EFTA Document EFTA01802986

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:[email protected]] 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> EFTA_R1_00146143 EFTA01802986 <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 cataracts was delayed by about 100 days, the treated mice had twice =s wide muscle fibers, and their spine curvature and fat deposits resembled=those of youthful mice. Next, the researchers gave the drug to older mice =hat already showed signs of aging, such as muscle loss. After S months, th= treated mice showed better improvement in treadmill tests than untreated =ice. Their muscle and fat cells did not show s=gns of aging <http://www.nature.com/nature/journalkaop/ncurrent/full/na=ure10600.html> , although the treatment didn't reverse aging that had alr=ady happened, the team reports online today in Nature.</=> "I think the results are quite striking," Sharpless says= But he cautions that further research is needed to understand the effects=of removing senescent cells. Although they may promote some age-related di=orders, they could prevent others. "Whether there are any unintended =esults of this has to be studied further," he says. "Yes, we mig=t make cataracts better, but will it come with the risk of cancer or infec=ions?" Since the work relied on genetically engineered mice, it's not directly translatable into humans, van Deursen says. =span style='background:yellow'>Researchers, however, can now screen drug= to find compounds that might activate cell death in senescent cells, he s=ys, or that might turn the immune system against senescent cells. <=:p> 2 EFTA_R1_00146144 EFTA01802987 The information con=ained in this communication is confidential, may be attorney-client pri=ileged, may constitute inside information, and is intended only for =he use of the addressee. It is the property of Jeffrey Epstein Unau=horized use, disclosure or copying of this communication or any part th=reof is strictly prohibited and may be unlawful. If you have received t=is communication in error, please notify us immediately by return e-=ail or by e-mail to [email protected] <mailto:[email protected]> , and destroy this communication and all c=pies thereof, including all attachments. copyright -all rights reserved=o:p> 3 EFTA_R1_00146145 EFTA01802988