EPSTEIN
page 1 / 279 . OCR, unverified
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From:
Larry Visoski
Sent:
Tuesday, February
AM
To:
jeffrey E.
Subject:
Re:
Jeffrey
Real flight plan, with today's winds.
8+52min (-42kt headwind)
<=div>
Mach .80
Thx
Larry
jeevacation@gmail.com> wrote:
<=div>
Real flight time Paris lsj..?
<=r>
please note
The information contained in this communication is
confidential, m=y be attorney-client privileged, may
constitute inside information, and i= intended only for
the use of the addressee. It is the property of
JE=
Unauthorized use, disclosure or copying of this
communication or any=part thereof is strictly prohibited
and may be unlawful. If you have rec=ived this
communication in error, please notify us immediately by
ret=rn e-mail or by e-mail to jeevacation@gmailcom <mailto:jeevacation@gmail.com> , and
destroy this communication and al= copies thereof,
including all attachments. copyright -all rights reserv=d
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From:
Boris Nikolic <
Sent:
Sunday, Novem er ,
:
To:
Jeffrey Epstein
Subject:
RE: you were right!!!
LOVE how it starts
"Memo to mature, health-minded vampires: You might want to consider limit=ng your treats to victims under age 30."
Jee was right al along!!!!=!!!!!!!
&nbs=;
=p class=MsoNormal>From: Jeffrey Epstein [mailto:jeevacation@gmail.com]
Sent: Saturday, November 05, 2011 9:59 PM
To: Boris Nikol=c
Subject: Re: you were right!!!
http://med.stanford.edu/ism/2011/august/aging-brain.html <http://med.stanford.edu/ism/2011/august/aging-
brain.h=ml>
On Sun, Nov 6, 2011 at 3:01 AM, Boris Nikoli=
wrote:
Being around old — even if these are your ow= cells can't be good for you!
It is a breakthrough...
<=pan style='color:#1F497D'>
<http://n=ws.sciencemag.oresciencenowk
Cellular Spring Cleaning Slows Aging=o:p>
by Sarah C.P. Williams on 2 November 2011, 2:04 PM I <=:p>
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<http://news.sci=ncemag.org/sciencenow/assets_c/2011/11/sn-aging-thumb-800xauto-11418.jpg>
Stay=ng young. The mouse on the left has aged normally and shows a curved s=ine and loss of muscle mass. The mouse
on the right was treated with drugs=that remove senescent cells from its body, keeping it more youthful.<=o:p>
Credit: Van Deursen Lab
The accumulati=n of old, stagnant cells in the body is to blame for some age-related dise=ses, a new study has found.
When researchers removed such cells from mice,=they were able to delay the onset of cataracts and slow age-related
muscle=loss.
"This i= really a technical tour de force," says geneticist Norman Sharpless =f the University of North Carolina School of
Medicine in Chapel Hill, who =as not involved in the study. "And then they went beyond this technic=l feat and made
findings that are really important to understanding the basic science of aging."
Most cells in the b=dy can't continue dividing forever. After a cell has duplicated itself a n=mber of times—around SO is
the average—a genetic switch turns =ff the division program. A cell that's no longer dividing is known as sene=cent; it
continues to live but no longer functions as it once did. While m=st senescent cells continue to behave as whatever cell
type they started a=, they also begin to secrete immune proteins that scientists hypothesize c=uld cause age-related
changes in the surrounding tissues. In elderly human=, at least VA of the total cells in the body are thought to be
senescent. =he cells accumulate in places particularly affected by aging—the eye= and muscles, for example.
"It has been hypothe=ized, since these cells are found at sites of age-related pathologies, tha= they are related to the
development of these pathologies," says biol=gist Jan van Deursen of the Mayo Clinic in Rochester, Minnesota, lead
auth=r of the new paper. But the connection hasn't been fully fleshed out, he s=ys.
Van Deursen and colleagues developed a way to kil= senescent cells in mice, clearing them from the body. They
engineered mic= so that when cells flipped on a gene called p161nk4a, a=marker for senescence, the cell would also turn
on the production of inact=ve cellular death genes, not normally produced by senescent cells. Then, w=en the
researchers gave the mice a drug, the death pathway would be activa=ed in all senescent cells. "Our met=od allowed us
to look at the consequences of removing senescent cells at d=fferent stages of the mouse life cycle," van Deursen says.
"We d=dn't just block senescence altogether."
F=rst, the researchers cleared senescent cells from the mice throughout thei= lives—giving the drug every 3 days
beginning as soon as the animals=were weaned. Although the mice did not have an increased life span, the on=et of