The silent missile that can cripple enemy’s electronics with PULSES


  • Named counter-electronics high-powered microwave advanced missile
  • Weapon destroys electronic systems without hurting people or buildings
  • Champ is now an ‘operational system already in [the] tactical air force’ 
  • Joint Air-to-Surface Standoff Missile-Extended Range has been chosen as the delivery vehicle

From Ocean’s Eleven to Star Trek, weapons that wipe out enemy electronics are a staple of science fiction films.

For years, scientists have been attempting to create such a weapon as part of Champ, or the Counter-electronics High-powered microwave Advanced Missile Project.

Now, the US Air Force claims it has advanced the technology, and says it can deploy it using the stealthy Joint Air-to-Surface Standoff Missile-Extended Range (JASSM).

For years, scientists have been attempting to turn fantasy into reality by working on a system known as Champ, or Counter-electronics High-powered microwave Advanced Missile Project

For years, scientists have been attempting to turn fantasy into reality by working on a system known as Champ, or Counter-electronics High-powered microwave Advanced Missile Project

HOW DOES IT WORK?

The missile is equipped with an electromagnetic pulse cannon.

This uses a super-powerful microwave oven to generate a concentrated beam of energy.

The energy causes voltage surges in electronic equipment, rendering them useless before surge protectors have the chance to react.

The aim is to destroy an enemy’s command, control, communication and computing, surveillance and intelligence capabilities without hurting people or infrastructure.

According to Foxtrot Alpha, once integrated into JASSM, Champ will be a ‘first day of war’ standoff weapon.

Because it can be launched by both bombers and fighters, Lockheed’s Joint Air-to-Surface Standoff Missile, or JASSM, is an ideal platform for Champ.

‘The capability is real … and the technology can be available today,’ said Major General Thomas Masiello, the Air Force Research Laboratory.

‘That’s an operational system already in our tactical air force’

In 2012, aircraft manufacturer Boeing successfully tested the weapon on a one-hour flight during which it knocked out the computers of an entire military compound.

During Boeing’s experiment, the missile flew low over the Utah Test and Training Range, discharging electromagnetic pulses on to seven targets, permanently shutting down their electronics.

Boeing said that the test was so successful even the camera recording it was disabled.

Although the project is shrouded in secrecy, experts believe the missile is equipped with an electromagnetic pulse cannon.

This uses a super-powerful microwave oven to generate a concentrated beam of energy which causes voltage surges in electronic equipment, rendering them useless before surge protectors have the chance to react.

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The 5 fastest ways that men die


Here are five other afflictions that are more likely to strike you down cold before you can even blink—and what to do to survive them.

 

Instant killer: Hypertrophic cardiomyopathy

About one in 500 people have some form of this heart disorder, which causes the walls of your heart muscle to thicken and lose their pumping power. Approximately 1 percent of people with the disorder die suddenly each year, usually because of a too-rapid heartbeat—and many of them are young and unaware they even have heart issues.

In fact, hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in people younger than 30. If you hear of an athlete falling dead on the field, this condition often takes the blame.

Survive it: Most cases of hypertrophic cardiomyopathy are genetic, says Jil Tardiff, M.D., Ph.D., of the University of Arizona College of Medicine.

Sit down with mom, dad, and grandma and ask if anyone in your family died young, of any cause. Many deaths that appear accidental—drowning, single-car wrecks, falls off a horse or motorcycle—actually occur when people with undetected cardiomyopathy go into sudden cardiac arrest, Dr. Tardiff says.

If you do have a suspicious family history, your doctor will probably recommend tests like an electrocardiogram and ultrasound. Plus, you should stay extra alert for warning signs, such as unusual shortness of breath, fainting, and fluttering heartbeats you haven’t had before.

People diagnosed with hypertrophic cardiomyopathy can work with a cardiologist to manage it—and avoid sudden death.

Medications, defibrillators, and sometimes surgery can help. And you’ll want to follow a carefully tailored exercise program. Sure, you might have to skip out on some sports that involve contact or start-and-stop action, like football, but you don’t want to be a couch potato with a heart condition, Dr. Tardiff says.

 

Instant killer: Faulty heart wiring

While cardiomyopathy changes your ticker’s shape and structure, another group of heart issues affects the electrical system that controls and synchronizes its beats, Dr. Wydro says. Rare but serious conditions such as Brugada syndrome, long QT syndrome, and Wolff-Parkinson-White syndrome scramble the signals that direct your heart to beat normally.

You might not have any signs until your heart’s lower chambers, the ventricles, start quivering instead of pumping properly—and you keel over.

Survive it: Genetics play a big role here, too, so climb your family tree with your doctor. Tests such as electrocardiograms and exercise stress tests can identify these conditions.

Like hypertrophic cardiomyopathy, you can work with a specialist to manage them using medications, pacemakers, and frequent follow-up visits, among other treatments.

The typical heart-healthy lifestyle can reduce the risk of sudden death even in people with these predispositions, Dr. Wydro says. Don’t smoke, and cut back on your boozing, since alcohol increases your likelihood of abnormal heart rhythms.

And tell your M.D. if you have bad dreams—nightmares and nighttime thrashing sometimes signal Brugada syndrome, which often kills people in their sleep.

 

Instant killer: Brain aneurysm

About 3 to 5 million Americans have one of these abnormal bulges in the wall of a brain blood vessel, according to the American Stroke Association.

Most linger silently, causing no symptoms. But according to a recent study in the journal Stroke, about one third of the aneurysms eventually rupture—an event that proves fatal about 40 percent of the time.

Survive it: Don’t blow off a sudden, severe headache—especially if it goes hand in hand with strange symptoms like a droopy eyelid, double vision, or a single dilated pupil. That might signal the aneurysm pressing against nerves in your brain.

Early detection is key: If doctors find an aneurysm before it bursts open, they can repair it with surgery or other treatments.

Step up your vigilance if your doc says your blood pressure is on the high side, Dr. Wydro says. The harder your blood pushes against an aneurysm, the greater the chance it ruptures.

 

Instant killer: Aortic dissection

In 2003, this condition struck down actor John Ritter, tearing a hole in the wall of the major artery leaving his heart.

Doctors aren’t sure exactly what causes these rips, but they can trigger blood to flow where it shouldn’t—or even a complete rupture of the aorta, which typically proves fatal. Aortic dissection occurs in only about two in every 10,000 people, but most are men ages 40 to 70, notes the National Institutes of Health.

Survive it: Sudden and excruciating pain in your chest or back serves as the main sign of aortic dissection, so get medical help if you experience it.

Before that, know your risk: It’s higher if you had a family member with the condition or if you have a connective tissue disorder like Ehlers-Danlos syndrome, which causes stretchy skin and super-flexible joints.

These diseases result in fragile blood vessels that rip more easily, Dr. Wydro says, so people who have them should seek medical attention for any unexplained chest or back pain (not just the most severe).

And, oddly, make sure you get a flu shot. According to research presented last year at the American Heart Association’s Scientific Sessions, hospital admissions for aortic dissections spike in peak flu season, perhaps because an inflammatory reaction to the virus triggers a tear in susceptible people.

 

Instant killer: Pulmonary embolism

Half of people with these blood clots in their lungs have no symptoms at all. But for 100,000 Americans per year, the clots block blood flow, jack up blood pressure in the lungs, and work the heart so hard it can’t keep up.

In fact, sudden death serves as the first symptom of a pulmonary embolism about a quarter of the time.

Survive it: Watch out for signs of blood clots elsewhere in your body, such as your legs and arms, Dr. Wydro says.

Treating them with blood-thinning medication can prevent them from breaking loose and traveling to your lungs.

Red flags include pain and swelling in one arm or leg that doesn’t go away within a day or two, especially if you’ve recently broken a bone, taken a long flight, or otherwise spent time not moving around very much.

Brain implant that decodes intention will let us probe free will .


Imagine a world where you think of something and it happens. For instance, what if the moment you realise you want a cup of tea, the kettle starts boiling?

That reality is on the cards, now that a brain implant has been developed that can decode a person’s intentions. It has already allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity.

But the implications go far beyond prosthetics. By placing an implant in the area of the brain responsible for intentions, scientists are investigating whether brain activity can give away future decisions – before a person is even aware of making them. Such a result may even alter our understanding of free will.

Fluid movement

“These are exciting times,” says Pedro Lopes, who works at the human-computer interaction lab at Hasso Plattner Institute in Potsdam, Germany. “These developments give us a glimpse of an exciting future where devices will understand our intentions as a means of adapting to our plans.”

The implant was designed for Erik Sorto, who was left unable to move his limbs after a spinal cord injury 12 years ago. The idea was to give him the ability to move a stand-alone robotic arm by recording the activity in his posterior parietal cortex – a part of the brain used in planning movements.

“We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, ‘I want to pick up that cup’,” Richard Andersen at the California Institute of Technology in Pasadena told delegates at the NeuroGaming Conference in San Francisco earlier this month.

Two tiny electrodes implanted in Sorto’s posterior parietal cortex were able to record the activity of hundreds of individual neurons. After some training, a computer could match patterns of activity with Sorto’s intended movement. Once this neuronal information had been collected, a computer translated Sorto’s intentions into movements of a robotic arm. This enabled him to control the speed and trajectory of the arm, so he could shake hands with people, play rock, paper, scissors and swig a beer at his own pace.

Read more about Sorto’s implant hereMovie Camera.

Desires laid bare

The breakthrough raises the tantalising possibility of using other intentions decoded from brain activity to control our environment. For example, could we identify the pattern that corresponds to the thought of wanting to watch a film, then have that switch on the television?

To investigate the feasibility, Andersen’s team had a person with a similar implant to Sorto’s play a version of the prisoner’s dilemma, where players can either collaborate or double-cross one another. The team was able to predict the volunteer’s decision based on the neural activity the implant recorded. This showed that more abstract decisions such as, in this case, the intention to snitch on a hypothetical partner, can indeed be decoded from the posterior parietal cortex.

Ori Cohen from the Advanced Virtuality Lab at the Interdisciplinary Center in Herzliya, Israel, says that using abstract commands for brain-computer interfacesMovie Camera is a promising idea. “After all, this is how we control our body – we have a goal such as getting coffee and our brain kick-starts a range of processes involving complex geometrical computations in order to achieve it,” he says.

Eventually, he believes that a person with paralysis could imagine themselves making a cup of coffee and have a humanoid robot automatically carry out the action. He is hopeful that such approaches could one day be achieved using non-invasive techniques, such as recording brain activity with an EEG headset, rather than having to embed electrodes in the brain.

Probing free will

Others are not so sure. “It’s hard to get really high-quality brain signals with non-invasive technology,” says Jörn Diedrichsen, a neuroscientist at University College London. He thinks this might be off-putting to those who have no medical need to link up with their environment. “You have to ask whether you’d want to have invasive surgery to not have to press a button on a remote control,” he says. “It might be technically possible in five to 10 years, but would you do it?”

The most intriguing aspect of Andersen’s work, he says, is that we are now able for the first time to record the brain activity underlying intentions while asking about a person’s conscious experience. For example, Andersen’s team has already started to repeat classic free will experiments in which researchers try to use brain activity to predict a person’s decisions before they are consciously aware of making any.

“We will be able to look carefully into big philosophical questions of whether a person’s future decisions can be decoded from their neural activity before the individual is aware of having formed them – and what that all means for our ideas on free will,” says Diedrichsen. “It really captures the imagination.”

Journal reference: Science, doi.org/4tp

Mind control in your living room

(Image: FOC.US)

As our ability to decode brainwaves improves, the market for mind-reading devices that can be used at home is growing. Some estimates predict this market could be worth as much as $6 billion by 2020. At the NeuroGaming Conference in San Francisco this month, companies were showing off a range of devices – scientifically validated to varying degrees.

An example is NeuroMage – one of the first computer games to harness the power of the mind to control a character using an EEG headset. Players must use certain kinds of thoughts to build up an armoury of spells to cast on opponents.

If you have trouble concentrating, MUSE might be more up your street. This app, combined with an EEG headset, teaches you to focus your attention using brain training exercises, and promises to improve your emotional well-being. The system is being tested by several US universities.

Then there’s Foc.us EDGE – the world’s first brain stimulation device aimed at improving your fitness. It involves a portable headset that sends a low current to the temporal lobe. The idea comes from astudy in which professional cyclists showed a 4 per cent improvement in stamina when they received a similar kind of stimulation. The researchers involved – who have not endorsed any Foc.us product – suggest that stimulating the temporal lobe can affect how difficult a workout feels.

While there is no evidence to suggest that short bursts of stimulation can damage the brain, many researchers at the conference were still wary of such devices, since they do not need to be approved by medical regulators.

This Self-Powered, Eco-Friendly Tiny House Lets You Dwell Anywhere On Earth


If you’ve ever wished you could post up on a mountaintop forever, then meet your new home.

Ecocapsule is a tiny, 86 square-foot living capsule that, as soon as next year, will enable owners to live virtually anywhere. Each mobile pod comes with sleeping space for two, a mini kitchen, a fully functional toilet and shower, storage space, a desk and two windows.

The pods, which are currently in pre-production, harvest rainwater and remove bacteria all on their own, while powering themselves with sun and wind. The capsule’s battery can also charge electric cars, Gizmodo reports, making the location possibilities breathtakingly endless — from beaches to jungles to wide-open prairies.

Pricing for the Ecocapsules is not yet available, but Slovakia-based Nice Architects doknow that shipping the pods to the U.S. will not be cheap — it’s estimated to cost about $2,400 to have a pod shipped to New York City.

Or you could just skip all the kerfuffle and build your own wooden cabin. Ahh, the great outdoors.

What ‘Type A’ people want you to know


Ambitious. High strung. Perfectionist.

Type A individuals are known for rather uptight behavior, but just like any other personality trait, there’s more to us than what you see on the surface. To know a Type A person is to love them — flaws and all. Below are just a few things Type A people want you to know about the personality.

1. We’re not impatient, just efficient.

Long lines? Traffic? Type A individuals loathe them all. This is because we feel as though they’re slowing our progress of a certain goal, according to John Schaubroeck, a professor of psychology and management at Michigan State University — even if that goal is just to deposit a check at the bank.

2. Arriving late to anything is agonizing.

If you tell us to be somewhere at 6:30, more likely than not, we’re rolling up to the parking lot at 6:25. Type A folks tend to have an oversensitivity to time, because we don’t want to feel like we’re wasting it.

3. We live by to-do lists.

How else are we supposed to track what we’re supposed to get done?!

4. Each task we’re assigned is urgent.

Because of this, we value team members who work with the same brevity and speed that we do. Once again, wasting time is our ultimate enemy. Type A workers “appreciate individuals that can communicate in a clear, concise and succinct manner,” psychologist and project management executive Bernado Tirado wrote in a Psychology Today blog post.

5. We’re extremely goal-oriented.

Once we commit to something, we see it through until the very end, whether it’s a work project or Friday night plans. “[Type A’s] are certainly more occupied with achieving outcomes,” Schaubroeck previously told HuffPost Healthy Living. “And given that they’re so occupied with achieving their goals, it makes sense that they would be more likely to do so.”

6. It’s hard for us to relax.

This is where time sensitivity comes into play again. We hate the idea of letting time pass if there’s something we need to be doing, so relaxing in the middle of our workday is a bit of a challenge (but necessary, as research shows). Downtime tends to feel unproductive to Type A folks — unless, of course, it’s on our to-do list.

7. We get stressed out easily.

According to Friedman, certain personalities — like Type A — are more sensitive to stress (which, as we know, is terribly bad for our health). We also tend to default on the worst possible outcome when working through a situation. Sorry in advance for the slight negativity.

8. We have nervous habits.

For me, it’s hair twirling. For others, it’s nail biting or teeth grinding. This behavior is common for Type A personalities, according to cardiologist and personality researcher Meyer Friedman.

9. We’re emotional.

The reason we behave the way that we do is because we care (some could even argue that we care just a little too much). Researchers suggest that Type A people are highly conscientious — so while it may seem like we’re uptight when we’re organizing our friend’s birthday party, it’s really just because we want it to be spectacular. They deserve it.

10. We’re constantly ruminating over something.

You know when you just replay a mistake over and over in your head? This is a common occurrence for Type A individuals. We are notorious for dwelling on our worries, sometimes to the point where it keeps us up at night.

11. We have a competitive side.

This is perhaps one of our most glaring flaws. Type A’s put a lot of pressure on themselves to be the best possible version of themselves, which sometimes is taken to mean “the best person in the room.” It doesn’t matter if it’s a work assignment or a board game, they’re all the same to a Type A personality.

Everyone has their strengths and weaknesses, and Type A people are no exception. We mean well though, we promise.

Study reveals autism’s ‘noisy’ secret


human brain artwork

3-D simulator provides multi-sensory experience of motion through a ‘star field,’ and reveals the inner workings of the autistic brain

Strapped into a motion-enabled simulator and wearing 3D glasses, 36 adolescent volunteers recently experienced what it was like to “travel” through a field of virtual stars. The experiments provided new and convention-busting data about how sensory stimuli are processed by the brains of individuals with autism spectrum disorder (ASD).

The study, entitled “Self-motion perception in autism is compromised by visual noise but integrated optimally across multiple senses,” is published online in the Proceedings of the National Academy of Sciences. The authors of the study are Adam Zaidel, of Israel’s Bar-Ilan University, and Robin P. Goin-Kochel and Dora E. Angelaki, of Baylor College of Medicine in the United States.

Perceptual Impairment in Autism – a “Noisy” Controversy

One of the hallmarks of ASD is superior low-level task performance alongside reduced performance in tasks that involve the processing of complex sensory data. This has led to the assumption that autism is characterized by a difficulty integrating individual units of perceptual data into global concepts. In line with this first assumption, it has further been proposed that individuals with autism have difficulty integrating multi-sensory input.

With its unique experimental set-up, the new study has successfully challenged this conventional wisdom. Moreover, it has identified a neurological phenomenon associated with autism pathology: a heightened sensitivity to “noisy” sensory signals.

“Theories of global and multisensory integration deficits in ASD are deeply rooted in the scientific conversation about autism,” says Dr. Adam Zaidel, a member of Bar-Ilan University’s Gonda (Goldschmied) Multidisciplinary Brain Research Center, who is the publication’s lead author. “Recently, this notion has come under scrutiny, as more and more investigators have observed discrepancies with experimental results.”

“In this study we show that heightened sensitivity to sensory noise – the random signals inserted into the visual tasks traditionally used by scientists to test sensory integration levels in autism – may provide an alternative explanation for impaired performance. When this noise is removed from the equation, the integration of visual motion stimuli in ASD is equal to, or maybe even superior to that of the control group. Moreover, our study demonstrates that the multi-sensory integration seen in autistic participants was comparable to that of the non-autistic control group.”

A Problematic “Twist” in Traditional Testing: Noise

Zaidel explains that visual motion processing in ASD has generally been examined through the use of a computer-based tool in which study participants are asked to designate the overall direction of motion of a field of dots, while a certain number of dots – the “noise” in an otherwise coherent picture – are randomly displaced. In these experiments, the level of noise at which participants can no longer determine overall direction is seen as a measure of the participant’s innate ability to integrate isolated visual stimuli into a global picture.

Zaidel’s new approach proves that such traditional methods – which depend on noise as a modulator of task difficulty – have led to widespread misinterpretation of how individuals with ASD integrate visual stimuli.

“Our study is carried out in a 3D environment in which a field of moving dots generates the feeling of traveling through space, with different trials ‘steering’ to the right or left of straight ahead,” Zaidel says. “By asking participants to indicate their perceived direction of movement, we test their ability to create a global picture out of individual details. Significantly – and this is where our method differs from previous tests – we can achieve measureable results both when randomized dots are included in the overall picture, and in a completely coherent, noise-free environment.”

Zaidel says that when there were no randomly-moving dots, autistic participants performed well, successfully determining the direction of movement at a level similar to that achieved by the non-ASD control group. When the noisy signals were introduced, however, the ASD group was significantly more affected than controls. This indicates that it is the presence of noise – rather than any innate integration deficit – that makes the task more difficult for people with autism.

No Deficit: Re-Thinking Multi-Sensory Integration in ASD

The unique experimental platform also allowed Zaidel to challenge another theory that has emerged more recently: that people with ASD are neurologically pre-disposed toward deficient integration of multi-sensory stimuli.

The simulator used in the study was equipped with an ability to introduce movement into the chair in which the study participant was sitting – requiring the participant to respond to and interpret visual and vestibular stimuli at the same time.

“By adding movement to the experiment, we created a situation in which participants didn’t just see the direction of the movement, but felt it as well,” he says. “In this scenario, people with autism displayed intact multi-sensory integration, completing tasks in a normative manner, both in a coherent, noiseless environment, and even when noise was present. These findings raise questions about prevalent theories related to multi-sensory integration deficits in ASD.”

Autism Thinks: Processing Sensory Stimuli vs. Accessing Prior Knowledge

According to Zaidel, the new study provides support for the idea that people with autism are highly sensitive to incoming sensory information. Moreover, he suggests, they are predisposed toward relying more highly on external stimulation – with less use of prior knowledge – when interpreting the world around them.

“Our results suggest that people with autism may experience a deficiency in what are known in the scientific literature as Bayesian priors – the ability to draw on existing knowledge to understand what we see and to predict what we will see in the near future,” Zaidel says. “If you’re more heavily weighted toward perceiving the world bottom up – from stimulus to perception – and relying less on rules of thumb from prior knowledge, perception will be both more taxing, and more sensitive to sensory noise.”

In the future, Zaidel says, it may someday be possible to study this phenomenon directly in the brain, or to create treatments that might help autistic individuals become more adept at re-connecting to and using prior knowledge. However, he adds, future advances will depend on getting a clearer picture how the autistic brain processes sensory information and priors.

“In recent years, predominant theories about the nature of autism have become the subject of debate in the scientific community,” he says. “At the same time, the incidence of ASD diagnosis is on the rise. It is vitally important to understand autism’s underlying neuropathology, so that scientists can create the studies that have the best chance of helping us face this challenge.”

Effects of Estradiol Withdrawal on Mood in Women With Past Perimenopausal Depression


Importance  Perimenopause is accompanied by an increased risk of new and recurrent depression. The coincidence of declining ovarian function with the onset of depression led to the inference that “withdrawal” from physiologic estradiol levels underpinned depression in perimenopause. To our knowledge, this is the first controlled systematic study to directly test the estrogen withdrawal theory of perimenopausal depression (PMD).

Objective  To examine the role of estradiol withdrawal in PMD.

Design, Setting, and Participants  Initial open-label treatment with estradiol followed by randomized, double-blind, placebo-controlled, parallel-design evaluation of continued estradiol treatment was evaluated at an outpatient research facility at the National Institutes of Health Clinical Center. An intent-to-treat analysis was performed between October 2003 and July 2012. Participants included asymptomatic postmenopausal women with past PMD responsive to hormone therapy (n = 26) and asymptomatic postmenopausal women with no history of depression (n = 30) matched for age, body mass index, and reproductive status who served as controls. Data were analyzed between November 2012 and October 2013 by repeated-measures analysis of variance.

Interventions  After 3 weeks of open-label administration of transdermal estradiol (100 µg/d), participants were randomized to a parallel design to receive either estradiol (100 µg/d; 27 participants) or matched placebo skin patches (29 participants) for 3 additional weeks under double-blind conditions.

Main Outcomes and Measures  Center for Epidemiologic Studies–Depression Scale and 17-item Hamilton Depression Rating Scale (completed by raters blind to diagnosis and randomization status), self-administered visual analog symptom ratings, and blood hormone levels obtained at weekly clinic visits.

Results  None of the women reported depressive symptoms during open-label use of estradiol. Women with past PMD who were crossed over from estradiol to placebo experienced a significant increase in depression symptom severity demonstrated using the Center for Epidemiologic Studies–Depression Scale and 17-item Hamilton Depression Rating Scale, with mean (SD) scores increasing from estradiol (ie, 2.4 [2.0] and 3.0 [2.5]) to placebo (8.8 [4.9] and 6.6 [4.5], respectively [P = .0004 for both]). Women with past PMD who continued estradiol therapy and all women in the control group remained asymptomatic. Women in both groups had similar hot-flush severity and plasma estradiol levels during use of placebo.

Conclusions and Relevance  In women with past PMD that was previously responsive to hormone therapy, the recurrence of depressive symptoms during blinded hormone withdrawal suggests that normal changes in ovarian estradiol secretion can trigger an abnormal behavioral state in these susceptible women. Women with a history of PMD should be alert to the risk of recurrent depression when discontinuing hormone therapy.

Japanese scientists reverse ageing in human cell lines.


By altering the behaviour of two genes responsible for the production of simple amino acids in human cells, scientists have gained a better understanding of how the process of ageing works, and how we could delay or perhaps even reverse it.

The team, led by Jun-Ichi Hayashi at the University of Tsukuba, targeted two genes that produce the amino acid glycine in the cell’s mitochondria, and figured out how to switch them on and off. By doing this, they could either accelerate the process of ageing within the cell, which caused signifiant defects to arise, or they could reverse the process of ageing, which restored the capacity for cellular respiration. Using this technique to produce more glycine in a 97-year-old cell line for 10 days, the researchers restored cellular respiration, effectively reversing the cell line’s age.

The finding brings into question the popular, but more recently controversial, mitochondrial theory of ageing, which puts forward the notion that an accumulation of mutations in mitochondrial DNA leads to age-related defects in the mitochondria – often referred to as the cell’s powerhouses because they are responsible for energy production and cellular respiration. Defects in the cell’s mitochondria lead to damage in the DNA, and an accumulation of DNA damage is linked to age-related hair loss, weight loss, spine curvature, osteoporosis, and a decreased lifespan.

But is this theory accurate? The results of Hayashi’s study support an alternative theory to ageing, which proposes that age-associated mitochondrial defects are caused not by the accumulation of mutations in mitochondrial DNA, but by certain crucial genes being turned on and off as we get older.

The team worked with human fibroblast cell lines gathered from young people – from foetus-age to 12 years old – and the elderly, from 80 to 97 years old. They compared the capacity for cellular respiration in the young and old cells, and found that while the capacity was indeed lower in the cells of the elderly, there was almost no difference in the amount of DNA damage between the two. This calls into question the mitochondrial theory of ageing, the team reports in the journal Scientific Reports,and suggests instead that the age-related effects they were seeing were being caused by a process known as epigenetic regulation.

Epigenetic regulation describes the process where the physical structure of DNA – not the DNA sequence – is altered by the addition or subtraction of chemical structures or proteins, which is regulated by the turning on and off of certain genes. “Unlike mutations that damage that sequence, as in the other, aforementioned theory of ageing, epigenetic changes could possibly be reversed by genetically reprogramming cells to an embryonic stem cell-like state, effectively turning back the clock on ageing,” says Eric Mack at Gizmag.

Hayashi and his team supported this theory by showing that they could turn off the genes that regulate the production of glycine to achieve cellular ageing, or turn them on for the restoration of cellular respiration. This suggests, they say, that glycine treatment could effectively reverse the age-associated respiration defects present in their elderly human fibroblasts.

“Whether or not this process could be a potential fountain of youth for humans and not just human fibroblast cell lines still remains to be seen, with much more testing required,” Mack points out at Gizmag. “However, if the theory holds, glycine supplements could one day become a powerful tool for life extension.”

We’ll just have to wait and see. The faster we can solve the debate over how ageing actually works, the faster we can figure out how to delay it.

Tattoos Can Cause Serious, Long-Term, Adverse Reactions


Whether it’s a skull, cross, rose, or mom’s name in a thorn bush wrapped around the bicep, about one quarter of American adults have a tattoo. But a new study says about one out of every 10 inkers does not anticipate something that can come along with them: a severe, ongoing skin reaction.

Study: Tattoos Can Cause Serious, Long-Term, Adverse Reactions

In the just-published NYU Langone Medical Center research that studied tattoo-clad New Yorkers, those who reacted to tattoos experienced a rash, itching or swelling that lasted anywhere from four months to several years, with the longest-lasting complications stemming from ink shades of red and black.

“While we know infections are a risk of tattoos and can be dependent on tattoo parlor practices, a lot of the complications in our study — and that I have seen in my patients — do not have to do with the tattoo artist or parlor practices, but rather the qualities of ink and how the body’s immune system responds to it,” Marie C. Leger, MD, PhD, study lead and Assistant Professor at the Ronald O. Perelman Department of Dermatology, tells Yahoo Health.

The 300 respondents ranged in age from 18 to 69, with most having no more than five tattoos — and 67 percent of studied tattoos were on the arms. “We were rather alarmed at the high rate of reported chronic complications tied to getting a tattoo. Given the growing popularity of tattoos, physicians, public health officials and consumers need to be aware of the risks involved,” added Leger.

While less than a third of the affected study participants saw a doctor for the reaction, the majority returned to the tattoo parlor to complain or ask for guidance. “Tattoo artists are ‘first responders’ when people have problems,” says Leger, who adds that a planned follow-up study will examine what kind of reactions artists see most frequently, and how clients are directed, in an effort to get people to the right place for help.

Experts are not surprised by the news. “While tattoos are popular among Americans, there is still little to no regulation of what exactly is being injected into the skin,” says Jeremy A. Brauer, MD, dermatologist and Director of Clinical Research at Laser & Skin Surgery Center of New York, where he has seen patients with tattoo reactions — most often to red ink. The majority of patients have allergic contact dermatitis, which is marked by redness, swelling and itching in the area of the tattoo.

Treatment of tattoo reactions “can be challenging” says Brauer, who uses oral antihistamines combined with oral or injectable steroids to quell the inflammation. Blistering sometimes occurs and requires wound care and dressings, while evidence of infection is treated with antibiotics. More recently, there have been reports of successful laser treatment with both ablative and non-ablative fractional lasers, adds Bauer.

For some, the discomfort never completely goes away, and they are even driven to remove the tattoo altogether. While nanosecond (“Q-switched”) lasers have been the tattoo removal standard, the newer PicoSure laser is now clearing tattoos in “far fewer treatments than before,” says Bauer. The laser also addresses and improves scarring that can be an accompanying issue with tattoos.

And when it comes to tattoo removal, there’s one design that stands out as the one most people want to get rid of: 52 percent of RealSelf.com doctors say tribal tattoos are the style they most frequently are asked to remove, for any number of reasons – from discomfort to regret.

Looking ahead, Leger also has plans for a bigger survey to determine what tattoo dye components are most closely tied to adverse reactions. She hopes her investigation might also reveal other factors that put some people at higher risk of suffering chronic complications.

Standard vs Modified Antiplatelet Preparation for Preventing Thromboembolic Events in Patients With High On-Treatment Platelet Reactivity Undergoing Coil Embolization for an Unruptured Intracranial AneurysmA Randomized Clinical TrialStandard vs Modified Antiplatelet Preparation in Patients With Coil EmbolizationStandard vs Modified Antiplatelet Preparation in Patients With Coil Embolization


Importance  Thromboembolism is the most common complication in coiling for an unruptured aneurysm and is frequent in patients with high on-treatment platelet reactivity (HTPR) who are prescribed a standard antiplatelet preparation for its prevention.

Objective  To evaluate the effect of a modified antiplatelet preparation compared with a standard preparation in patients with HTPR undergoing coiling.

Design, Setting, and Participants  A prospective randomized open-label active-control trial with blinded outcome assessment at the Seoul National University Bundang Hospital from May 27, 2013, to April 7, 2014. Patients with HTPR were randomly assigned (1 to 1) to the standard or modified preparation group. Patients without HTPR were assigned to the non-HTPR group. A total of 228 patients undergoing coiling for unruptured aneurysms were enrolled and allocated to the study, 126 in the HTPR group (63 to the standard preparation group and 63 to the modified preparation group) and 102 to the non-HTPR group. Intent-to-treat analysis was performed.

Interventions  The modified preparation (HTPR to aspirin, 300 mg of aspirin and 75 mg of clopidogrel bisulfate; and HTPR to clopidogrel, 200 mg of cilostazol added to the standard regimen) was performed before coiling in the modified preparation group. Standard preparation (100 mg of aspirin and 75 mg of clopidogrel) was maintained in the standard preparation and non-HTPR groups.

Main Outcomes and Measures  The primary outcome was a thromboembolic event defined as thromboembolism during coiling and a transient ischemic attack or ischemic stroke within 7 days after coiling. The principal secondary outcome was a bleeding complication according to Thrombolysis in Myocardial Infarction bleeding criteria within 30 days after coil embolization.

Results  The thromboembolic event rate was low in the modified preparation group (1 of 63 [1.6%]) compared with the standard preparation group (7 of 63 [11.1%]; adjusted risk difference, −11.7% [95% CI, −21.3% to −2.0%]; P = .02), which had a higher thromboembolic risk than the non-HTPR group (1 of 102 [1.0%]; adjusted risk difference, 8.6% [95% CI, 1.0% to 16.3%]; P = .03). All bleeding complications were of minimal grade according to Thrombolysis in Myocardial Infarction bleeding criteria. The bleeding rate was not different between the modified (6 of 63 [9.5%]) and standard (4 of 63 [6.3%]) preparation groups (adjusted risk difference, 5.6% [95% CI, −4.2% to 15.4%]; P = .26).

Conclusions and Relevance  Modified antiplatelet preparation for patients with HTPR compared with standard antiplatelet preparation reduced the thromboembolic event rate in coiling for an unruptured aneurysm without increasing bleeding.