It is an open secret: while athletes dope their bodies, regular office workers dope their brains. They buy prescription drugs such as Ritalin or Provigil on the internet’s flourishing black market to boost their cognitive performance.
It is hard to get reliable data on how many people take such “smart drugs” or “pharmacological cognitive enhancement substances”, as scientists call them. Prevalence studies and surveys suggest, though, that people from different walks of life use them, such as researchers, surgeons, and students. In an informal poll among readers of the journal Nature, 20% reported that they had taken smart drugs. And it seems that their use is on the rise.
So, if you are in a demanding and competitive job, some of your colleagues probably take smart drugs. Does this thought worry you? If so, you are not alone. Studies consistently find that people see brain doping negatively.
A main concern is fairness. Imagine that while you are going for a run to boost your mental energy, your colleague is popping Ritalin instead. While you believe in your afternoon nap to regain concentration, your office mate relies on Provigil. Unfair? The general public thinks that taking smart drugs is cheating, because it can give users a competitive edge. In fact, even several academics have argued that brain doping is unfair towards people who don’t do it.
I’m writing this on the UK’s hottest day of the year. There is a light breeze, but everyone I have seen today has beads of sweat on their forehead. Seeing someone wiping their brow is a fairly common sight in midsummer, but it reveals a simple and fascinating truth about our species: without sweat, we would not still be here. Without this absolutely amazing technology we would not have climbed our way to the top of the evolutionary pile. Many animals perspire, but no others use it as such an efficient and refined cooling technology. So how does it work and why do we owe it so much?
We often assume that it is our brain power that differentiates us from other animals. It is obvious that we are able to process more intellectual stimuli than other mammals, but any PC owner knows that computational power is completely useless if the cooling system fails. And this is what really sets us apart. It is our ability to maintain an effective working temperature, not just so that we can keep moving, but so that we can keep thinking while in motion, efficiently chasing down the quarry.
As a species, over short distances, we are hopeless runners. We might be able to go a long way but what use is that if we can’t catch anything? The truth is that we never could if it weren’t for several factors that make us identifiably human. And it is our ability to perspire which renders them all effective. So we may have perfect bodies for distance running, but those features that enable us to move so effectively are useless without correct temperature control.
Open-heart surgery is risky and can take patients months to recover from. Researchers at the University of Maryland Medical Center have developed a device that eliminates the need for such surgery for those suffering degenerative mitral regurgitation (MR). Not only does the device reduce time spent on the operating table, but it could eventually see patients heading home from hospital the day after a heart operation.
Degenerative mitral regurgitation is a common heart valve disorder that affects around eight million people in the US alone. It is caused by a leaky heart valve, in which the small cords that control the valve's flaps are broken or stretched and cause blood to flow in the wrong direction. To repair the valve, invasive open-heart surgery is carried out to replace the small cords in a procedure that requires surgical skill and experience.
The Harpoon TSD-5 device built by Harpoon Medical of Baltimore is based on technology developed by the University of Maryland Medical Center and makes the job easier for surgeons and safer and less intrusive for patients.
Are you middle-aged or older and having problems remembering details, like where you left the keys or parked your car?
Cheer up, it may simply be the result of a change in what information your brain focuses on during memory formation and retrieval, rather than a decline in brain function, according to a study by McGill University researchers.
In the study, published in the journal, NeuroImage, 112 healthy adults ranging in age from 19 to 76 years were shown a series of faces. Participants were then asked to recall where a particular face appeared on the screen (left or right) and when it appeared (least or most recently). The researchers used functional MRI to analyze which parts of brain were activated during recall of these details.
Different parts of the brain involved
Senior author Natasha Rajah, Director of the Brain Imaging Centre, and colleagues found that young adults activated their visual cortex while successfully performing this task.
But for middle-aged and older adults, their medial prefrontal cortex was activated instead. That’s a part of the brain known to be involved with information having to do with one’s own life and introspection. This may reflect changes in what adults deem “important information” as they age, she said.
Rajah says middle-aged and older adults can improve their recall abilities by learning to focus on external rather than internal information, using mindfulness meditation, for example.*
Rajah is currently analyzing data from a similar study to discern if there are any gender differences in middle-aged brain function as it relates to memory. “At mid-life women are going through a lot of hormonal change. So we’re wondering how much of these results is driven by post-menopausal women.”
The research was supported by the Canadian Institutes of Health Research and by a grant from the Alzheimer’s Society of Canada.
In Evelyn De Morgan’s numinous painting, Night and Sleep (1878), Nyx, the mighty Greek goddess of night, hovers across a dusky sky with her beloved son Hypnos, the sweet-natured god of sleep. The painting and the Greek gods it captures depict a radically different way of understanding and relating to sleep. In antiquity sleep was personified, transcendent, even romantic.
Both Nyx and Hypnos had personality. Nyx was beautiful, shadowy and formidable – the only goddess Zeus ever feared. A Mother Nature figure with attitude, she was most protective of her son, even when he engaged in divine mischief. Which he did. But Hypnos was also gentle and benevolent, an androgynous mamma’s boy. Occupying a liminal zone between sleep and waking, he often seemed a bit dreamy. If he showed up at a sleep clinic today, he would likely be diagnosed with narcolepsy – a disorder of heightened permeability in the boundary between waking and sleep.
Nyx and Hypnos were denizens of the underworld. She was the original night owl, a fierce guardian of nature’s circadian rhythms who magically transformed day into night. With her support, as seen in De Morgan’s painting, Hypnos gently scatters crimson poppies, sleep elixirs, over the planet below. As in the more recent tale of the Sandman who sprinkles sleepy dust over the eyes of children, sleep is bequeathed from above. That sleep is grace.
Nyx and Hypnos were a dynamic duo of sorts – supernatural heroes who romanticised night and sleep. Nyx gave birth to sleep and created an aesthetic of darkness where Hypnos could flourish. And Hypnos loved sleep. Surrounded by fields of wild poppies on the River of Oblivion, his lair was a sanctuary – a cool, magical retreat open to all in celebration of the sensual, even sexy, mysteries of sleep.
Today, mother and son have been largely forgotten. Nyx has been in exile for well over a century as our night sky is eroded by light pollution. And Hypnos is remembered mainly by his namesakes, hypnosis and, surely to his chagrin, hypnotics. Sleep is no longer personal, transcendent and romantic – it is medical, mundane and pragmatic.
We all like to think of ourselves as totally unique, independent individuals, in charge of our own destinies. But new research has found evidence that our behaviour, and maybe even our personalities, could be influenced by something totally unexpected - our immune systems.
Researchers have shown that by switching off just one immune molecule in mice, they can change the way the animals behave and interact with each other - which suggests the immune system may play a role in conditions such as autism-spectrum disorder or schizophrenia.
Before we get too carried away, this is early research that's only been conducted in rodents for now. But the researchers from the University of Virginia School of Medicine were able to clearly show that by simply changing the way the immune system responds to pathogens, they could trigger antisocial behaviour in mice.
Restoring the molecule returned the mouse personalities to normal.
"It’s crazy, but maybe we are just multicellular battlefields for two ancient forces: pathogens and the immune system," said lead researcher, Jonathan Kipnis. "Part of our personality may actually be dictated by the immune system."
Being overweight or obese puts men at a greater risk of dying prematurely than women, the largest ever study on obesity and death suggests.
Scientists say though the reasons behind the trend are unclear, the study supports others that suggest obese men are at higher risk of diabetes and have higher levels of dangerous liver fat.
The authors say second to smoking, obesity is the most significant cause of death in Europe and North America.
The report appears in the Lancet. 'Obesity challenges'
A global consortium of researchers pulled together data from 189 studies across the world, involving almost four million people.
They focused on people who had never smoked and did not have a long-term illnesses when the studies started - in an attempt to exclude people who had lost weight through heavy smoking or serious ill health.
Overall, they found the risk of death increased the more overweight a person was.
And the links between obesity and death were strongest for men.
Giving an example of an obese but otherwise healthy man in North America, they estimate the risk of death before the age of 70 to be about 29%, compared with 19% for a man of normal weight.
Meanwhile, they say the risks for a woman in North America would rise from 11% at a healthy weight to 14.6% if she were moderately obese.
Prof Sir Richard Peto, said: "Smoking causes about a a quarter of all premature deaths in Europe and North America, and smokers can halve their risk of premature death by stopping.
Activating particular neurons may be a way to control alcohol-drinking, a new study suggests.
Prior research has shown that alcohol consumption alters the physical structure and function of medium spiny neurons, in the dorsomedial striatum. Essentially, this means that activation of one type of neuron, called D1, determines whether one drink leads to two. Now, scientists have discovered the ones that tell us to stop.
These neurons can be thought of like a tree, with branches, and small protrusions, or spines, coming off of them. Each neuron has one of two types of dopamine receptors—D1 or D2—and so can be thought of as either D1 or D2 neurons.
D1 neurons are informally called part of a “go” pathway in the brain, while D2 neurons are in the “no-go” pathway. In other words, when D2 neurons are activated, they discourage action—telling you to wait, to stop, to do nothing.
“At least from the addiction point of view, D2 neurons are good,” says Jun Wang, assistant professor of neuroscience and experimental therapeutics at Texas A&M University College of Medicine. “When they are activated, they inhibit drinking behavior, and therefore activating them is important for preventing problem drinking behavior.”
The trouble is, even in individuals without alcoholism, D2 neurons tend to become deactivated when we drink too much. This deactivation means there is nothing telling us to stop drinking, so we drink more, in a self-perpetuating cycle.
There could be a very serious problem with the past 15 years of research into human brain activity, with a new study suggesting that a bug in fMRI software could invalidate the results of some 40,000 papers.
That's massive, because functional magnetic resonance imaging (fMRI) is one of the best tools we have to measure brain activity, and if it’s flawed, it means all those conclusions about what our brains look like during things like exercise, gaming, love, and drug addiction are wrong.
"Despite the popularity of fMRI as a tool for studying brain function, the statistical methods used have rarely been validated using real data," researchers led by Anders Eklund from Linköping University in Sweden assert.
The main problem here is in how scientists use fMRI scans to find sparks of activity in certain regions of the brain. During an experiment, a participant will be asked to perform a certain task, while a massive magnetic field pulsates through their body, picking up tiny changes in the blood flow of the brain.
These tiny changes can signal to scientists that certain regions of the brain have suddenly kicked into gear, such as the insular cortex region during gaming, which has been linked to 'higher' cognitive functions such as language processing, empathy, and compassion.
Getting high on mushrooms while connected to an fMRI machine has shown evidence of cross-brain activity - new and heightened connections across sections that wouldn’t normally communicate with each other.
It’s fascinating stuff, but the fact is that when scientists are interpreting data from an fMRI machine, they’re not looking at the actual brain. As Richard Chirgwin reports for The Register, what they're looking at is an image of the brain divided into tiny 'voxels', then interpreted by a computer program.
"Software, rather than humans ... scans the voxels looking for clusters," says Chirgwin. "When you see a claim that ‘Scientists know when you're about to move an arm: these images prove it,' they're interpreting what they're told by the statistical software."
Prostate exams aren't exactly an enjoyable experience, but if you ever need one, you'll want the doctor to know what they're doing. Unfortunately, the procedure is difficult for med students to learn, thanks to the internal nature of the examination and a lack of willing test subjects. Scientists at Imperial College London wanted to solve that problem by developing a robotic rectum that recreates the feel of the real thing and even provides haptic feedback.
The cheek-clench-inducing procedure involves a doctor snapping on a glove and probing a man's back passage, which is the most direct path to the prostate gland. A hardened or enlarged prostate is often a warning sign for prostate cancer, and the procedure is commonly used to determine if a patient needs to undergo further tests.
"Internal examinations are really challenging to learn – and to teach," says Dr Fernando Bello of Imperial College London. "Because the examinations occur in the body, the trainer cannot see what the trainee is doing, and vice versa. In addition to this, medics rarely get the chance to practice the examination, as few patients would volunteer as practice subjects. In fact there is only one person registered in the country as a test subject, called a Rectal Teaching Assistant (RTA) in the UK."
Rather than rely on that one person with a pain-in-the-butt job, the scientists' robobottom is designed to feel far more authentic than existing plastic models. The user slips their finger inside a silicone thimble, and small robotic arms apply pressure to recreate the sensation of living tissue. Using a screen to display a 3D image of the anatomy allows both trainer and trainee to see what's happening in there.
The robotic rectum is customizable too, allowing trainers to program in a variety of scenarios and teach students the difference between a healthy and a potentially cancerous prostate gland.
Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.
Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.
GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains. Treating depression
An experiment in 2011 showed that a different type of gut bacteria, called Lactobacillus rhamnosus, can dramatically alter GABA activity in the brains of mice, as well as influencing how they respond to stress. In this study, the researchers found that this effect vanished when they surgically removed the vagus nerve – which links the gut to the brain – suggesting it somehow plays a role in the influence gut bacteria can have on the brain.
Strandwitz is now looking for other gut bacteria that consume or even produce GABA, and he plans to test their effect on the brains and behaviour of animals. Such work may eventually lead to new treatments for mood disorders like depression or anxiety.
“Although research on microbial communities related to psychiatric disorders may never lead to a cure, it could have astonishing relevance to improving patients’ quality of life,” said Domenico Simone of George Washington University in Ashburn, Virginia.
If you're having trouble shaking your cravings for doughnuts, hamburgers and pizza, the key to curbing them could come from a new supplement based on a compound released by gut bacteria. The appetite-suppressing supplement developed by scientists from England and Scotland is called inulin-propionate ester and was found to only affect cravings for high calorie foods.
As its name suggests, the inulin-propionate ester supplement developed by the researchers from the Imperial College in London and the University of Glasgow in Scotland is made from a type of fiber called inulin that contains propionate, a molecular compound released in the intestines by gut microbiota that sends signals to a person's brain to make them feel full.
The digestion of inulin on its own has previously been shown to trigger the release of appetite-suppressing propionate by bacteria in the gut, but the team discovered that eating inulin-propionate ester resulted in the release of much more propionate in the intestines than inulin alone, and therefore had a much greater effect on appetite and weight gain. The team's latest study has now shed light on the reasons for this.
Imagine a pill-dispensing, health-focused version of Amazon Echo, and you'll get an idea of what Pillo is designed to be. Utilizing facial and voice recognition software, the internet-connected device can reportedly recognize multiple family members on sight, giving them their daily medication while also addressing their health and wellness-related inquires.
The tamper-proof dispenser can store different pills for multiple users, keeping track of who has and has not taken their daily dosage. In cases of medication that can't be stored onboard (such as liquids), audio and visual reminders are still offered. Users are notified when their pill supply is running low – Pillo can even order refills for them online, from a pharmacy of their choice.
Up to 250 medium-sized pills can be stored in the device at once. If a user doesn't take their medication for whatever reason, Pillo can send an alert to the smartphone of a caretaker or family member.
The brain looks like a featureless expanse of folds and bulges, but it’s actually carved up into invisible territories. Each is specialized: Some groups of neurons become active when we recognize faces, others when we read, others when we raise our hands.
On Wednesday, in what many experts are calling a milestone in neuroscience, researchers published a spectacular new map of the brain, detailing nearly 100 previously unknown regions — an unprecedented glimpse into the machinery of the human mind.
Scientists will rely on this guide as they attempt to understand virtually every aspect of the brain, from how it develops in children and ages over decades, to how it can be corrupted by diseases like Alzheimer’s and schizophrenia.
“It’s a step towards understanding why we’re we,” said David Kleinfeld, a neuroscientist at the University of California, San Diego, who was not involved in the research.
Scientists created the map with advanced scanners and computers running artificial intelligence programs that “learned” to identify the brain’s hidden regions from vast amounts of data collected from hundreds of test subjects, a far more sophisticated and broader effort than had been previously attempted.
Coxsackievirus B can be deadly, leading to heart disease and, in some cases, death. Now scientists at Colorado State University (CSU) have developed a method to combat the virus. Described as a "genetic poison pill," the technique restricts the ability of the virus to replicate and can even cause it to self-destruct. The approach could one day lead to a vaccine against coxsackievirus B and similar viruses.
Led by CSU professor Olve Peersen, previous research into how coxsackievirus copies itself and mutates focused on the RNA-dependent RNA polymerase responsible for replication. For this follow-up project, Peersen and the team worked with the specific strain, coxsackievirus B3, and modified that replicating polymerase so it fights against itself.
As the polymerase replicates the virus genome, it makes several random mistakes in order to continue evolving. The researchers were able to "outsmart Mother Nature," as Peersen puts it, by swapping out one amino acid in the polymerase for another, resulting in a checkmate effect on the virus.
Not so far in the future, your doctor might prescribe playing a few games in virtual reality to ease aches and pains, rather than popping a pill.
That’s Matthew Stoudt’s hope, anyway. He’s the CEO of AppliedVR, a startup that’s building a library of virtual-reality content for alleviating pain and anxiety before, during, and after medical procedures. The company is working with hospitals and doctors to get patients using the technology on Samsung’s Gear VR headset and to study its effectiveness as well.
So far, the company has created three different virtual-reality pain applications, as well as one for reducing anxiety, Stoudt says, and it’s using some third-party content, too. Headsets running AppliedVR’s platform are being used in hospitals, doctors’ offices, and clinics for things like drawing blood and administering epidurals, as well as for pain management after operations.
Scientists have for the first time watched the human brain making a purely voluntary decision to act.
Unlike in brain imaging studies where researchers watch as people respond to cues or commands, Johns Hopkins researchers found a way to observe people’s brain activity as they made choices entirely on their own.
The findings, which pinpoint parts of the brain involved in decision-making and action, were recently published in the journal Attention, Perception, and Psychophysics.
“How do we peek into people’s brains and find out how we make choices entirely on our own?” asks Susan Courtney, a professor of psychological and brain sciences and senior author of the study. “What parts of the brain are involved in free choice?”
Early in our 40s, we may start to notice it’s harder to remember things, like where we left our car keys. But researchers say this decline in memory may not really be a decline at all.
Rather, they say it may be the result of a change in what information the brain focuses on during memory formation and retrieval.
“This change in memory strategy with age may have detrimental effects on day-to-day functions that place emphasis on memory for details such as where you parked your car or when you took your prescriptions,” says Natasha Raj, associate professor in the psychiatry department at McGill University.
Brain changes associated with dementia are now thought to arise decades before the onset of symptoms. So a key question in current memory research concerns which changes to the aging brain are normal and which are not.
But Rajah says most of the work on aging and memory has concentrated on understanding brain changes later in life.
“So we know little about what happens at midlife in healthy aging and how this relates to findings in late life. Our research was aimed at addressing this issue.”
The mere mention of a 'faecal transplant' might be something that makes a lot of us squirm, but the truth is that poo transplants from one person to another are an increasingly popular treatment for a range of illnesses.
But what's actually in a poo transplant that makes it so beneficial to the recipient? A new study has shed light on exactly what our poo is made of, in the hopes of figuring out how poo transplants actually work.
"There is no doubt that poo can save lives," says biologist Seth Bordenstein from Vanderbilt University. "Right now faecal transplants are used as the treatment of last resort, but their effectiveness raises an important question: When will doctors start prescribing them, or some derivative, first?"
Faecal transplants actually go way back, with evidence of the treatment being used in China as long ago as the 4th century. More recently, in the 16th century, poo transplants were given the nickname "yellow soup", but it's only been in the past five years that interest in the treatment in contemporary Western science has picked up.
Alcohol can be a destructive substance when drinking gets out of control, but a recent neurological discovery could lead to a way to help people break addictive cycles. Scientists from the Texas A&M College of Medicine identified the neurons in the brain that enable and discourage drinking habits in mice.
The study, which was published in the most recent issue of the medical journal Biological Psychiatry, says that neurons located in the dorsomedial striatum, the part of the brain that facilitates goal-driven behavior located in the subcortical part of the forebrain, could play a major role in controlling alcohol addiction.
The neurons studied have small, spiny protrusions branching off of them called D1 or D2. Neurons with D1 protrusions encourage actions while neurons with D2 protrusions discourage actions. A previous study by the same team of researchers published in August of last year in the Journal of Neuroscience found that the D1 neuron drove mice to consume more alcohol. The newest study extends from that research and identifies the D2 neuron as the receptor that can stop mice from seeking out another drink when they've had a few too many already.
The next time you feel hungry even though you've already eaten a big meal, the culprit may be a certain protein. A new study shows that the protein AMPK regulates the neurons in the brain responsible for making you feel hungry. The findings may have implications in the treatment of obesity.
Researchers from Tufts University School of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School participated in the study that discovered a link between the protein and the neurons. The study indicates that the metabolic sensor protein AMPK activates agouti-related peptide (AgRP) neurons located in the brain's hypothalamus.
Researchers used mice to examine the role that the AMPK plays in the neurological behavior patterns of feeling hungry. They engineered some of the mice to continuously activate the AMPK protein whether or not they had been fed, and found these mice also had an increase in AgRP neuron activity, food consumption and weight gain. The mice with increased AMPK activity also showed an increase in the formation of AgRP dendritic spines, the membranous structures along neurons that receive synaptic inputs from other neurons.
Regenerative dental fillings that allow teeth to heal themselves have been developed by researchers, potentially eliminating the need for root canals.
The treatment, developed by scientists from the University of Nottingham and Harvard University, earned a prize from the Royal Society of Chemistry after judges described it as a “new paradigm for dental treatments.”
The tooth filling works by stimulating stem cells to encourage the growth of dentin—the bony material that makes up the majority of the tooth—allowing patients to effectively regrow teeth that are damaged through dental disease.
This is a significant step forward from current methods to treat cavities, which involve drilling out the decay and putting in a filling. When these fail, a root canal is needed to remove the pulp of the tooth and damage it even further.
“Existing dental fillings are toxic to cells and are therefore incompatible with pulp tissue inside the tooth,” said Adam Celiz, a Marie Curie research fellow at the University of Nottingham. “In cases of dental pulp disease and injury a root canal is typically performed to remove the infected tissues.
“We have designed synthetic biomaterials that can be used similarly to dental fillings but can be placed in direct contact with pulp tissue to stimulate the native stem cell population for repair and regeneration of pulp tissue and the surrounding dentin.”
The scientists are now hoping to develop the technique with industry partners in order to make it available for dental patients as an alternative to traditional fillings.
In an attempt to gain new ground in the battle against obesity, the Food and Drug Administration recently approved a device, called the AspireAssist, that enables users to empty the contents of their stomach via a surgical-inserted tube following consumption of a meal. Dean Kamen, inventor of the Segway, came up with the idea for the device and developed it with the help of physicians that specialize in the treatment of obesity. About 20 to 40 minutes after eating, users just pop to the bathroom, connect a longer tube to a hole in their body that is directly connected to their stomach, and drain 30 percent of their consumed food right into the toilet.It’s clear how the device might lend itself well to reflexive disgust. Online media outlets coined the term “medical bulimia” to describe the immediately apparent similarities with the eating disorder bulimia nervosa—compulsive eating and purging. “Is this new device simply a condemnable medical bulimia machine?” read the first line of one story. Another concluded “this terrifying invention is also, let’s face it, an automatic bulimia machine.” But to dismiss this device as “medical bulimia” shows both a misunderstanding of the eating disorder and also vastly overestimates how easy it is for those with morbid obesity to lose weight.
The birth of Dolly the sheep seemed one of those moments in scientific research that would change the world forever.
The cloning of the first animal from an adult cell was a remarkable scientific achievement. It promised new treatments for debilitating diseases. But it also raised fears of cloned human beings, designer babies and a dystopian future.
Twenty years on, neither the hopes nor the hype have been realised. So what is Dolly's legacy?
I first saw Dolly in 1997 at the Roslin Institute just outside Edinburgh. She stood apart from the other sheep in the pens at this agricultural research centre. She stood prouder, her fleece seemed like a lion's mane and there was an aura about her.
Dolly's creation had echoes of Mary Shelley's classic novel Frankenstein, in which inanimate tissue was brought to life by electricity.
Dolly was created from a skin cell taken from a frozen leg of a sheep that was long dead. The technique involved zapping it with electricity which turned the skin cell into an embryo.
Researchers at Roslin then implanted the embryo into the womb of a sheep which grew into Dolly - an exact genetic copy of the sheep from which the skin cell was taken.
It took 277 attempts to clone Dolly. There were many miscarriages and deformed births on the way.
There were also genuine concerns that it would not be long before cloned humans would soon be walking the Earth - people would try to clone themselves to achieve a kind of immortality or they might try to resurrect a beloved dead relative.
The airwaves were filled with conversations about what it meant to be human, whether the clones would be exactly the same as the person from which they were cloned and what kind of world the scientists were tumbling us into.
Sufferers of type 1 diabetes are required to constantly monitor their blood glucose levels and administer insulin as needed. But the daily hassle of self-care for patients could soon be reduced, with a new study concluding that automated "artificial pancreas" systems could be available in as little as two years.
The study, authored by Doctors Roman Hovorka and Hood Thabit of Cambridge University, reviews the overall progress of technology in these automated systems, including the bionic pancreas being developed by Boston University scientists.
Currently, treatment for type 1 diabetes generally requires two separate processes. Patients need to manually monitor their blood glucose levels several times a day with a fingerstick blood test, and if readings are low they may need to use an insulin pump. These pumps are automated devices which clip to clothing and administer a base-line level of insulin through a catheter under the skin, with patients manually telling the pump to inject additional doses when they eat.
The artificial pancreas combines those two separate processes into one "closed-loop" system. A needle under the skin continuously monitors blood glucose levels and automatically administers insulin as required, removing the burden of patient self-care and ensuring a more consistent glucose level than current pumps.
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