The Argument Against Quantum Computers


  The mathematician Gil Kalai believes that quantum computers can’t possibly work, even in principle.

Sixteen years ago, on a cold February day at Yale University, a poster caught Gil Kalai’s eye. It advertised a series of lectures by Michel Devoret, a well-known expert on experimental efforts in quantum computing. The talks promised to explore the question “Quantum Computer: Miracle or Mirage?” Kalai expected a vigorous discussion of the pros and cons of quantum computing. Instead, he recalled, “the skeptical direction was a little bit neglected.” He set out to explore that skeptical view himself.

Today, Kalai, a mathematician at Hebrew University in Jerusalem, is one of the most prominent of a loose group of mathematicians, physicists and computer scientists arguing that quantum computing, for all its theoretical promise, is something of a mirage. Some argue that there exist good theoretical reasons why the innards of a quantum computer — the “qubits” — will never be able to consistently perform the complex choreography asked of them. Others say that the machines will never work in practice, or that if they are built, their advantages won’t be great enough to make up for the expense.

Kalai has approached the issue from the perspective of a mathematician and computer scientist. He has analyzed the issue by looking at computational complexity and, critically, the issue of noise. All physical systems are noisy, he argues, and qubits kept in highly sensitive “superpositions” will inevitably be corrupted by any interaction with the outside world. Getting the noise down isn’t just a matter of engineering, he says. Doing so would violate certain fundamental theorems of computation.

Kalai knows that his is a minority view. Companies like IBM, Intel and Microsoft have invested heavily in quantum computing; venture capitalists are funding quantum computing startups (such as Quantum Circuits, a firm set up by Devoret and two of his Yale colleagues). Other nations — most notably China — are pouring billions of dollars into the sector.

Quanta Magazine recently spoke with Kalai about quantum computing, noise and the possibility that a decade of work will be proven wrong within a matter of weeks. A condensed and edited version of that conversation follows.

When did you first have doubts about quantum computers?

At first, I was quite enthusiastic, like everybody else. But at a lecture in 2002 by Michel Devoret called “Quantum Computer: Miracle or Mirage,” I had a feeling that the skeptical direction was a little bit neglected. Unlike the title, the talk was very much the usual rhetoric about how wonderful quantum computing is. The side of the mirage was not well-presented.

And so you began to research the mirage.

Only in 2005 did I decide to work on it myself. I saw a scientific opportunity and some possible connection with my earlier work from 1999 with Itai Benjamini and Oded Schramm on concepts called noise sensitivity and noise stability.

What do you mean by “noise”?

By noise I mean the errors in a process, and sensitivity to noise is a measure of how likely the noise — the errors — will affect the outcome of this process. Quantum computing is like any similar process in nature — noisy, with random fluctuations and errors. When a quantum computer executes an action, in every computer cycle there is some probability that a qubit will get corrupted.

Kalai argues that limiting the noise in a quantum computer will also limit the computational power of the system.

Video: Kalai argues that limiting the noise in a quantum computer will also limit the computational power of the system.

And so this corruption is the key problem?

We need what’s known as quantum error correction. But this will require 100 or even 500 “physical” qubits to represent a single “logical” qubit of very high quality. And then to build and use such quantum error-correcting codes, the amount of noise has to go below a certain level, or threshold.

To determine the required threshold mathematically, we must effectively model the noise. I thought it would be an interesting challenge.

What exactly did you do?

I tried to understand what happens if the errors due to noise are correlated — or connected. There is a Hebrew proverb that says that trouble comes in clusters. In English you would say: When it rains, it pours. In other words, interacting systems will have a tendency for errors to be correlated. There will be a probability that errors will affect many qubits all at once.

So over the past decade or so, I’ve been studying what kind of correlations emerge from complicated quantum computations and what kind of correlations will cause a quantum computer to fail.

In my earlier work on noise we used a mathematical approach called Fourier analysis, which says that it’s possible to break down complex waveforms into simpler components. We found that if the frequencies of these broken-up waves are low, the process is stable, and if they are high, the process is prone to error.

That previous work brought me to my more recent paper that I wrote in 2014 with a Hebrew University computer scientist, Guy Kindler. Our calculations suggest that the noise in a quantum computer will kill all the high-frequency waves in the Fourier decomposition. If you think about the computational process as a Beethoven symphony, the noise will allow us to hear only the basses, but not the cellos, violas and violins.

These results also give good reasons to think that noise levels cannot be sufficiently reduced; they will still be much higher than what is needed to demonstrate quantum supremacy and quantum error correction.

Why can’t we push the noise level below this threshold?

Many researchers believe that we can go beyond the threshold, and that constructing a quantum computer is merely an engineering challenge of lowering it. However, our first result shows that the noise level cannot be reduced, because doing so will contradict an insight from the theory of computing about the power of primitive computational devices. Noisy quantum computers in the small and intermediate scale deliver primitive computational power. They are too primitive to reach “quantum supremacy” — and if quantum supremacy is not possible, then creating quantum error-correcting codes, which is harder, is also impossible.

What do your critics say to that?

Critics point out that my work with Kindler deals with a restricted form of quantum computing and argue that our model for noise is not physical, but a mathematical simplification of an actual physical situation. I’m quite certain that what we have demonstrated for our simplified model is a real and general phenomenon.

My critics also point to two things that they find strange in my analysis: The first is my attempt to draw conclusions about engineering of physical devices from considerations about computation. The second is drawing conclusions about small-scale quantum systems from insights of the theory of computation that are usually applied to large systems. I agree that these are unusual and perhaps even strange lines of analysis.

And finally, they argue that these engineering difficulties are not fundamental barriers, and that with sufficient hard work and resources, the noise can be driven down to as close to zero as needed. But I think that the effort required to obtain a low enough error level for any implementation of universal quantum circuits increases exponentially with the number of qubits, and thus, quantum computers are not possible.

How can you be certain?

I am pretty certain, while a little nervous to be proven wrong. Our results state that noise will corrupt the computation, and that the noisy outcomes will be very easy to simulate on a classical computer. This prediction can already be tested; you don’t even need 50 qubits for that, I believe that 10 to 20 qubits will suffice. For quantum computers of the kind Google and IBM are building, when you run, as they plan to do, certain computational processes, they expect robust outcomes that are increasingly hard to simulate on a classical computer. Well, I expect very different outcomes. So I don’t need to be certain, I can simply wait and see.

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YALE UNIVERSITY STUDY FINDS LINK BETWEEN VACCINES & MULTIPLE BRAIN DISORDERS


It’s become a common question to ask if someone is anti- or pro-vaccination. With heavy arguments on either side and truths and lies at every turn, the controversy surrounding the topic seems only to heighten with each passing year. So when researchers find valuable information that is for or against vaccinations, it’s worth reading up.

 

Over the last 50 years, we’ve seen a devastating rise in brain disorders like Autism, ADHD, and major depressive disorders — a phenomenon that, understandably, has people searching for answers, particularly those directly affected. In this regard, an overwhelming amount of parents have reported that their children went from being seemingly healthy to suddenly suffering from disorders like Autism or ADHD as a result of vaccinations.

Now a team of researchers from the Yale School of Medicine and Penn State College of Medicine have lent further weight to many of these parents’ words. The study, which analyzed five years’ worth of private health insurance data on children ages 6-15, discovered that young people vaccinated in the previous three to 12 months were much more likely to be diagnosed with certain neuropsychiatric disorders than their non-vaccinated counterparts.

The study raises more questions among an already growing list regarding whether over-vaccination can cause immunological and neurological damage in vulnerable children. The research was published in the peer-reviewed journal Frontiers in Psychiatry, Jan. 19.

Over 95,000 children in the database that were analyzed were found to have one of  seven neuropsychiatric disorders: anorexia nervosa, anxiety disorder, attention deficit and hyperactivity disorder (ADHD), bipolar disorder, major depression, obsessive-compulsive disorder (OCD), and tic disorder. The children with these disorders were measured against those without such disorders, as well as children with two other conditions unrelated to vaccination: open wounds and broken bones.

The control subjects without brain disorders were matched with subjects based on age, geographic location, and gender. The researchers found, as they had imagined they would, that broken bones and open wounds had no association with vaccinations worth noting. Additionally, new cases of major depression, bipolar disorder, or ADHD showed no noteworthy link with vaccinations.

 The study did find, however, that children who had been vaccinated were 80% more likely to be diagnosed with anorexia and 25% more likely to be diagnosed with OCD than those who had not been vaccinated. Furthermore, vaccinated children had a higher risk of being diagnosed with an anxiety disorder and with tics compared to the controls.

“This pilot epidemiologic analysis implies that the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals,” the researchers wrote. “These findings warrant further investigation, but do not prove a causal role of antecedent infections or vaccinations in the pathoetiology of these conditions.”

They also caution that their research should by no means serve as a deciding factor for whether or not people should vaccinate their children. “Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines,” they said.

Scientists Officially Link Processed Foods To Autoimmune Disease.


microwave meals could be to blame for a sharp increase in autoimmune diseases such as multiple sclerosis, including alopecia, asthma and eczema.

processed-foodsA team of scientists from Yale University in the U.S and the University of Erlangen-Nuremberg, in Germany, say junk food diets could be partly to blame.

‘This study is the first to indicate that excess refined and processed salt may be one of the environmental factors driving the increased incidence of autoimmune diseases,’ they said.

Junk foods at fast food restaurants as well as processed foods at grocery retailers represent the largest sources of sodium intake from refined salts.

The Canadian Medical Association Journal sent out an international team of researchers to compare the salt content of 2,124 items from fast food establishments such as Burger King, Domino’s Pizza, Kentucky Fried Chicken, McDonald’s, Pizza Hut and Subway. They found that the average salt content varied between companies and between the same products sold in different countries.

U.S. fast foods are often more than twice as salt-laden as those of other countries. While government-led public health campaigns and legislation efforts have reduced refined salt levels in many countries, the U.S. government has been reluctant to press the issue. That’s left fast-food companies free to go salt crazy, says Norm Campbell, M.D., one of the study authors and a blood-pressure specialist at the University of Calgary.

Many low-fat foods rely on salt–and lots of it–for their flavor. One packet of KFC’s Marzetti Light Italian Dressing might only have 15 calories and 0.5 grams fat, but it also has 510 mg sodium–about 1.5 times as much as one Original Recipe chicken drumstick. (Feel like you’re having too much of a good thing? You probably are.

Bread is the No. 1 source of refined salt consumption in the American diet, according to the Centers for Disease Control and Prevention. Just one 6-inch Roasted Garlic loaf from Subway–just the bread, no meat, no cheeses, no nothing–has 1,260 mg sodium, about as much as 14 strips of bacon.

How Refined Salt Causes Autoimmune Disease

The team from Yale University studied the role of T helper cells in the body. These activate and ‘help’ other cells to fight dangerous pathogens such as bacteria or viruses and battle infections.

Previous research suggests that a subset of these cells – known as Th17 cells – also play an important role in the development of autoimmune diseases.

In the latest study, scientists discovered that exposing these cells in a lab to a table salt solution made them act more ‘aggressively.’

They found that mice fed a diet high in refined salts saw a dramatic increase in the number of Th17 cells in their nervous systems that promoted inflammation.

They were also more likely to develop a severe form of a disease associated with multiple sclerosis in humans.

The scientists then conducted a closer examination of these effects at a molecular level.

Laboratory tests revealed that salt exposure increased the levels of cytokines released by Th17 cells 10 times more than usual. Cytokines are proteins used to pass messages between cells.

Study co-author Ralf Linker, from the University of Erlangen-Nuremberg, said: ‘These findings are an important contribution to the understanding of multiple sclerosis and may offer new targets for a better treatment of the disease, for which at present there is no cure.’

It develops when the immune system mistakes the myelin that surrounds the nerve fibres in the brain and spinal cord for a foreign body.

It strips the myelin off the nerves fibres, which disrupts messages passed between the brain and body causing problems with speech, vision and balance.

Another of the study’s authors, Professor David Hafler, from Yale University, said that nature had clearly not intended for the immune system to attack its host body, so he expected that an external factor was playing a part.

He said: ‘These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment.

‘Humans were genetically selected for conditions in sub-Saharan Africa, where there was no salt. It’s one of the reasons that having a particular gene may make African Americans much more sensitive to salt.

‘Today, Western diets all have high salt content and that has led to increase in hypertension and perhaps autoimmune disease as well.’

The team next plan to study the role that Th17 cells play in autoimmune conditions that affect the skin.

‘It would be interesting to find out if patients with psoriasis can alleviate their symptoms by reducing their salt intake,’ they said.

‘However, the development of autoimmune diseases is a very complex process which depends on many genetic and environmental factors.’

Stick to Good Salts

Refined, processed and bleached salts are the problem. Salt is critical to our health and is the most readily available nonmetallic mineral in the world. Our bodies are not designed to processed refined sodium chloride since it has no nutritional value. However, when a salt is filled with dozens of minerals such as in rose-coloured crystals of Himalayan rock salt or the grey texture of Celtic salt, our bodies benefit tremendously for their incorporation into our diet.

“These mineral salts are identical to the elements of which our bodies have been built and were originally found in the primal ocean from where life originated,” argues Dr Barbara Hendel, researcher and co-author of Water & Salt, The Essence of Life. “We have salty tears and salty perspiration. The chemical and mineral composition of our blood and body fluids are similar to sea water. From the beginning of life, as unborn babies, we are encased in a sack of salty fluid.”

“In water, salt dissolves into mineral ions,” explains Dr Hendel. “These conduct electrical nerve impulses that drive muscle movement and thought processes. Just the simple act of drinking a glass of water requires millions of instructions that come from mineral ions. They’re also needed to balance PH levels in the body.”

Mineral salts, she says, are healthy because they give your body the variety of mineral ions needed to balance its functions, remain healthy and heal. These healing properties have long been recognised in central Europe. At Wieliczka in Poland, a hospital has been carved in a salt mountain. Asthmatics and patients with lung disease and allergies find that breathing air in the saline underground chambers helps improve symptoms in 90 per cent of cases.

Dr Hendel believes too few minerals, rather than too much salt, may be to blame for health problems. It’s a view that is echoed by other academics such as David McCarron, of Oregon Health Sciences University in the US.

He says salt has always been part of the human diet, but what has changed is the mineral content of our food. Instead of eating food high in minerals, such as nuts, fruit and vegetables, people are filling themselves up with “mineral empty” processed food and fizzy drinks.

Study Source: 
This is the result of a study conducted by Dr. Markus Kleinewietfeld, Prof. David Hafler (both Yale University, New Haven and the Broad Institute of the Massachusetts Institute of Technology, MIT, and Harvard University, USA), PD Dr. Ralf Linker (Dept. of Neurology, University Hospital Erlangen), Professor Jens Titze (Vanderbilt University and Friedrich-Alexander-Universitat Erlangen-Nurnberg, FAU, University of Erlangen-Nuremberg) and Professor Dominik N. Muller (Experimental and Clinical Research Center, ECRC, a joint cooperation between the Max-Delbruck Center for Molecular Medicine, MDC, Berlin, and the Charite — Universitatsmedizin Berlin and FAU)

Ketamine Alternative Shows Promise.


Researchers show that lanicemine is an effective antidepressant without the adverse effects of the related hallucinogenic drug.

Ketamine can reduce depressive symptoms, but it induces side effects that make its street drug counterpart, “Special K,” popular at parties: hallucinations, altered perception, and dissociative behavior. But now researchers have shown that a ketamine alternative, lanicemine, can reduce depression without the adverse effects, according to a study published in Molecular Psychiatry this week (October 15).

Researchers from Yale University, the French pharmaceutical company Forenap, and AstraZeneca conducted a double-blind, placebo-controlled study to test the effectiveness of lanicemine in 152 people with treatment-resistant major depressive disorder (MDD). They found that study participants who received lanicemine injections three times a week for three weeks had a greater decrease in depressive symptoms than patients who received the placebo. The patients who received lanicemine also reported no serious adverse effects.

“This is the largest study to date evaluating the antidepressant effects of an NMDA receptor antagonist,” first author Gerard Sanacora, a professor of psychiatry at Yale University, told Everyday Health. Lanicemine and ketamine block NMDA receptors, but it is still not well understood why this seems to reduce depression.

Ketamine has been shown to relieve depressive symptoms within 24 hours, and while lanicemine did not work as quickly in this study—it took up to three weeks to see symptom improvement—the delayed effects could have been due to the study design, in which patients continued to take other medications while participating in the trial. “This could be revolutionary—the first new drug treatment for depression in 50 years,” David Nutt of Imperial College London, who was not involved in the work, told New Scientist.

“What this tells us is some of the concerns around ketamine might not be such big problems as originally thought,” senior author Mike Quirk of AstraZeneca told New Scientist. “There are ways around them with the right molecule,” he added.

Scientists Officially Link Processed Foods To Autoimmune Disease.


The modern diet of processed foods, takeaways and microwave meals could be to blame for a sharp increase in autoimmune diseases such as multiple sclerosis, including alopecia, asthma and eczema.

A team of scientists from Yale University in the U.S and the University of Erlangen-Nuremberg, in Germany, say junk food diets could be partly to blame.

‘This study is the first to indicate that excess refined and processed salt may be one of the environmental factors driving the increased incidence of autoimmune diseases,’ they said.

Junk foods at fast food restaurants as well as processed foods at grocery retailers represent the largest sources of sodium intake from refined salts.

The Canadian Medical Association Journal sent out an international team of researchers to compare the salt content of 2,124 items from fast food establishments such as Burger King, Domino’s Pizza, Kentucky Fried Chicken, McDonald’s, Pizza Hut and Subway. They found that the average salt content varied between companies and between the same products sold in different countries.

U.S. fast foods are often more than twice as salt-laden as those of other countries. While government-led public health campaigns and legislation efforts have reduced refined salt levels in many countries, the U.S. government has been reluctant to press the issue. That’s left fast-food companies free to go salt crazy, says Norm Campbell, M.D., one of the study authors and a blood-pressure specialist at the University of Calgary.

Many low-fat foods rely on salt–and lots of it–for their flavor. One packet of KFC’s Marzetti Light Italian Dressing might only have 15 calories and 0.5 grams fat, but it also has 510 mg sodium–about 1.5 times as much as one Original Recipe chicken drumstick. (Feel like you’re having too much of a good thing? You probably are.

Bread is the No. 1 source of refined salt consumption in the American diet, according to the Centers for Disease Control and Prevention. Just one 6-inch Roasted Garlic loaf from Subway–just the bread, no meat, no cheeses, no nothing–has 1,260 mg sodium, about as much as 14 strips of bacon.

How Refined Salt Causes Autoimmune Disease

The team from Yale University studied the role of T helper cells in the body. These activate and ‘help’ other cells to fight dangerous pathogens such as bacteria or viruses and battle infections.

Previous research suggests that a subset of these cells – known as Th17 cells – also play an important role in the development of autoimmune diseases.

In the latest study, scientists discovered that exposing these cells in a lab to a table salt solution made them act more ‘aggressively.’

They found that mice fed a diet high in refined salts saw a dramatic increase in the number of Th17 cells in their nervous systems that promoted inflammation.

They were also more likely to develop a severe form of a disease associated with multiple sclerosis in humans.

The scientists then conducted a closer examination of these effects at a molecular level.

Laboratory tests revealed that salt exposure increased the levels of cytokines released by Th17 cells 10 times more than usual. Cytokines are proteins used to pass messages between cells.

Study co-author Ralf Linker, from the University of Erlangen-Nuremberg, said: ‘These findings are an important contribution to the understanding of multiple sclerosis and may offer new targets for a better treatment of the disease, for which at present there is no cure.’

It develops when the immune system mistakes the myelin that surrounds the nerve fibres in the brain and spinal cord for a foreign body.

It strips the myelin off the nerves fibres, which disrupts messages passed between the brain and body causing problems with speech, vision and balance.

Another of the study’s authors, Professor David Hafler, from Yale University, said that nature had clearly not intended for the immune system to attack its host body, so he expected that an external factor was playing a part.

He said: ‘These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment.

‘Humans were genetically selected for conditions in sub-Saharan Africa, where there was no salt. It’s one of the reasons that having a particular gene may make African Americans much more sensitive to salt.
‘Today, Western diets all have high salt content and that has led to increase in hypertension and perhaps autoimmune disease as well.’

The team next plan to study the role that Th17 cells play in autoimmune conditions that affect the skin.
‘It would be interesting to find out if patients with psoriasis can alleviate their symptoms by reducing their salt intake,’ they said.

‘However, the development of autoimmune diseases is a very complex process which depends on many genetic and environmental factors.’

Stick to Good Salts

Refined, processed and bleached salts are the problem. Salt is critical to our health and is the most readily available nonmetallic mineral in the world. Our bodies are not designed to processed refined sodium chloride since it has no nutritional value. However, when a salt is filled with dozens of minerals such as in rose-coloured crystals of Himalayan rock salt or the grey texture of Celtic salt, our bodies benefit tremendously for their incorporation into our diet.

“These mineral salts are identical to the elements of which our bodies have been built and were originally found in the primal ocean from where life originated,” argues Dr Barbara Hendel, researcher and co-author of Water & Salt, The Essence of Life. “We have salty tears and salty perspiration. The chemical and mineral composition of our blood and body fluids are similar to sea water. From the beginning of life, as unborn babies, we are encased in a sack of salty fluid.”

“In water, salt dissolves into mineral ions,” explains Dr Hendel. “These conduct electrical nerve impulses that drive muscle movement and thought processes. Just the simple act of drinking a glass of water requires millions of instructions that come from mineral ions. They’re also needed to balance PH levels in the body.”
Mineral salts, she says, are healthy because they give your body the variety of mineral ions needed to balance its functions, remain healthy and heal. These healing properties have long been recognised in central Europe. At Wieliczka in Poland, a hospital has been carved in a salt mountain. Asthmatics and patients with lung disease and allergies find that breathing air in the saline underground chambers helps improve symptoms in 90 per cent of cases.

Dr Hendel believes too few minerals, rather than too much salt, may be to blame for health problems. It’s a view that is echoed by other academics such as David McCarron, of Oregon Health Sciences University in the US.

He says salt has always been part of the human diet, but what has changed is the mineral content of our food. Instead of eating food high in minerals, such as nuts, fruit and vegetables, people are filling themselves up with “mineral empty” processed food and fizzy drinks.

Source: preventdisease.com

         

Skin drug may treat type 1 diabetes


A drug that was used to treat a skin disorder has shown signs of being able to treat aspects of type 1 diabetes.

A small trial on US patients suggests that alefacept helps the body produce its own insulin, which is key for people with type 1 diabetes.

Type 1 diabetes affects around 400,000 people in the UK.

Researchers said the drug could be better than other treatments because it protects the immune system – but more research was needed.

The findings are published in The Lancet Diabetes & Endocrinology.

Alefacept (sold as Amevive) was used to treat the skin disorder psoriasis in the US before it was withdrawn by its manufacturer in 2011. The drug was never approved for the European drug market.

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“Start Quote

Type 1 diabetes will one day be cured. It’s a matter of time, money and excellent research”

Karen Addington Chief executive of JDRF

Psoriasis, like type 1 diabetes, is an autoimmune disorder that occurs when the immune system attacks healthy skin cells.

In clinical trials of the drug on psoriasis, the drug was found to attack specific types of T-cells that were also involved in attacking insulin-producing cells in type 1 diabetes.

So researchers, led by a team at Indiana University, Indianapolis, decided to investigate if it could have any effect on newly diagnosed type 1 patients.

Preserve insulin

In the trial, which is continuing, 33 patients received weekly injections of alefacept for 12 weeks, followed by a break of 12 weeks, and then another 12 weekly doses.

Another 16 participants were given placebo injections following the same schedule.

The researchers found no difference in how well the pancreas produced insulin two hours after eating food, but they did find “significant differences” between the two groups four hours after eating.

At this point, the group who received the drug showed they were able to preserve insulin while the placebo group‘s insulin levels decreased.

What is type 1 diabetes?

Type 1 diabetes is an autoimmune condition, where the immune system attacks the cells of the pancreas that produce insulin.

This results in insulin deficiency and the body being unable to regulate blood sugar.

Scientists suspect the condition often follows a trigger such as a viral infection.

After 12 months, the same group showed no significant increase in insulin use, yet those in the placebo group did.

The first group also had fewer episodes of hypoglycaemia, low blood glucose levels. which are common in people with type 1 diabetes.

‘Small successes’

Lead researcher Prof Mark Rigby, of Indiana University, said the first 12 months of the trial were encouraging.

“Although the primary endpoint was not met, several key secondary endpoints were significantly different between treatment groups, suggesting that alefacept might preserve pancreas cell function during the first 12 months after diagnosis.”

He said the initial findings meant that in the future the drug “could be used to stabilise type 1 diabetes and prevent its progression” – but it was unlikely to be a cure.

He added that the trial would continue and further measurements would be taken after 18 months and 24 months.

Writing about the study in The Lancet, Dr Kevan Herold, of Yale University, said: “It is important to underscore these small successes since, as in other fields such as oncology and infectious diseases, the small achievements acquire greater significance when they are combined.”

Karen Addington, chief executive of JDRF, the type 1 diabetes charity that helped fund the study, said the outcome was promising.

“The results of this study appear worthy of further exploration. Small steps forward such as this take us closer to a world without type 1 diabetes.

“It is a challenging and complex condition. But type 1 diabetes will one day be cured. It’s a matter of time, money and excellent research.”

Words prompt us to notice what our subconscious sees.


It’s a case of hear no object, see no object. Hearing the name of an object appears to influence whether or not we see it, suggesting that hearing and vision might be even more intertwined than previously thought.

Studies of how the brain files away concepts suggest that words and images are tightly coupled. What is not clear, says Gary Lupyan of the University of Wisconsin in Madison, is whether language and vision work together to help you interpret what you’re seeing, or whether words can actually change what you see.

Lupyan and Emily Ward of Yale University used a technique called continuous flash suppression (CFS) on 20 volunteers to test whether a spoken prompt could make them detect an image that they were not consciously aware they were seeing.

CFS works by displaying different images to the right and left eyes: one eye might be shown a simple shape or an animal, for example, while the other is shown visual “noise” in the form of bright, randomly flickering shapes. The noise monopolises the brain, leaving so little processing power for the other image that the person does not consciously register it, making it effectively invisible.

Wheels of perception

In a series of CFS experiments, the researchers asked volunteers whether or not they could see a specific object, such as a dog. Sometimes it was displayed, sometimes not. When it was not displayed or when the image was of another animal such as a zebra or kangaroo, the volunteers typically reported seeing nothing. But when a dog was displayed and the question mentioned a dog, the volunteers were significantly more likely to become aware of it. “If you hear a word, that greases the wheels of perception,” says Lupyan: the visual system becomes primed for anything to do with dogs.

In a similar experiment, the team found that volunteers were more likely to detect specific shapes if asked about them. For example, asking “Do you see a square?” made it more likely than that they would see a hidden square but not a hidden circle.

James McClelland of Stanford University in California, who was not involved in the work, thinks it is an important study. It suggests that sight and language are intertwined, he says.

Lupyan now wants to study how the language we speak influences the ability of certain terms to help us spot images. For instance, breeds might be categorised differently in different languages and might not all become visible when volunteers hear their language’s word for “dog”. He also thinks textures or smells linked to an image might have a similar effect on whether we perceive it as words.

Source: http://www.newscientist.com

Obesity Gene Linked to Hunger Hormone.


Researchers think they’ve hit on why a common obesity gene causes weight gain: Those who carry a version of it don’t feel full after eating and take in extra calories. That’s because the variant of the FTO gene in question, which one in six individuals carry, leads to higher levels of ghrelin, a hormone involved in mediating appetite and the body’s response to food, researchers have discovered. While most studies on FTO have relied on mice, the new work analyzed blood samples and brain scans from humans.

“This is a very exciting piece of research,” says geneticist Andrew Hattersley of the Peninsula Medical School in Exeter, U.K., who was not involved in the new study. “There is a lot of work that’s been done on the mechanism of FTO in animals, but you have to be careful about applying those lessons to people. So it’s nice to finally see work done in humans.”

Hattersley was part of a team that in 2007 reported that people who had one version of the FTO gene, called AA, weighed an average of 3 kilograms more than those with the TT version of the gene. Since then, studies in mice have shown that in everyone, there are high levels of the FTO protein in brain areas that control energy balance. Researchers have also found that animals with the AA version tend to eat more and prefer high-fat food compared with those with the TT version. But why FTO had this effect wasn’t known.

Rachel Batterham, an endocrine and obesity researcher at University College London, thought that gut hormones that mediate the body’s response to eating could be the missing link between FTO and food intake. One such hormone is ghrelin, known to be produced by gut cells to stimulate hunger. So Batterham and her colleagues measured levels of ghrelin in the blood of nonobese men with the AA or TT versions of FTO. In those with the TT variant, ghrelin levels rose before a meal, when the person experienced hunger, and fell after eating, as expected. But in those with the obesity-associated AA version, ghrelin levels stayed relatively high even after eating. Moreover, the AA individuals reported a faster increase in hunger after a test meal. And MRI scans revealed that, when the test subjects were shown images of food before or after eating, brain activity in areas associated with motivation and rewards remained high before and after the meal in AA individuals. This suggests that the increased ghrelin levels were impacting the brain’s response to food—which “fits very well with what we already know the effects of ghrelin,” Batterham says.

But could higher ghrelin levels be unrelated to FTO? The researchers don’t think so, in part because they found that in isolated human cells, increased levels of FTO protein led to more ghrelin production. The reason this happens, the group showed, is because that the FTO protein actually alters the ghrelin gene, causing methyl chemical groups to be removed, a so-called epigenetic modification that impacts how much protein the ghrelin gene produces. The AA gene variant, the researchers report online today in The Journal of Clinical Investigation, removed more methyl groups from the gene, leading to increased levels of the hunger hormone.

Whether that proves true, the full story is FTO remains to be uncovered, Hattersley says. “What we don’t know is whether FTO is changing many things that alter appetite, of which ghrelin is just one,” he says. “I suspect human appetite and obesity is more complex than a single hormone.”

Neurobiologist Tamas Horvath of Yale University agrees. “This is a beautiful piece of work at face value,” he says. “But I think it’s reasonable to continue pursuing many other avenues to see what else might be going on here.”

Source: sciencemag.org

 

Everolimus 

Neuroenhancement of Kids ‘Not Justifiable,’ Neurology Groups Say.


Neuroenhancement — the use of prescription drugs (e.g., stimulants) by healthy people in order to increase normal brain function — “is not justifiable” for children without diagnosed neurological disorders, according to a new position paper published in Neurology.

The paper also notes that for “nearly autonomous” adolescents, neuroenhancement is “inadvisable because of numerous social, developmental, and professional integrity issues.”

The authors offer a series of discussion points to guide physicians’ conversations with parents who request neuroenhancement medications for healthy children and teens.

The position paper is endorsed by the American Academy of Neurology, Child Neurology Society, and American Neurological Association.

Source: Neurology 

Salt Linked to Autoimmune Diseases .


 

salt-linked-to-autoimmune-diseases_1

Nanowires used to disarm single genes in cells without harming or altering them were used to reveal that sodium chloride might cause harmful T cell growth

The incidence of autoimmune diseases, such as multiple sclerosis and type 1 diabetes, has spiked in developed countries in recent decades. In three studies published today in Nature, researchers describe the molecular pathways that can lead to autoimmune disease and identify one possible culprit that has been right under our noses — and on our tables — the entire time: salt.

To stay healthy, the human body relies on a careful balance: too little immune function and we succumb to infection, too much activity and the immune system begins to attack healthy tissue, a condition known as autoimmunity. Some forms of autoimmunity have been linked to overproduction of TH17 cells, a type of helper T cell that produces an inflammatory protein called interleukin-17.

But finding the molecular switches that cause the body to overproduce TH17 cells has been difficult, in part because conventional methods of activating native immune cells in the laboratory often harm the cells or alters the course of their development.

So when researchers heard a talk by Hongkun Park, a physicist at Harvard University in Cambridge, Massachusetts, about the use of silicone nanowires to disarm single genes in cells, they approached him immediately, recalls Aviv Regev, a biologist at the Massachusetts Institute of Technology (also in Cambridge) and a co-author on two of the studies.

Park showed last year that these nanowires can be used to manipulate genes in immune cells without affecting the cells’ functions. For the first of the Nature studies, Regev and her colleagues used Park’s technology to piece together a functional model of how TH17 cells are controlled, she says. “Otherwise,” she says, they would have been only “guessing in the dark.”

In the second study, an affiliated team of researchers observed immune cell production over 72 hours. One protein kept cropping up as a TH17-signal: serum glucocorticoid kinase 1 (SGK1), which is known to regulate salt levels in other types of cells. The researchers found that mouse cells cultured in high-salt conditions had higher SGK1 expression and produced more TH17 cells than those grown in normal conditions.

“If you incrementally increase salt, you get generation after generation of these TH17 cells,” says study co-author Vijay Kuchroo, an immunologist at Brigham and Women’s Hospital in Boston, Massachusetts.

In the third study, researchers confirmed Kuchroo’s findings, in mouse and human cells. It was “an easy experiment — you just add salt”, says David Hafler, a neurologist at Yale University in New Haven, Connecticut, who led the research.

But could salt change the course of autoimmune disease? Both Kuchroo and Hafler found that in a mouse model of multiple sclerosis, a high-salt diet accelerated the disease’s progression.

All this evidence, Kuchroo says, “is building a very interesting hypothesis [that] salt may be one of the environmental triggers of autoimmunity”.

But Kuchroo and other researchers say that evidence so far cannot predict the effect of salt on human autoimmunity. “As a physician, I’m very cautious,” Hafler says. “Should patients go on a low-salt diet? Yes,” he says, adding that “people should probably already be on a low-salt diet” for general health concerns.

Other experts are intrigued by the findings. “They have a very clear effect in vitro,” says John O’Shea, scientific director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases Intramural Research Program in Bethesda, Maryland. But Hafler and others note that there are likely many cell types and environmental factors involved in triggering autoimmunity.

The results offer tantalizing leads for drug targets for autoimmune conditions. But O’Shea notes that it is unclear whether TH17 proliferation is a factor in all autoimmune disease. A targeted drug that might work to relieve psoriasis might not subdue rheumatoid arthritis. “When we say autoimmunity, we’re implying that it’s one thing,” O’Shea says. “But it’s not one thing — it’s heterogeneous.”

Source: Scientific American.