Doc uses Google Glass to live-stream surgery


Google Glass is finding its way into operation rooms: A surgeon in Ohio recently became one of the first to livestream an operation and use the technology to consult with a colleague.

On Aug. 21, Dr. Christopher Kaeding, director of sports medicine at Ohio State University Wexner Medical Center, wore Google Glass a wearable computer that has a frame similar to traditional eyeglasses as he performed surgery on the anterior cruciate ligament (ACL) in the knee of a 47-year-old woman.

The procedure was livestreamed to a group of medical students, who watched on laptops, and to Dr. Robert Magnussen, an assistant professor of clinical orthopedics at Ohio State, who watched from his office.

During the operation, Kaeding consulted with Magnussen about what he was seeing during the surgery.


‘Once we got into the surgery, I often forgot the device was there.’

– Dr. Christopher Kaeding, director of sports medicine at Ohio State University Wexner Medical Center


Kaeding said he did not find wearing the device to be a distraction.

“To be honest, once we got into the surgery, I often forgot the device was there. It just seemed very intuitive and fit seamlessly,” Kaeding said in a statement.

The device does not have lenses, but instead, has a small glass screen that sits above the right eye. Using voice commands, wearers of Google Glass can pull up information on that screen like they would on a computer. The device also has a camera that can take photos and videos that show the viewpoint of the user. [Video: Google Glass Used in Surgery]

So far, a select group of about 1,000 people have had the opportunity to test Google Glass. One of Kaeding’s colleagues applied and was accepted as a tester, and the two partnered for the surgery.

One day, doctors may use the technology to view X-rays, MRI images or other medical information about their patient as they conduct surgeries, although this was not done in the current surgery.

“We just have to start using it. Like many technologies, it needs to be evaluated in different situations to find out where the greatest value is, and how it can impact the lives of our patients in a positive way,” said Dr. Clay Marsh, chief innovation officer at the medical center.

In June, a doctor in Maine used Google Glass to livestream a surgery on Google Hangout. The surgery was a gastrostomy, a relatively simple procedure that involves the placement of a feeding tube into a patient’s stomach.

Copyright 2013 LiveScience, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

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Ohio man comes back to life after being dead for 45 minutes

After showing no signs of life for 45 minutes and being declared dead, a 37-year-old Ohio man suddenly came back to life, reported.

Anthony Yahle was taken to Kettering Medical Center in Kettering, Ohio on the morning of August 5 when his wife Melissa noticed his breathing didn’t sound right.  She and her 17-year-old son, Lawrence, performed CPR on Yahle until first responders arrived.

At the hospital, doctors treated Yahle with every medicine they could for 45 minutes, but he didn’t respond and was officially declared dead.

According to, Lawrence said that when he found out his father had died, he ran down the hall to his father’s room and yelled, “Dad, you’re not going to die today.”  Shortly after that, doctors noticed Yahle had a faint heartbeat again, and they decided to make another effort to revive him.

Their attempts were successful, and Yahle returned home on August 10 with no need for a heart transplant.  The cause for his medical emergency has not yet been reported.

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Clinically dead woman revived after 42 minutes

News Corp Australian Papers
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Australian doctors have saved the life of a woman who was clinically dead for 42 minutes.

The miracle patient was rushed to hospital after a major heart attack, but was declared clinically dead soon after arrival.

With the aid of a hi-tech machine that kept blood flowing to her brain, doctors at Melbourne’s MonashHeart managed to unblock vital arteries and return her heart to a normal rhythm.

The hospital today described her survival as “astonishing”.

Doctors say Vanessa Tanasio, 41, a mother of two from the suburb of Narre Warren, needed numerous defibrillator shocks, including one in the ambulance on her way to hospital.

In a telephone interview from the hospital, she said she was eager to get home. “I’m feeling excellent. For someone who has been dead for nearly an hour of this week I am feeling tremendously well.”

Emergency medics used a device called LUCAS 2 to keep her blood flowing last Monday while cardiologist Dr Wally Ahmar worked to unblock the arteries to her heart.

Tanasio, a sales representative for an earthmoving equipment company, said she had no history of heart problems.

“This has taken me completely by surprise. I am relieved to still be here for my children. The doctors and the nurses have been awesome. The machine is awesome.”

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Researchers develop rabbits that glow in the dark

Discovery News
  • glowingrabbits.jpg

    University of Hawaii Manoa collaboration with two Turkish Universities produced transgenic rabbits using the technique created at UH Manoa. (Turkish Universities/John A. Burns School of Medicine)

A glowing bunny sounds like a creature from Jefferson Airplane’s psychedelic-laced song, “White Rabbit,” but real fluorescent rabbits were recently born at the University of Istanbul, Turkey.

Rabbits join a growing list of fluorescent fur-bearers. Genetic engineers have created glowing dogs, cats, pigs and mice by inserting a gene from a jellyfish into the mammals’ DNA. The jellyfish gene codes for a protein that emits light when exposed to ultraviolet light.

The jellyfish gene adds an obvious physical change to an engineered animal. This allows scientists to know that genetic material successfully transferred into a new organism.

For example, when Mayo Clinic researchers genetically engineered cats to carry a protein that defends the animals from infection by the feline immunodeficiency virus (FIV, the cat version of HIV), the scientists added the fluorescent gene along with the FIV-resistance gene. That way they knew that any cat that fluoresced also carried protein protection against FIV, a trait that would otherwise be invisible.

The fluorescent rabbits could eventually produce proteins as well. Re-engineered rabbits could manufacture molecules that biologists would then collect from female fluorescent rabbits’ milk. Producing medicines and other chemicals using rabbits could be less expensive than fabricating the materials in factories.

University of Hawaiʻi – Mānoa geneticists, Ryuzo Yanagimachi and Stefan Moisyadi, collaborated with Turkish scientists at the University of Istanbul and Marmara University to create the fluorescent rabbits.

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A potential cure for Alzheimer’s? Scientists discover new culprit behind brain-wasting disease
  • brain neuron

The accumulation of a specific protein in the aging brain may be the cause of numerous devastating neurodegenerative diseases – most notably Alzheimer’s disease.

But it’s not amyloids – the proteins that most health experts blame for the brain-wasting condition.  It’s an entirely new culprit.

In a groundbreaking study from Stanford University School of Medicine, researchers detailed the significance of a protein called C1q, which was previously known as the initiator of the immune system response. After analyzing brain tissue in mice of varying ages, as well as postmortem samples of a 2-month-old infant and an elderly person, they discovered that C1q exponentially increases in the aging brain – creating as much as a 300-fold buildup. Comparatively, most age-associated increases of proteins in the brain are only three- or four-fold.

The research team revealed that as the brain ages, C1q accumulates around the brain’s synapses – contact points that connect the brain’s nerve cells to one another.  Rather than being naturally cleared by the brain, the C1q sticks, making these synapses vulnerable to destruction from the brain’s immune cells.

According to study author Dr. Ben Barres, the findings could fundamentally change the way scientists and doctors perceive neurodegenerative diseases, as well as lead to treatments that could alleviate the devastating effects of age-related brain disorders.  Classic symptoms of neurodegneration range anywhere from severe memory loss to problems with motor function and complete loss of limb movement.

“We’re suggesting the reason the old brain is so vulnerable to Alzheimer’s disease is because of this massive buildup of C1q,” Barres, professor and chair of neurobiology at Stanford, told  “One of the things that’s very interesting about this pattern is that the earliest accumulation of C1q starts in regions of the brain that are well-known to be most vulnerable to neurodegenerative disease – the hippocampus and substantia nigra.”

The complement system

C1q is a well-established component of what is known as the complement system – a group of 20 proteins that help antibodies and macrophages clear pathogens from the body.  Considered the initiator of the system, C1q is responsible for recognizing the body’s “garbage,” such as bacteria, dying cells, and other harmful agents.

After locating these potentially dangerous cells, C1q binds to them and triggers a molecular reaction known as the amplifying cascade, in which the remaining 19 complement proteins bind to and coat the debris.  This allows the macrophages (immune cells) to recognize the complement-tagged junk and eliminate it from the body.

“In the body, this system makes a lot of sense,” Barres said.  “All the cells in the body contain inhibitors to the complement, so normal cells aren’t targeted and destroyed.  For example, a normal liver cell will be fine, so it doesn’t have to worry about showers of complement protein.”

It was previously thought that the complement system did not exist in the brain, but in 2007, Barres’ group discovered that this system is actually hard at work in the brains of infants.  As a young brain grows, it generates an excess of synapses that will potentially form new neural circuits.  However, since too many synapses are created, the brain had to develop a mechanism for eliminating the ones deemed unnecessary.

“The mystery was nobody knew how the extra synapses were removed,” Barres explained.

Through their research, they found that this synaptic pruning was done by the complement system. The microglia – the brain’s version of immune cells – were secreting C1q, while other brain cells called astrocytes were responsible for secreting the rest of the complement proteins.  As a result, the microglia would then attack the complement coated synapses, eliminating the excess from the brain.

“This is what really got us interested,” Barres said. “Neurodegenerative disorders are well described as unwanted synapse degeneration.  So there is massive synapse loss, but no one knows why.  We thought maybe the complement system is way overactive in Alzheimer’s.  It’s not normally active in the typical adult brain, but in Alzheimer’s, it turns on like a switch.”

Complement gone wrong

Barres explained that when the complement system gets reactivated in the aging brain, an overabundance of C1q is created by the microglia, while the other complement proteins are somehow not activated.  The C1q then targets the synapses but does not get cleared from the brain, so the protein remains on the neural connectors – causing more and more damage.

Barres’ explanation for this is that the synapses in the aging brain are different from those in the developing brain.

“We infer the existence of aging synapses that aren’t present in young brains – what we call senescent synapses,” Barres said.  “We don’t know why they become this way.  We infer that the old synapses are changing with age.  One of the things about the brain that makes it different from most other tissues is the cells don’t turnover.  The neurons you’re born with you’ll have your entire life.”

It’s possible that the senescent synapses become “sticky,” Barres theorized, which allows for this accumulation of C1q.  This leaves the synapses on the brink of catastrophe, since a traumatic brain event such as a trauma or a stroke could trigger an activation of the remaining complement proteins, leading to massive synapse destruction.

According to Barres, his findings stand in contrast to current ways of thinking, as most scientists believe the pathology of Alzheimer’s begins with the buildup of amyloid plaque, which causes the loss of brain synapses and subsequent inflammation.  Instead, he believes the amyloid buildup is a symptom of the disease rather than the cause.

“We think people have the ordering backwards,” Barres said.  “We believe the complement turns on first and starts to kill synapses.  If that’s true, the implication is we just need to block this complement cascade to treat Alzheimer’s.”

Barres is so confident about his findings that he is already developing a drug to target the complement system in the brain.  In 2011, he co-founded a company, Annexon, which has been working on creating a drug that binds and inhibits the C1q protein.  While their main focus has been on alleviating the effects of Alzheimer’s, Barres said this kind of drug could potentially help those suffering from a full range of neurodegenerative disease.

“One thing is clear is that the compliment mechanism is activated very highly in all neurodegenerative diseases – Parkinson’s, multiple sclerosis, Alzheimer’s, Huntington’s, etc.,” Barres said. “If we can block this pathway, we should be able to block the neurodegeneration process in many, many people.”

The research was published in the Journal of Neuroscience.

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Helmet grows food, keeps you fed with algae
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    A duo of UK designers developed an Algaculture Symbiosis Suit that grows algae while you wear it. (AfterAgri/Vimeo)

Don’t always have time to pack a snack? The Algaculture Symbiosis Suit is your solution.

Desingers Michiko Nitta and Michael Burton have developed a new kind of gagdet that grows food while wearers go about their daily activities. With a little help from the sun, a series of tubes placed in front of the mouth use the carbon dioxide we inhale to fuel the ever-growing population of suit-embedded algae.

“Algaculture designs a new symbiotic relationship between humans and algae. It proposes a future where humans will be enhanced with algae living inside new bodily organs, allowing us to be semi-photosynthetic,” Burton Nitta write on their website.

If a diet full of algae does not sound appetizing, know that you actually consume algae on a regular basis. That slice of pizza you had last night for dinner and the bagel you had this morning for dinner all contain derivatives of algae.

The suit made its debut last year outside of the Victoria and Albert Museum in London where an opera singer wore the device while singing to an intrigued crowd. Watch as the singer created enough algae to feed the crowd below.

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‘Grid cells’ help rats, humans with navigation, researchers say
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    Grid neurons in the brain activate during navigation to help humans keep track of where they are, scientists say. (Drexel University)

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    Scientists study an MRI targeting the area of the hippocampus where electrodes were placed. (John F. Burke)

Like a GPS in your brain, a newly discovered type of cell helps people keep track of their location while navigating an unfamiliar environment, researchers say.

Using direct human brain recordings, scientists from Drexel University, the University of Pennsylvania, UCLA and Thomas Jefferson University found the “grid cell,” so called for its triangular grid pattern.

This grid pattern, which needs to be consistent, is critical as it shows how people can keep track of their location even in new environments, notes Joshua Jacobs, an assistant professor from Drexler and the study’s primary investigator.

“Without grid cells, it’s likely that humans would frequently get lost or have to navigate based only on landmarks. Grid cells are thus critical for maintaining a sense of location in an environment,” Jacobs explained.

The cell is activated during navigation and allows the brain to keep track of navigational cues, such as how far a person is from their starting point and their last turn. Navigation in this manner is known as path integration.

The team, which included Michael Kahana of Penn, and Itzhak Fried of UCLA, discerned the cells after having a rare opportunity to study brain recordings of epileptic patients.

With electrodes placed deep inside their brains, 14 participants played a video game, challenging them to navigate from one point to another, collecting objects while riding a virtual bicycle. They then had to recall how to how to get back to places where each object was located.

After trail runs – with each of the objects visible by the gamers in the distance – they were returned to the start of the game and the objects were hidden until the virtual bicycle was right in front of them. Scientists then told the participants to travel to particular objects in different orders.

After studying the relationship between navigation and the activity of individual neurons, Jacobs stated that the triangular grid pattern appears to play a fundamental role in navigation.

The findings in this experiment mark the first positive identification of such cells in humans. Prior experiments showed the existence of grid cells in rats and human hippocampal place cells, according to Kahana, a professor of psychology. The new findings also suggest that grid patterns may be more prevalent in humans. Human grid cells were found in the entorhinal cortex – same as the rats – but also in the cingulate cortex.

The entorhinal cortex is a critical part of the human memory system and the findings will hopefully shed new light on a region of the brain that is first to be affected in Alzheimer’s disease, according to Fried.

It could also help researchers understand why people with Alzheimer’s often become disoriented, while showing them how to improve brain function of people with this disease, Jacobs explained

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Genetic ‘Adam’ and ‘Eve’ uncovered

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    Human sex-determining chromosomes: X chromosome (left) and the much smaller Y chromosome. (University of Arizona)

Almost every man alive can trace his origins to one man who lived about 135,000 years ago, new research suggests. And that ancient man likely shared the planet with the mother of all women.

The findings, detailed Thursday, Aug. 1, in the journal Science, come from the most complete analysis of the male sex chromosome, or the Y chromosome, to date. The results overturn earlier research, which suggested that men’s most recent common ancestor lived just 50,000 to 60,000 years ago.

Despite their overlap in time, ancient “Adam” and ancient “Eve” probably didn’t even live near each other, let alone mate. [The 10 Biggest Mysteries of the First Humans]

“Those two people didn’t know each other,” said Melissa Wilson Sayres, a geneticist at the University of California, Berkeley, who was not involved in the study.

Tracing history
Researchers believe that modern humans left Africa between 60,000 and 200,000 years ago, and that the mother of all women likely emerged from East Africa. But beyond that, the details get fuzzy.

The Y chromosome is passed down identically from father to son, so mutations, or point changes, in the male sex chromosome can trace the male line back to the father of all humans. By contrast, DNA from the mitochondria, the energy powerhouse of the cell, is carried inside the egg, so only women pass it on to their children. The DNA hidden inside mitochondria, therefore, can reveal the maternal lineage to an ancient Eve.

But over time, the male chromosome gets bloated with duplicated, jumbled-up stretches of DNA, said study co-author Carlos Bustamante, a geneticist at Stanford University in California. As a result, piecing together fragments of DNA from gene sequencing was like trying to assemble a puzzle without the image on the box top, making thorough analysis difficult.

Y chromosome
Bustamante and his colleagues assembled a much bigger piece of the puzzle by sequencing the entire genome of the Y chromosome for 69 men from seven global populations, from African San Bushmen to the Yakut of Siberia.

By assuming a mutation rate anchored to archaeological events (such as the migration of people across the Bering Strait), the team concluded that all males in their global sample shared a single male ancestor in Africa roughly 125,000 to 156,000 years ago.

In addition, mitochondrial DNA from the men, as well as similar samples from 24 women, revealed that all women on the planet trace back to a mitochondrial Eve, who lived in Africa between 99,000 and 148,000 years ago almost the same time period during which the Y-chromosome Adam lived.

More ancient Adam
But the results, though fascinating, are just part of the story, said Michael Hammer, an evolutionary geneticist at the University of Arizona who was not involved in the study.

A separate study in the same issue of the journal Science found that men shared a common ancestor between 180,000 and 200,000 years ago.

And in a study detailed in March in the American Journal of Human Genetics, Hammer’s group showed that several men in Africa have unique, divergent Y chromosomes that trace back to an even more ancient man who lived between 237,000 and 581,000 years ago. [Unraveling the Human Genome: 6 Molecular Milestones]

“It doesn’t even fit on the family tree that the Bustamante lab has constructed. It’s older,” Hammer told LiveScience.

Gene studies always rely on a sample of DNA and, therefore, provide an incomplete picture of human history. For instance, Hammer’s group sampled a different group of men than Bustamante’s lab did, leading to different estimates of how old common ancestors really are.

Adam and Eve?
These primeval people aren’t parallel to the biblical Adam and Eve. They weren’t the first modern humans on the planet, but instead just the two out of thousands of people alive at the time with unbroken male or female lineages that continue on today.

The rest of the human genome contains tiny snippets of DNA from many other ancestors they just don’t show up in mitochondrial or Y-chromosome DNA, Hammer said. (For instance, if an ancient woman had only sons, then her mitochondrial DNA would disappear, even though the son would pass on a quarter of her DNA via the rest of his genome.)

As a follow-up, Bustamante’s lab is sequencing Y chromosomes from nearly 2,000 other men. Those data could help pinpoint precisely where in Africa these ancient humans lived.

It’s very exciting,” Wilson Sayres told LiveScience. “As we get more populations across the world, we can start to understand exactly where we came from physically.”

Copyright 2013 LiveScience, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

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The price of anarchy: How contagion spreads

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    The price of anarchy, two weeks after an epidemic starts from each county in the East Coast of the United States. The price of anarchy measures the difference in spread of a disease between selfish (uncoordinated) and policy-driven (coordinated). (C. Nicolaides/Juanes Research Group/MIT)

During infectious disease outbreaks, personal freedom comes at a price: the welfare of the public as a whole, a new study finds.

In the research, scientists investigated whether, in the event of an outbreak, people should be allowed to move about freely or if authorities should enforce travel restrictions to halt the disease’s spread.

“What we were trying to understand better is how actions, in terms of routing humans, could affect the spread of disease,” said study researcher Ruben Juanes, a geoscientist at MIT in Cambridge, Mass. [The 5 Most Likely Real-Life Contagions]

The findings suggest that highly connected regions of dense commuter traffic carry the gravest consequences of allowing free movement.

The price of anarchy

The researchers borrowed a concept from game theory known as the “price of anarchy,” which they defined as “the loss of welfare due to selfish rerouting compared with the policy-driven coordination.”



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Juanes and colleagues modeled the epidemic problem as two scenarios. In a free-movement scenario, people act selfishly to avoid infected areas, regardless of whether or not they themselves are infected, Juanes told LiveScience. In a policy-driven scenario, government agencies dictate that infected individuals move only within infected areas, while healthy individuals keep to unaffected areas, he said.

If the price of personal freedom is low — the spread of the disease is similar whether or not movement controls are imposed — it provides a clear answer regarding restrictions, Juanes said. “You come to the conclusion that it’s not worth doing,” he said, adding that these restrictions could be very costly and unpopular.

But if the price of such freedom is high, and movement restrictions could significantly slow the disease’s progression, government agencies might want to implement these policies, Juanes said.

The researchers looked at census data on the passage of commuters within and among U.S. counties. Scientists compared how the disease would spread in different counties under the two different scenarios.

Not all areas would benefit equally from such restrictions, the findings showed. Places that had high traffic both within and among counties saw the most benefit from restricting travel. For example, counties near a major interstate highway, such as I-80 from New York to San Francisco or I-95 from the Canadian border to Miami, had a higher cost of anarchy — meaning travel restrictions would be helpful.

By contrast, low traffic areas did not benefit much from travel restrictions, so their cost of anarchy was lower, the model showed.

Surprisingly, some densely trafficked areas still wouldn’t benefit much from travel restrictions. The policies only benefitted high-traffic regions that were near other high-traffic areas. “It was only when we established the longer-range correlation [with neighboring high-traffic areas] that we could make sense of it,” Juanes said.

Understanding disease spread

Physicist Alessandro Vespignani of Northeastern University in Boston, who was not involved with the study, called it an interesting contribution to scientists’ understanding of social behavior and of how people adapt to learning of an epidemic. Still, “many elements of realism are still missing in the modeling approaches,” Vespignani cautioned. More studies are needed “to fully understand the effects of behavioral reactions in the spreading of large-scale epidemics,” he said.

Even if travel restrictions can limit disease spread, implementing these policies may be unrealistic, Juanes said. The economic cost of rerouting a large population could be immense, he said, and people may be reluctant to give up their freedom.

Nonetheless, “there are events in which people understand that some extreme measures are perhaps admissible,” Juanes said, citing the lockdown of Boston while police searched for the Boston Marathon bombers.

“In some extreme cases, it is conceivable to impose far-reaching travel restrictions,” he said.

Copyright 2013 LiveScience, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

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Return of the mammoth? Dolly scientist says beast should be cloned
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    An artist’s illustration depicts a herd of woolly mammoths. (Mauricio Anton/PLoS)

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    A researcher holding a test tube with what the scientists called a sample of well-preserved blood they found in a carcass of a female mammoth discovered on a remote island in the Arctic Ocean. (AFP / Northeastern Federal University)

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    A researcher working near a carcass of a female mammoth found on a remote island in the Arctic Ocean. (AFP / Northeastern Federal University)

The astonishingly well-preserved blood from a 10,000-year-old  frozen mammoth could lead to mammoth stem cells, said Ian Wilmut, the scientist responsible for Dolly, the world’s first cloned animal — and might ultimately lead to a cloned mammoth.

There are several hurdles to such a venture, of course, and it may ultimately prove unsuccessful.

But Wilmut’s weight lends credibility to the growing possibility of bringing back the mammoth — the “de-extinction” of a long-lost species.


‘If there are reasonable prospects of them being healthy, we should do it.’

– Ian Wilmut, emeritus professor at the MRC Center for Regenerative Medicine at University of Edinburgh


“I think it should be done as long as we can provide great care for the animal,” Wilmut told The Guardian. “If there are reasonable prospects of them being healthy, we should do it. We can learn a lot about them,” he said.

PHOTOS: Ten Most Wanted “Extinct” Amphibians

In an essay on The Conversation, Wilmut spelled out the two main methods for turning an ancient pile of mammoth bones and blood into a living, breathing creature. The two he focused on were the use of elephant eggs to grow an embryo — similar to the process that led to Dolly — and the creation of embryonic mammoth stem cells.

“Stem cells of this type can also be induced to form gametes. If the cells were from a female, this might provide an alternative source of eggs for use in research, and perhaps in breeding, including the cloning of mammoths,” Wilmut wrote.

Wilmut, emeritus professor at the MRC Center for Regenerative Medicine at University of Edinburgh, made headlines in 1996 when he and his colleagues cloned Dolly the sheep. Their technique involved injecting DNA into a special egg cell and transferring the product into a third sheep, which carried the egg to term. While Dolly lived a brief life, dying in 2003, her very existence was hailed as a medical marvel.

That such a noted scientist could even discuss the process of bringing back the mammoth stems from an astonishing find on a remote Russian island in the Arctic Ocean: blood so well preserved that it flowed freely from a 10,000- to 15,000-year-old creature.

PHOTOS: “Extinct” Monkeys With Sideburns Found in Borneo

“The fragments of muscle tissues, which we’ve found out of the body, have a natural red color of fresh meat. The reason for such preservation is that the lower part of the body was underlying in pure ice, and the upper part was found in the middle of tundra,” said Semyon Grigoriev, the head of the expedition and chairman of the Mammoth Museum, after announcing the discovery.

Wooly mammoths are thought to have died out around 10,000 years ago, although scientists think small groups of them lived longer in Alaska and on Russia’s Wrangel Island off the Siberian coast.

A growing chorus of scientists have been targeting the mammoth for so called “de-extinction” in recent years, at the same time that others argue against tampering with Mother Nature’s plans. Bringing back a dead species raises a host of issues, wrote two ethicists recently.

RELATED: Boy in Alaska Finds Mammoth Tooth

“The critical ethical issue in re-creating extinct species, or in creating new kinds of animals, is to first determine through careful scientific study what is in their interests and to ensure that they live good lives in the world in which they are create,” wrote Julian Savulescu, who studies ethics at Monash University, and Russell Powell, a philosophy professor at Boston University.

“If we are confident that a cognitively sophisticated organism, such as a mammoth, would lead a good life, this may provide moral reasons to create it — whether or not that animal is a clone of a member of an extinct lineage.”

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