Brooklyn Man Convicted of Black Market Organ Sales

Rosenbaum.jpgIn what is the first conviction under the U.S. federal statute outlawing black-market organ sales, a Brooklyn man named Levy Izhak Rosenbaum pleaded guilty Thursday to brokering three illegal kidney transplants for at least $120,000 each (a huge markup) and conspiring to arrange yet another sale. He boasted on tape that he actually handled “quite a lot” during the decade-long scheme.

At 60 years of age, Rosenbaum is but one of 46 people arrested in 2009 in a massive federal corruption probe dubbed “Operation Big Rig” that ensnared dozens of officials, politicians, community and religious leaders involved in organ sales, money laundering, and political corruption over an investigative period of 10 years.

From January 2006 to February 2009, Rosenbaum conspired to obtain kidneys from paid donors in exchange for payments of $120,000, $150,000 and $140,000 from three recipients of the organs.

“Rosenbaum admitted he was not new to the human kidney business when he was caught brokering what he thought was a black-market deal,” U.S. Attorney Paul Fishman said in a release.

“A black market in human organs is not only a grave threat to public health, it reserves lifesaving treatment for those who can best afford it at the expense of those who cannot [...] We will not tolerate such an affront to human dignity.”

Rosenbaum faces up to 20 years in prison when he’s sentenced February 2. He agreed to forfeit $420,000 he received in connection with the three transplants and admitted that he invented cover stories and fictitious relationships between donors and recipients so doctors wouldn’t know a kidney was being sold.

His black market involvement was exposed with the help of Solomon Dwek, a cooperating criminal defendant who helped prosecutors develop charges against defendants in the “Operation Big Rig” case. Posed as an employee of Dwek and claiming that her uncle needed a transplant, an undercover agent met with Rosenbaum in mid-February 2008. He told them that it was illegal to buy and sell organs but that he had been “doing this a long time” and explained that he would help the recipient and donor concoct a false story to support the appearance of a legitimate donation, Fishman said. Rosenbaum also claimed he would be in charge of “babysitting” the donor after the person arrived from overseas.

“I am what you call a matchmaker,” he told the snitch. “I’ve never had a failure.”

During Thursday’s plea, Rosenbaum admitted that he typically located Israelis who were willing to be paid for giving up their kidneys and that he was responsible for travel arrangements for the donor to the United States along with their accomodations pre- and post-operation. He arranged for blood samples and helped each paid donor and recipient fabricate stories to fool hospital staff. His lawyers noted that the surgeries took place in “prestigious American hospitals and were performed by experienced and expert” surgeons. He remains free on bail and under house arrest pending sentencing scheduled for February 2, 2012.

Methuselah Foundation’s New Organ Prize not only serves to catalyze progress in tissue and organ regeneration but it also aims to make the crimes of the black market a thing of the past. In a future where an individual in need of an organ can have one made with their own cells, the market for organs exploited from the disadvantaged and weak will eventually shrink and disappear altogether.

We at Methuselah Foundation echo the words of Attorney Fishman: “We will not tolerate such an affront to human dignity.”


Golson, Jennifer. “Brooklyn Man Who Sold Kidneys on Black Market Pleads Guilty.” Thomson Reuter News and Insight. Thomson Reuters, 28 Oct. 2011. Web. 28 Oct. 2011.

Photo Credit: Tony Kurdzuk | The Star-Ledger

Aging Does Not Necessarily Mean A Weakening Immune System


When you think about old age, what comes to mind? Most people associate old age with disability and cognitive and physical impairment but researchers from the University of Pittsburgh and Children’s Hospital of Pittsburgh of UPMC have found that old age is not synonymous with impairment and disability. According to the study published by the Public Library of Science in the online journal PLoS ONE, exceptional cognitive and physical function in old age leaves behind a tell-tale immunologic fingerprint.

“Our study indicates that getting older does not necessarily mean that the immune system gets weaker, as many of us assumed,” says lead investigator Abbe N. de Vallejo, Ph.D., associate professor of pediatrics and immunology at University of Pittsburgh School of Medicine. “The immune system is dynamic, and the changes it undergoes over time very much influence function.”

Previous studies showed that immune cells called T-cells become more like natural killer (NK) cells, which typically targets virus-infected cell and tumor cells. For this new study, the team collected blood samples from a body of 140 participants who had been followed in the Cardiovascular Health Study for nearly 20 years and were 78-94 years old. Only two were younger than 82–the average age of the group was 86. The researchers gathered information about the participants’ health and function, medical history, hospitalizations, self-rated health, and cognitive and physical function assessments via standardized tests.

A closer look at the new study revealed that those who were most physically and cognitively resilient had a dominant pattern of stimulatory NK receptors on the surface of the T-cell. These unusual T-cells can be activated directly through these NK receptors in a manner independent of the conventional ones. The functionally resilient elders also have a distinct profile of blood proteins called cytokines that reflect an immune-enhancing environment.

The group that showed mild health impairment had a dominant pattern of inhibitory NK receptors on their T-cells, with a cytokine profile indicating a pro-inflammatory environment. Both of these immunologic features might suggest greater susceptibility to illness.

“These findings indicate that there is remodeling or adaptation of the immune system as we age that can be either protective or detrimental,” Dr. de Vallejo said. “Now we have an immunological fingerprint that can identify individuals who are more likely to stay physically and cognitively well.”


“Exceptional Cognitive and Physical Health in Old Age Leaves Immunologic Fingerprint, Study Finds.” Science Daily. Science Daily, 21 Oct. 2011. Web. 25 Oct. 2011.

Abbe N. Vallejo, David L. Hamel, Robert G. Mueller, Diane G. Ives, Joshua J. Michel, Robert M. Boudreau, Anne B. Newman. NK-Like T Cells and Plasma Cytokines, but Not Anti-Viral Serology, Define Immune Fingerprints of Resilience and Mild Disability in Exceptional Aging. PLoS ONE, 2011; 6 (10): e26558 DOI: 10.1371/journal.pone.0026558

Sonia Arrison’s Illuminating New Book 100 Plus Sheds Light on Healthy Life Extension


“We are at the cusp of a revolution in medicine and biotechnology that will radically increase not just our life spans but also, and more importantly, our health spans. That is, we will live longer and with a higher quality of life. [We] will examine the fascinating new technologies that will allow doctors to repair or replace worn-out body parts, re-engineer our bodies, and take preventative measures that will radically lengthen our lives.” -Sonia Arrison, 100+ Chapter 2: How Science and Technology Will Increase Life Span

sonia-arrison-headshot-med.jpgWith her new book 100 Plus, Sonia Arrison introduces us to the people and the innovations that are transforming our lives while bringing to the fore a very comprehensive picture of how life-extending discoveries will impact our personal, social, and economic spheres. After a decade of research and writing experience on the breakthrough advances in science and biotechnology, Arrison’s wide-angle approach to healthy life extension is both sparklingly informative and thought-provoking.

What will your life look like after reaching your 100th year? Will over-population be a major issue? How will living longer and with more vigor affect your family life, your personal belief system, even your finances? Her work is a fantastic attempt in addressing these questions.

Peter Thiel graces 100 Plus with the following words in his foreward:
“Arrison’s book begins with a history of the many great men and women of the past who sought human longevity. She surveys he current generation of scientists and technologists who promise to usher in a new era, demonstrating that aging is a foe that can be hobbled and potentially even beaten. From here Arrison goes to the heart of things by directly confronting opposition to longer and healthier lives and outlining the extraordinary economic, social, and cultural changes that will happen as the world wakes up from history…”

The Methuselah Foundation team is voraciously reading 100 Plus with growing excitement for Arrison’s well-informed candor and refreshing perspective on the advances of healthy life extension technologies that cover a wide range of angles.

And as if you needed more reason to go read this book as soon as you can get your hands on it, CEO Dave Gobel had this to say about it from his Amazon review:

“The best thing about 100+ is that it documents the increases in healthy longevity that are already happening right now. Refreshingly, it treats widely held cultural and religious values with legitimate respect, without resorting to the typical elitist/dismissive tone others have taken. 100+ carefully covers new ground on topics that I’ve not seen covered in detail before – such as how longevity will affect the future of childbearing and the family – based on little known trends and science happening right now. This book is also the best survey of the field of life extension to date, giving useful and actionable insights on such topics as population growth, the environment, economics, medical trials and advances in biotech without burdening the reader with red-herring issues like immortality or demonizing the “opposition”. The book is an easy and compelling read and even though I’ve read extensively on the subject, each page of 100+ offers up new facts with real value – no filler or arm waving here! Highly recommended.”

Now how’s that for a review? Pick it up, read it, think about it, and tell us how it’s affected the way you think about living to see a healthy 100… and beyond!


Arrison, Sonia. 100 Plus. New York: Basic, 2011. Print.

Future of Organ Regeneration Addressed by Anthony Atala


Credit: Teresa Kelly

Our friend and scientific advisory board member Anthony Atala of the Wake Forest University for Medicine discussed the advances of regenerative medicine in the fourth installment of The University of Rhode Island’s Honors Colloquium. The lecture began with a progress report for the new field of regenerative medicine and, reminding the audience that it was only in a few decades ago in 1954 that surgeons transplanted an organ into a human for the first time in history, it’s astonishing that as 2012 quickly approaches, medical science has progressed to allow organs such as kidneys, uteruses, bladders, urethras, and even the skin to regrow.

“Is this science fiction?” Atala asks. “Not really. We see it in biology all the time.”

bioprintingskin.jpgHe outlined the process a surgeon goes through to regenerate an organ–the easiest organs being flat, such as the skin. For the larger, tubular organs such as the kidney and liver, that happens to be a different, much more difficult ball game.

For skin regeneration, the surgeon simply extracts a bit of cells the size of less than half a postage stamp from the patient. Then, after being mixed with a solution to keep the cells alive, the cells are then sprayed back onto the patient. Should the patient be immobile, he would be scanned by a machine and his cells delivered to a bio-printer. The printer would produce a sticky sheet of gel cells to be administered to the patient to help regenerate his skin.

Nearing the end of his presentation, Atala played a short clip of an interview with former patient Luke M., whose surgery was performed 10 years ago. A new bladder was engineered for him out of his own cells. Prior to the operation, he said he was faced with a lifetime of dialysis. He could barely get out of bed, constantly missed school, and couldn’t play basketball with his friends without feeling faint.

“After surgery, I was able to do more things, like wrestle in high school,” said Luke, proudly. “I even became captain of the team. Because they used my own cells to build this bladder, I got it for life. So I’m all set.”

Atala reminded the audience how 50 years ago, the iron lung was thought to be revolutionary technology. Now, we look back on it and think “Boy, wasn’t that primitive?” The goal of medical science is to keep pushing forward and breaking boundaries, he said, so that in the next 50 years, people can look back on his technology and find it primitive as well.

“My goal tonight was to make this look easy to you,” he stated. “But I assure you, the work we do is anything but easy. We still have many challenges ahead, but the promise this field holds is to try and make our patients better.”


Delande, Kimberly. “Colloquium Speaker Addresses Future of Organ Regeneration through Technology.” The Good 5¢ Cigar. College Media Network, 5 Oct. 2011. Web. 6 Oct. 2011.

Training the Immune System to Kill Cancer

When chemotherapy proved ineffective for 65-year-old William Ludwig, a retired corrections officer from New Jersey a year ago, he signed up to be the first to receive treatment in a bold experiment at the University of Pennsylvania. By then, his life was draining away, as he put it. He thought he had nothing to lose.

The research team, led by Dr. Carl June, removed a billion of William’s T-cells (white blood cells that fight viruses and tumors) and engineered them with new genes that reprogram the cells to attack his cancer. A disabled form of H.I.V. -1, the virus that causes AIDS, was employed to transport cancer-fighting genes into the patient’s own T-cells. In essence, the team trained Ludwig’s own immune system to kill cancer cells. The process is detailed in The New England Journal of Medicine as well as in Science Translational Medicine.


There were no reactions at first but after 10 days, he shook with chills, his temperature skyrocketed while his blood pressure plummeted–William had so rapidly become ill that the doctors moved him into intensive care, warning him that he might die. Fearing the worst, his family gathered at the hospital.

Fast forward a few weeks later. No fever. No leukemia.

All traces of leukemia vanished. No leukemic cells were to be found in his blood or bone marrow; his CT scan was clean. The doctors calculate that the treatment destroyed up to two pounds of cancer cells. One year later, and William is still in complete remission. Before the treatment, there were days when he could barely get out of bed. Now he revels on the green of gulf and works on his yard.

“I have my life back,” says William.

“It’s great work,” said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients’ recoveries remarkable, exciting and significant. “I feel very positive about this new technology. Conceptually, it’s very, very big.”

Tcells.jpgThough Ludwig’s doctors do not claim that he is cured, as it is too soon to tell – the research has far to go and the treatment is still experimental and unavailable outside of clinical studies – the treatment has obviously helped Ludwig tremendously. This may be a turning point in the long struggle to develop effective gene therapies to combat cancer. And not just for leukemia–other cancers may also be vulnerable to this breakthrough approach.

Two other chronic lymphocytic leukemia patients were also treated in the experiment; one had a partial remission–his disease lessened but did not completely go away. Another, like William, experienced complete remission. All three were at an advanced stage of the disease, ran out of chemotherapy options, and were not candidates for bone-marrow transplantation.

Dr. Carl June said the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. Of course they had hoped to see some benefit of the experimentation, but had not dreamed of seeing complete, prolonged remissions in the patients. When Mr. Ludwig began running fevers, the doctors did not initially realize that it was a sign that his T-cells were furiously battling with his leukemia.

Dr. Walter J. Urba said he thinks the approach would ultimately be used against other types of cancer along with leukemia and lymphoma though he cautions that “For patients today, we’re not there yet.” And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.

WilliamLudwig.jpgBut what profound hope we have for this to be validated!

When Ludwig entered the trial, Dr. June said that he was “almost dead”. The trial was Phase 1, meaning that the main goal was to find out if the treatment was safe, and if so, at what doses. Ludwig thought that if the trial study could give him six months to a year, it would be worth it, but even if it didn’t help him personally, he felt that it would still be worth helping the study.

“I feel wonderful,” Mr. Ludwig said in an interview. “I walked 18 holes on the golf course this morning.”

William Ludwig was tremendously week before the study, suffering repeated bouts of pneumonia and wasting away. Now, he is full of energy. He has gained 40 pounds. He and his wife bought an R.V., in which they travel with their grandson and nephew.

“I feel normal, like I did 10 years before I was diagnosed,” Mr. Ludwig said. “This clinical trial saved my life.”


Grady, Denise. “An Immune System Trained to Kill Cancer.” The New York Times | Health. The New York Times Company, 12 Sept. 2011. Web. 14 Sept. 2011.

The Aging Brain and the Role of Blood

A blood-borne immune factor present in elderly mice contributes to signs of mental decline when injected into young mice. By inhibiting this blood-born immune factor, youthfulness is restored in old mice, implying that it may be possible to change some of the symptoms of aging in the brain by altering the levels of immune factors in the blood.

neurons.jpgThe hippocampus, an important sea-horse shaped component of the brain that plays a role in memory, spatial memory, and navigation, loses function and ceases to produce new neurons as it ages. Though this deterioration can be partially reversed when animals regularly exercise thereby stimulating circulation and releasing chemicals and metabolites into the blood, Tony Wyss-Coray of Stanford University School of Medicine wondered if there was a blood-borne element that might contribute to these changes.

Published in August 31, 2011 in Nature, his study implies that it may be possible to change some of the aging symptoms of the brain by altering the levels of immune factors in the blood.

By stitching the flank of a young mouse to the flank of an old one, Wyss-Coray and colleagues formed a conjoined-twin effect, allowing the blood of both mice to mingle. They found that the young animals showed a decline in neurogenesis while the old ones showed new growth as compared to young and old stitched to partners of similar age.

“There seemed to be rejuvenation in the old brain,” said Wyss-Coray.

So the researchers extracted only blood plasma devoid of the cells of old mice and injected into the young mice. They saw a similar decline in neurogenesis. It appeared as though an extracellular blood protein was responsible. These mice were then administered a battery of memory tests and mazes. The mice with old blood plasma did not form as robust memories and did not remember the solution to a maze as well as normal young mice–similar impairments found in old mice.

In order to identify the element in the plasma that caused this effect, comparisons were made on the concentrations of blood proteins in the conjoined animal; of six candidate proteins whose levels that changed after the mice were stitched together, CCL11 or eotaxin, a chemokine, demonstrated the most significant change.

“The factor [CCL11] is a surprising character,” said Richard Ransohoff from the Cleveland Clinic Lerner College of Medicine. “It’s a chemokine that has zero prior neurobiology,” he added. Known only for its role in attracting eosinophils or immune cells that play a major role in allergy and asthma, when the researchers injected this chemokine into young mice, a decrease in new neuron formation was observed. This effect was then reversed with an injection of a CCL11-blocking antibody! Observing too how CCL11 fluctuates with age, Wyss-Coray and researchers saw that its blood-levels elevated in mice and in humans with age.

Wyss-Coray agrees that this study opens a floodgate of new questions. But he’s encouraged by the possibilities. For example, “if we could rejuvenate or maintain the brain in general,” he said, it might delay some of the detrimental effects that cause dementia or Alzheimer’s.


S. A. Villeda et al., “The ageing systemic milieu negatively regulates neurogenesis and cognitive function,” Nature, 477:90-96, doi:10.1038/nature10357, 2011.

Lifestyle of Centenarians Defy Expectations

We’re all interested in living a healthy, long life. For those of us who really mean it, our lifestyle reflects the discipline, restraint, and healthy moderation we think it takes to achieve a vibrant 100 years of life (at least). If you fit that category, reading things like “People who live to 95 or older are no more virtuous than the rest of us in terms of their diet, exercise routine or smoking and drinking habits” may be a bit of an irritation. Yes, you did just read that and we did just quote from a study conducted by researchers of Albert Einstein College of Medicine of Yeshiva University published yesterday, August 3, 2011 in the online edition of Journal of American Geriatrics Society entitled “Lifestyle Factors of People with Exceptional Longevity”. Feeling a little grumpy? Bear with me.

oldhandsw:cig.jpgThe age-old debate between Nature and Nurture rages on in the field of healthy life extension research– you can guess which side this study seems to lean more towards. “Nature” in this case comes in the form of protective longevity genes while “nurture” represents lifestyle behaviors and habits. This study, involving a few hundred centenarians, suggests that one’s genes may play more of an important role in living an exceptionally long life than one’s way of living.

The centenarians indulged in smoking and drinking just as much as their shorter-lived contemporaries. Their diets followed the same vein as others in the general population and they were just as likely to be overweight, perhaps even exercising less than the average person. What gives?

Senior author of the study, Nir Barzilai, M.D., the Ingeborg and Ira Leon Rennert Chair of Aging Research and Director of the Institute for Aging Research at Einstein, together with his colleagues, interviewed 477 independent Ashkenazi Jews aged 95 or older, a group more genetically homogenous than other populations. In this manner, the identification of genetic differences contributing to life span would be simplified. This population was questioned about current habits as well as their lifestyle in earlier years.

Now these researchers were intent on peering into the mystery of longevity through wide lenses–data collected in the 1970s were used to compare the long-lived group with another group of some 3,000 individuals from the general population born around the same time but generally didn’t get to make it 95 years of age.

To put it plainly: What they found was that people who lived to 95+ did not seem to have healthier lifestyles than those who died younger. Check out these numbers: 43% male centenarians reported exercising regularly at moderate intensity compared with 57% of men of the other group. Almost 30% of the long-lived females were smokers, a bit higher than the 26% in the comparison population who smoked. With the men, that percentage was significantly higher at 60% of the centenarian group compared to the 74% of their shorter-lived counterparts. About 24% of the men in the older group drank alcohol on a daily basis whereas 22% made that a habit from the younger group.

However, men and women from both groups were just as likely to be overweight. But there was one difference. Centenarians were less likely to be obese with only 4.5% of men in the older group compared to the 12% of the other male subjects. A similar pattern was found among women. When asked why they believed they had lived so long, most did not attribute their advanced age to lifestyle habits. 20% believed that physical activity played a role, 19% claimed a positive attitude, 12% to a busy or active life, 15% for less smoking and drinking, 8% believed it was good luck, and 6% attributed their longevity to religion or spirituality.

One finding that came as no surprise from the study was that about a third of the centenarians reported having many long-lived family members and relatives–previous studies of Ashkenazi Jews have helped locate a gene variant in the population that causes significantly elevated levels of HDL or “good” cholesterol in the centenarians that appeared to confer resistance Alzheimer’s and heart disease. For those of us who can’t claim the gene variant, there is potential good news, Dr. Barzilai says. There is a drug currently being developed that has the same effect on HDL as that particular gene.

“In previous studies of our centenarians, we’ve identified gene variants that exert particular physiology effects, such as causing significantly elevated levels of HDL or ‘good’ cholesterol,” said Dr. Barzilai, who is also professor of medicine and of genetics at Einstein. “This study suggests that centenarians may possess additional longevity genes that help to buffer them against the harmful effects of an unhealthy lifestyle…We’re identifying genes that play a role in aging and then we can design drugs to mimic their actions.”

While longevity genes may protect centenarians from bad habits, healthy lifestyle choices remain critical for the vast majority of the population. The U.S. Census Bureau estimates there were nearly 425,000 people aged 95 and older living in the U.S. in 2010 – a fraction (.01) of the 40 million U.S. adults 65 and over.

“Although this study demonstrates that centenarians can be obese, smoke and avoid exercise, those lifestyle habits are not good choices for most of us who do not have a family history of longevity,” said Dr. Barzilai. “We should watch our weight, avoid smoking and be sure to exercise, since these activities have been shown to have great health benefits for the general population, including a longer lifespan.”


O’ Connor, Anahad. “Centenarians Have Plenty of Bad Habits Too.” The New York Times Health. The New York Times Company, 4 Aug. 2011. Web. 4 Aug. 2011.

Newman, Kimberly. “Lifestyles of the Old and Healthy Defy Expectations.” EurkAlert! AAAS, the Science Society, 3 Aug. 2011. Web. 4 Aug. 2011.

Cornell Bio-Engineered Spinal Disc Implants Could Spell Relief for Back / Neck Pain Sufferers

If you’ve ever been struck with painful, almost total immobility because of your back or neck, then you know how excruciating it can be. Millions every year haul themselves to doctors for treatment and become part of a statistic for a broad category of illness called degenerative disc disease, a leading cause of disability worldwide. But now Cornell engineers in Ithaca are working in collaboration with doctors at Weill Cornell Medical College on a bio-engineered spinal implant that could someday spell relief for these millions.

“We’ve engineered discs that have the same structural components and behave just like real discs,” says Lawrence Bonassar, Ph.D, associate professor of biomedical engineering and mechanical engineering, together with Roger Härtl, M.D., associate professor of neurosurgery at Weill Cornell Medical College and chief of spinal surgery at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

rat spine.jpg

“The hope is that this promising research will lead to engineered discs that we can implant into patients with damaged discs.”

This new research will be published online Aug. 1, 2011 in the Proceedings of the National Academy of Sciences. Their other colleagues on the paper are Robby Bowles, Cornell Ph.D. ’11, and Harry Gebhard, M.D., of Weill Cornell Medical College. 40-60 percent of American adults suffer from chronic back or neck pain annually and though there might be a surgery called a discectomy (removing the spinal disk and fusing the vertebrate bones to stabilize the spine), they are for those diagnosed with severe degenerative disc disease or herniated discs. But the patient’s back will not likely feel the same as before.

(Bonassar Lab)
From left, a natural rat IVD compared with a tissue engineered IVD.

“Bone or metal or plastic implants are complicated structures which come with a mechanical risk of the structures moving around, or debris from the metal or plastic particles accumulating in the body from wear and tear,” says Härtl.

From a biological perspective, the new discs could create a “huge advantage” over traditional implants because of how they integrate and mature with the vertebrae. This major surgery would become less invasive, safer and come with fewer long-term side effects, he says.

How’d they do it? Focusing on the regeneration and analysis of musculoskeletal tissue, Bonasser and colleagues engineered artificial discs of two polymers- collagen, which wraps around the exterior and a hydrogel alginate in the middle. These were seeded with cells that repopulate the structures with new tissue. Extraordinarily, though artificial implants today degrade over time, the researchers are finding that the implants actually improve as they mature in the body due to the cell growth. Now that’s progress!

“Our implants have maintained 70 to 80 percent of initial disc height. In fact, the mechanical properties get better with time,” says Bonassar.

The scientists began collaborating on the project in 2006, first funded by an Ithaca-Weill seed grant. Since then, the project has moved into animal testing stages and has received several awards and accolades, a $325,000 grant from Switzerland’s AOSpine foundation and $100,000 in support from NFL Charities.

Isn’t this fantastic news? Regenerative breakthroughs are growing in frequency and affectiveness– help us get there faster!


Ju, Anne. “Back, Neck Pain Sufferers Could Find Relief with Cornell-developed Spinal Disc Implants.” Cornell University | Chronicle Online. Cornell University, 1 Aug. 2011. Web. 2 Aug. 2011.

Shrinking Brains: How Human


Jessica McConnell Burt / George Washington University

Researcher Chet Sherwood, holding a chimpanzee brain

“We are very weird animals,” said Emory University anthropologist Todd Preuss at the Yerkes National Primate Research Center in Atlanta, who wasn’t involved in the study. “Among neuroscientists, the assumption has been that species are all the same, but this shows there is something really unusual about the late-life biology of the human species.”

It’s estimated that as much as one in every five people in the US will be over the age of 65 by 2030, more than twice the number of elderly just a decade ago, according to the US Administration on Aging. Unfortunately for us, unlike chimpanzees and other primates, elderly humans are vulnerable to a host of neurodegenerative diseases such as Alzheimer’s–the hope of researchers is that understanding the basic biology of the brain can lead to new treatment and measures to postpone the mental demise of aging.

In this study, the first direct comparison of humans to chimps, a team of brain-scanning scientists led by George Washington University anthropologist Chet Sherwood find that chimps don’t experience such memory loss and that humans are uniquely afflicted by this oddity of longevity. They used MRI technology to scan and measure changes in five crucial brain structures involved in memory, reasoning and mental processing, and overall brain volume and density. Measurements were compared from 87 adult human brains (that’s, ahem, a lot of brains) ranging from 22 – 88 years of age with brain volumes of 99 adult chimps ranging from coinciding 10 – 51 years of age. The gray matter of neurons and white matter of connecting neural fibers were also measured. Chimps’ brains were found to only weigh a third as much as the average 3 lb human brain. The 3 lb human brain was found to shrink by up to a surprising 15% in later years.

aging brain.jpg

The results? “We found no age-related changes in chimpanzees,” said Dr. Sherwood. The human brains lost significant volume over time while the chimpanzees’ remained intact with age. But what humans eventually won’t have in brain volume, they make up for with longevity– a human being can expect to live up to 80 years or more, almost twice the normal lifespan of a chimpanzee in the wild.

“It seems that this is the cost,” said Dr. Sherwood. “We experience more extensive atrophy in the brain that results in this obvious shrinkage, of a kind that is not seen even in our closest relatives, chimpanzees.”

“We were most surprised that chimpanzees, who are separated from humans by only 6-8 million years of independent evolution, did not more closely resemble the human pattern of brain aging,” said Sherwood. “It was already known that macaque monkeys, separated from humans by about 30 million years, do not show humanlike, widespread brain atrophy in aging.”

“This is an excellent example of research that has implications for societal benefits,” said NSF Physical Anthropology Program Officer Kaye Reed. “While Dr. Sherwood and colleagues are interested in the evolutionary significance of brain differences between chimpanzees and humans, the results of this research can be used as a basis to explore degenerative brain diseases, such as Alzheimer’s, in a medical context.”


Hotz, Robert L. “Brain Shrinkage: It’s Only Human.” The Wall Street Journal | Health. Dow Jones & Company, Inc, 26 July 2011. Web. 30 July 2011.

Plant-Based Compound Effectively & Selectively Kills Cancer Cells

Though cancer cells seem to rebel against orderly cell life and death, breaking all the rules like a misfit, growing wildly and dangerously, there is actually a balance between a cancer cell’s fiery metabolism and skyrocketing levels of cellular stress–it is dependant on a hyperactive metabolism to fuel its rapid growth as well as antioxidant enzymes to rein in potentially toxic reactive oxygen species (ROS) generated by such high metabolic demand.

Long Pepper sw (1).jpgNow a study from scientists at the Broad Institute and Massachusetts General Hospital (MGH) reveals a novel compound that successfully but selectively blocks this response to oxidative stress in cancer cells, sparing normal cells. In fact, its effectiveness surpasses even a chemotherapy drug currently used for breast cancer. The compound? It’s actually derived from the fruit of a pepper plant native to southern India and Southeast Asia, a compound called plant-based piperlongumine or PL. Cancer cells are killed by jamming the machinery that dissipates high oxidative stress and the resulting ROS. Because of their more modest metabolism, normal cells maintain low levels of ROS, making high levels of the anti-oxidant enzymes unnecessary once they pass a certain threshold.

“Piperlongumine targets something that’s not thought to be essential in normal cells,” said Stuart L. Schreiber, a senior co-author and director of the Broad’s Chemical Biology Program. “Cancer cells have a greater dependence on ROS biology than normal cells.”

Some of the best discoveries in history are found by accident, and Sam w. Lee and Anna MAndinova, both senior co-authors from the Cutaneous Biology Research Center (CBRC) at MGH certainly weren’t looking for a ROS inhibitor when they found PL. Their target was in the tumor suppressor gene p53, mutated in more than haf of all cancer types. They were looking for something to increase the levels of the properly functioning p53 gene. A promising signal for PL occurred, but they only assumed it worked by the enhancement of the p53 gene. When PL induced cancer cell death independent of the p53′s activity as the tumor suppressor gene, they sat up and took notice. PL was tested in normal cells – they weren’t killed.

“The novelty of this compound was that it was able to recognize cancer cells from normal cells,” said Mandinova, a Broad associate member and a faculty member at MGH and Harvard Medical School. “It has a mode of action that targets something especially important to the cancer cell.”

And yet another surprise- after the Proteomics Platform’s quantitative analysis identified the target of PL, they found an indirect process on which cancer cells depend, in the stead of the assumed oncogene (a protein encoded by a cancer-causing gene being inhibited). There is a small number of new cancer drugs that target oncogenes directly, but they may not be the only promising new direction for treating cancers. See, cancer genes don’t act alone and PL exploits a dependency developed after oncogenes transform normal cells into cancer cells.

“Our studies suggest that piperlongumine’s ROS-associated mechanism is especially relevant to the transformed cancer cell,” said co-author Andrew M. Stern, associate director of Novel Therapeutics at the Broad. “And this in part may underlie the observed selectivity of PL.”

The scientists tested PL against cancer and normal cells engineered to develop cancer in mice injected with human bladder, lung, breast, or melanoma cancer cells. The PL inhibited tumor growth but showed no toxicity in normal mice. The tougher test of mice that spontaneously developed breast cancer revealed PL blocking both tumor growth and metastasis, whereas the chemotherapy drug paclitaxel (Taxol), even at high levels, proved less effective.

“This compound is selectively reducing the enzyme activity involved in oxidative stress balance in cancer cells, so the ROS level can go up above the threshold for cell death,” said Lee, a Broad associate member and associate director of CBRC at MGH. “We hope we can use this compound as a starting point for the development of a drug so patients can benefit.”

Much more work needs doing to gain a better understanding of how the ROS process differs between normal and cancer cells before the launch of clinical trials. Further studies will focus on different forms of cancer and their genotypes, or genetic information. So while the authors remain cautious, they’re hopeful.

“Our next set of goals is to learn if there are specific cancer genotypes that will be more sensitive to this compound than others,” said Alykhan F. Shamji, associate director of the Broad’s Chemical Biology Program. “We hope our experiments will help be predictive of whether patients with the same genotypes in their tumors would respond the same way. It would help us to pick the right patients.”


Cooney, Elizabeth. “Taking out a Cancer’s Co-dependency.” Broad Institute News and Multimedia. Broad Institute, 13 July 2011. Web. 25 July 2011.