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It is clear to me that TEATE (Reiki) which is energy that is part of the law of

sevens in some way (angles-angels) must play some role in reversing dark
intention to manipulate genes, dna, blood, bone and all physical things.

Genetic Makeup of Aggression & Bipolar Disorder

Mice have long been used for studying human diseases, behavior, and our
biology due to the fact that they have a surprisingly similar genetic makeup
to us. Scientists have gone even farther now by studying the ability to
change one's behavior due to genetic manipulation.

In 2002, researchers at the University of British Columbia's Centre for
Molecular Medicine and Therapeutics accidentally made a form of highly
aggressive mice.

The scientists unintentionally deleted a gene that influences their brain

The absence of this gene led to the mice becoming vicious towards their
caretakers as well as the other mice that they were with. Some even killed
their mates, others chewed on their siblings' tails.

Now scientists attempted to give the mice their "niceness" back by giving
them the gene that they were missing, except this time, from humans.
Researchers gave the aggressive mice's embryos the "human version" of the
gene that was currently absent from their makeup. Abraham (2005) stated,
"Simpson said that gene, called NR2E1, is found on a region of
chromosome 6 in humans and has been associated with bipolar disorder, a
serious mental illness resulting in dramatic mood swings.

The gene produces molecules that regulate other genes, suggesting it plays
multiple roles in the human body, including those involved in brain
development and function. That a similar version exists in the mouse
suggests the gene is a primitive one, passed down to mice and people from a
common ancestor many millennia ago." ( SHEREE: or passed down some
other way)
Once the human version of the gene was implanted into the
embryos they became normal and lost their aggressive
This study shows that behavior can be manipulated by the absence or
presence of particular genes.
The use of human genes being added to the mice (which led them to become
"nicer") exemplifies the potential that the absence or presence of that gene
in humans could lead to similar affects. This could lead to our discovery of
how to alter aggressive behavior in humans and potentially alter the
disorders that lead to aggression, supposing that gene NR2E1 or another
gene is involved. But the possibility of changing human behavior by
manipulating one's genetic makeup is as scary as it is promising.

The source of this article was The Canadian Press & Globe and,
written by Carolyn Abraham.

You can access the full article from Globe and Mail at: http://tinyurl.
The Globe and Mail homepage is at: http://www.theglobe
Posted by at July 9, 2005 12:52 PM

N R 2 E 1
14 18 2 5 1 = 22 h 40 v 62 hv

reverse is 04 + 22 = 26

26 + 62 = 88
N R2 E1 = 22 H
GENE = 22 H
In 2002, researchers at the University of British Columbia's Centre for
Molecular Medicine and Therapeutics accidentally made a form of highly
aggressive mice.
Chubby Blonde? Slim and Dark? Lab Mice Take After Mom's Diet

Sharon Begley
Science Journal
Wall Street Journal

The baby mice looked as different as night and day.

Those in one litter were dirty blondes, while those in the other were, well,
mousy brown. Yet the mice's genes for coat color were identical, down to
the last A, T, C and G that make up the twisting strands of DNA.

The reason some animals were yellow and some were brown lay deep in
their fetal past, biologists at Duke University Medical Center, Durham,
N.C., reported this month: Some of the mothers consumed supplements high
in very simple molecular compounds that zip around the genome turning off
genes. One silenced gene was for yellow fur; when it is turned off, the
mouse's fur color defaults to brown.

For the mice, it wasn't just that "you are what you eat," but that you are what
your mother ate, too.

The ink on the final draft of the complete human genome sequence is hardly
dry, but scientists are seeing more and more instances in which the sequence
of those celebrated A's, T's, C's and G's constituting the genome is only part
of the story.

Biologists have long known that having a particular gene is no guarantee
you will express the associated trait, any more than having a collection of
CDs will fill your home with music. Like CDs, genes are silent unless they
are activated. Because activating and silencing doesn't alter the sequence of
the gene, such changes are called epigenetic.

"Epigenetics is to genetics as the dark matter in the universe is to the stars;
we know it's important, but it's difficult to see," says geneticist Andrew
Feinberg of Johns Hopkins University School of Medicine, Baltimore.
"What we're thinking now is that, in addition to genetic variation, there may
be epigenetic variation that is very important in human disease."

Epigenetic variation may explain such long-running mysteries as why
identical twins are, in many ways, no such thing, including whether they
have such supposedly genetic diseases as schizophrenia and cancer.

Epigenetics may also help explain how the seeds of many adult diseases
may be planted during fetal life. ( OR BEFORE? ) Studies suggest that the
nutrition a fetus receives -- as indicated by birth weight -- might influence
the risk of adult-onset diabetes, heart disease, hypertension and some
cancers. The basis for such "fetal programming" has been largely an enigma,
but epigenetics may be key.

There is no doubt that, in the case of the brown or yellow mice, the "you are
what your mom ate" phenomenon reflects just such epigenetic influences.

The Duke scientists fed female mice dietary supplements of vitamin B12,
folic acid, betaine and choline just before and throughout their pregnancy.
Offspring of mice eating a regular diet had yellowish fur; pups of the
supplemented mothers, although genetically identical to the yellow mice,
were brown.

When they grew up, the brown mice also had much lower rates of obesity,
diabetes and cancer, Robert Waterland and Randy Jirtle of Duke's
Department of Radiation Oncology report in the journal Molecular and
Cellular Biology. Whatever the extra nutrients did to the fetal mice's genes
didn't stop with fur color.

Actually, that "whatever" isn't quite fair. The Duke team knows exactly what
the supplements did. All of the compounds contain a simple molecule called
a methyl group, which is one carbon and three hydrogen atoms. For a little
guy, methyl wields a big stick: It can turn genes off.

That's what happened in the brown mice. Methyl from the supplements
switched off a gene called Agouti, which both gives a mouse a yellowish
coat and makes it obese. The yellowish babies weren't suffering from any
nutritional deficiency; it's just that their Agouti gene was still activated.

"Nutritional supplementation to the mother can permanently alter gene
expression in her offspring without mutating the genes themselves at all,"
says Prof. Jirtle.

That's the very essence of epigenetics.

The reason the Agouti gene was silenced is that it had the misfortune to lie
next to an interloper. Mammalian genomes are riddled with bits of DNA that
leap around like so many jumping beans. Called transposons, they
sometimes wind up beside the on/off switch for an important gene, and are
sitting ducks for those gene-silencing methyl groups.

In the offspring of mouse moms eating methyl-rich dietary supplements, just
such a jumping gene was silenced, with the result that the Agouti gene it had
snuggled up to was also struck dumb.

This isn't just about yellow and brown mice. "About 40% of the human
genome is transposons, " notes Prof. Jirtle.

That means an awful lot of human genes could be targets of methylation,
and so silenced. Whether that is good or bad depends on what the gene does.
Silencing a gene that raises the risk of schizophrenia would be welcome.
Silencing a tumor-suppressor gene wouldn't be.

What's clear, he adds, is that "we, too, have genes -- including those
influencing susceptibility to cancer, obesity and diabetes -- that can be
turned off or on by epigenetic factors triggered by early nutrition and
exposure to chemical agents."

here's my questions:
what about CHEMTRAILS?
what about the chemicals in our water, milk, toothpaste, etc.

FOUND AT : http://www.biotech- moms_diet. html
** NOTICE: In accordance with Title 17 U.S.C. Section 107, this material
is distributed for research and educational purposes only. **

Turn On Gene, Turn Off Cancer?

P53 Gene May Thwart Cancers, Lab Tests Suggest By Miranda Hitti

WebMD Health News Reviewed by Louise Chang, MD

May 9, 2007 -- Cancer may have met its match in the p53 gene, reports a
Spanish cancer expert.

The p53 gene normally springs into action in DNA-damaged cells. It can
prompt those cells to die, stopping cancer before it starts.

The p53 gene can also stop DNA-damaged cells from dividing. That
process, called senescence, prevents a cancer from growing.

But if the p53 gene isn't working right, DNA-damaged cells may keep on
growing, paving the way for cancer to take root.

Manuel Serrano, PhD, works in Madrid at the Spanish National Cancer
Research Center.

He reviewed three recent studies on the p53 gene. The studies were done by
three teams of scientists who studied mice, not people.

The studies included mice with liver cancer, lymphoma (cancer of the lymph
system), and sarcoma (cancer of areas that include muscle, fat, and bone).
The mice were born with the p53 gene turned off.

In their labs, the scientists stimulated the p53 gene, turning the gene on. In
two of the three studies, the mice's cancers faded when the p53 gene was
turned on.

"The results were spectacular: in some cases, near-complete regression was
achieved just two days after p53 activation. In other cases, regression took
longer (about 10 days)," Serrano writes.

In the third study, p53 gene activation delayed -- but didn't completely
repress -- the progression of an aggressive lymphoma in the mice, according
to Serrano.
In the studies, activating the p53 gene didn't appear to harm the mice's
healthy cells.

http://www.webmd. com/cancer/ news/20070509/ turn-on-gene- turn-off-

http://www.dnaftb. org/dnaftb/33/concept/

Behind the Scenes of Gene Expression
Elizabeth Pennisi

As the units of DNA that define the proteins needed for life, genes have
played biology's center stage for decades. But work over the past few years
shows that gene expression is not determined solely by the DNA code itself
but by an assortment of proteins and, sometimes, RNAs that tell the genes
when and where to turn on or off.

Such epigenetic phenomena orchestrate the many changes through which a
single fertilized egg cell turns into a complex organism. And throughout
life, they enable cells to respond to environmental signals conveyed by
hormones, growth factors, and other regulatory molecules without having to
alter the DNA itself.

Scientists Create Human Male-Female Hybrid

AgapePress ^ | 7/11/03 | Bill Fancher and Jody Brown
Posted on Friday, July 11, 2003 8:01:27 AM by truthandlife

Private researchers experimenting on human embryos have developed a
being that is part male and part female.

A Chicago researcher, Dr. Norbert Gleicher of the Foundation for
Reproductive Medicine, has announced the creation of "she-males," the
result of injecting male cells into a female embryo. MSNBC reports that the
work "provoked repulsion" when presented at a meeting of the European
Society of Human Reproduction and Embryology in Madrid.

Dr. Nancy Jones, a pathologist at Wake Forest University in North Carolina
and a member of the Christian Medical and Dental Associations, was
shocked at Gleicher's announcement -- but says she expects such
experiments will continue until federal regulations are enacted prohibiting

"They injected male cells -- probably a stem cell line -- into the embryo and
then asked where these cells went. Similar experiments have been done on
animals in developmental models," Jones says.

Researchers tracked the male cells for six days before destroying the human
embryo. Jones, who serves on Wake Forest's standing committee for ethics
in research, says U.S. law forbids such experiments when federal funds are
involved. However, no restrictions apply for private facilities conducting
this kind of research.

"There are no guidelines available for the privately-funded facilities -- it's
just whoever they are beholden to, if they have some sort of ethics
committee. To me it clearly shows that we need more comprehensive
regulation on what is and isn't ethical research on the human embryo," Jones

http://www.freerepu focus/f-news/ 944217/posts

Re: Who was the first? Male or Female?

Creationist nonsense aside, the actual default sex for humans in female. It is
the presence of the Y chromosome that causes the differences in the sex
organs to develop. In has been shown in cases where people are born with
abnormal sex chromosomes. The variations are Klinefelter Syndrome (XXY,
XXYY, XXXY, XXXXY, XY/XXY are all variants of Klinefelter) and
Turner Syndrome (where the subject only has one X chromosome, or only
one functioning X chromosome). People affected by Klinefelter Syndrome
are always male (Y chromosome is present), but the testicles do not develop
at the onset of puberty and injections of testosterone are necessary for
normal physical development. The most common shared characteristics of
this are sterility, breast development, incomplete masculine development,
and learning disorders. People with Turner Syndrome are female (no Y
chromosome present), but their sex organs are also similarly undeveloped.
Common shared characteristics are infertility, short (average height ~4'7"),
ear/eye/heart/ thyroid/kidney problems, and occasionally webbed fingers
and lowset hairlines and ears.

Not so much which came first in original sexual development, but in the
immediate development we all experience in the womb. A bit of an answer
to the "chicken or egg" question. The genders developed at about the same
time, but female is the default.

http://science. php?thread= 30610&did=multLife%