of guilt?

I wonder if many people, as a believers, had to ebmrace any kind of a
religion WHY it had to be the monotheistic one (!) ?  Why leave the
heaven just to one god? I wonder if more democracy in heaven would
allow more democracy on earth?

Monotheism seems to be deeply ingrained in the psychology of most
people, far too prone to take the monotheistic side for granted. This
seems to contributes to a great deal of the cultural anxiety we

Why not many gods, when Greek mythology offers the most complete
catalogue of images produced: forming the tragedy; the source of poetry
and literature; building the foundation of philosophy. etc. Had we
embraced all the Gods AND the Goddesses, and created more democratic
religion, would we be more democratic today? Would we be more flexible?
Would we be more hedonistic? Less anxiety? More pleasure? Less guilt?

One can almost say that monotheism can be equated with guilt. In all
its variations, many cultures can be very guilt-ridden cultures. Where
guilt was fundamentally alien to the Greek spirit.

James Joyce seems to be a great example of a life lived under the
pressure of cultural anxiety. Ulysses, the tour-de-force of Western
literature: the hero, the modern Ulysses, is, paradoxically, a Jew
married to an Irish Catholic woman. The guilt-ridden Jesuitical
Catholicism and the different kinds of paganisms – the Mediterranean
and the author’s own Irish Celtic. Great work revealing the
fragmentation and the madness of the cultural anxiety in the soul of a
genius. With reference to Bloom, W.B. Stanford wrote: "Originally a
Jew, then vaguely Protestant and Catholic in turn, Bloom is now an
agnostic humanist."

"Some see things as they are and say "Why?" Others dream things that
never were and say "Why not?"
– G.B.Shaw

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