The Deadly Mystery of Prions

Deer that became zombies

zomDeer in at least 22 U.S. states and parts of Canada have died from a neurological disease called “chronic wasting disease,” according to the Centers for Disease Control and Prevention (CDC). Authorities are concerned that this illness, which is sometimes dubbed “zombie deer disease,” might spread to people, just as “mad cow disease” has done in the past.
Chronic wasting disease can cause a number of symptoms in animals, including drastic weight loss, a lack of coordination, drooling, listlessness or a “blank” facial expression, and a lack of fear of people, according to the CDC. It infects members of the deer (cervid) family, including white-tailed deer, mule deer, reindeer, moose and elk.
The disease was first discovered in Colorado in 1967, according to the CDC, and so far, no cases in humans have ever been reported.
Indeed, the infectious proteins that cause chronic wasting disease — called prions — don’t easily jump between species, said Mark Zabel, associate director of the Prion Research Center at Colorado State University. But it’s known that these proteins can evolve to infect other species, Zabel said. For example, the type of prion that causes so-called bovine spongiform encephalopathy, or “mad cow disease,” was transmitted to people who ate infected meat (mostly in the United Kingdom in the 1980s and ’90s), resulting in several hundred human infections.
“We have every reason to suspect” that chronic wasting disease could pass to humans, Zabel told Live Science. The disease “may still be evolving, and it may be just a matter of time before a prion evolves in a deer or elk that is capable of infecting a human, he said.” [10 Deadly Diseases That Hopped Across Species]

Concerns

Recently, researchers in Canada raised concerns about the possibility that the disease could jump to humans, after a study showed that macaque monkeys could get the disease from eating infected meat. Out of five monkeys that were fed infected white-tailed-deer meat, three tested positive for chronic wasting disease, according to The Tyee, a Canadian news outlet. This is the first time that the disease has been found to spread to primates through the consumption of infected meat, according to the Associated Press.
Infectious prions cause disease when they start to fold abnormally and trigger the misfolding of other, similar proteins. Studies by Zabel’s lab and others have shown that the prion proteins that cause chronic wasting disease are “flexible,” meaning they can “adopt many different shapes relatively easily,” Zabel said.
Moreover, some studies have shown that researchers can artificially evolve the prions that cause chronic wasting disease (either in a test tube or animal models) so that the altered prion proteins can cause human proteins to misfold, Zabel said.
This suggests that if chronic-wasting-disease prions evolve in nature, they could potentially cross the species barrier, he said.

The mystery of prions

prnp-prp-prion
A number of fatal neurodegenerative diseases in humans–such as Creutzfeldt-Jakob disease (CJD), kuru and Gerstmann-Straussler-Scheinker (GSS) disease–are thought to be caused by a mysterious infectious agent known as a prion. Prions also cause disease in a wide variety of other animals, including scrapie in sheep and bovine spongiform encephalopathy (BSE) in cows.

Just, what are prions and how do they cause disease?

Prions are proteins that have changed their normal shape. Proteins are the building blocks of living cells that are used by our bodies either as structural elements or as signaling molecules that carry information throughout our body. They consist of chains of amino acids folded into complex shapes. When the shape of a protein changes the spectrum of waves it is emitting changes. The prion protein is now transmitting a different informational message into your body. In effect, your body is now tuned to a new radio station and instead of classical music you may be getting hard-rock. When the prion creates a “disease” in the body it is known as a “mutant prion” since it can start a chain reaction and persuade other proteins to follow its example. That process can spread the disease through the cells and eventually to the brain. Just as we have “informational medicine” like homeopathy that can be used to heal us, we now have “informational disease” that can kill us.

Western science, and therefore our approach to the way in which we handle our food supply, has been confronted with an informational disease — mad-cow disease. The phenomenon was not a part of classical biochemistry and was only officially recognized in 1997 when Dr. Stanley Prusiner of UCSF won the Nobel Prize in Medicine for “his pioneering discovery of an entirely new genre of disease-causing agents.” Dr. Prusiner had discovered that altered versions of proteins, which he dubbed prions, are to blame for a family of human and animal diseases. Prusiner had pursued his specific area of research since 1972 but was met with incredulity, criticism, and controversy. Unlike bacteria, virus, or parasites, an “infectious” prion cannot be destroyed by heat, freezing or radiation. For example, to destroy mutant-prion infected meat the USDA facility at Ames, Iowa uses a tissue digestor, a large stainless steel vat that melts the carcasses in boiling lye under pressure, then dries the liquid into a powder that is incinerated.

Initially, mad-cow disease was a scientist’s worst nightmare since no one knew how it was transmitted. Early estimates were that millions of people in the United Kingdom could get the brain-wasting degenerative disease. Even through in the United Kingdom more than 185,000 cattle were found to be infected, only 143 cases of the always-fatal human version of the disease have been diagnosed. The number of new human cases has now leveled off at fewer than 20 a year. Only 10 people outside of the United Kingdom are known to have died from the human form of the disease. One cause for the low death rate could be the body’s quality control system for handling misfolded proteins. When a cell detects such prions it sends a signal to the nucleus to activate a program to destroy these mistakes. However, a disturbing note is that Britain, on Dec. 17, 2003, reported the first case of a person dying after a blood transfusion from an infected donor.

 

Mad cow disease

Glow in cattle’s eyes may be a sign of mad cow disease

Mad-cow disease, officially known as bovine spongiform encephalopathy (BSE) was first diagnosed in 1986 in Britain. Researchers quickly decided that cattle had gotten the disease from eating brains and nerve tissue of sheep infected with scrapie a variant of mad-cow disease. The tissues had been mixed into cattle feed along with the ground-up carcasses of other animals – including other cows. Such “rendered” feed has now been banned for most food animals. Today Japan tests every cow that enters the food supply for BSE, and Europe tests every animal older than 30 months (the age at which the incidence of BSE starts to climb). However, currently in the United States only about 20,000 of the 35 m5 million cattle slaughtered each year are tested for BSE, i.e., an insignificant 0.06% are tested.

If BSE is an “informational” disease than there should be other variations. We know that mad-cow disease can be caused by a mutation of a single gene, a so-called spontaneous case. Similar spongy-brain diseases have also appeared in at least 10 animal species. Included are farmed mink, domestic cats, cougars, bison, and African antelope (kudu & oryx). The so-called chronic wasting disease also strikes mule deer, white-tailed deer, and elk in the wild. Sheep carry a variant of mad-cow disease known as scrapie. Shepherds and pathologists have recognized it since the 18th century. Sheep haven’t been known to transmit their brain disease to people despite centuries of opportunity. In fact, potted sheep’s brain is a national dish in Scotland. This has raised questions about current theories regarding the scrapie as the trigger of BSE in Britain.

Is there maybe another underlying cause for these diseases, and the unparalleled large surge of mad-cow disease in the United Kingdom?

The link to food supply and heritage factors

An organic farmer, Mark Purdey, and a number of researches are putting forth an

hypothesis based upon environmental causal factors. They implicate a warble fly eradication program mandated in the early 1980s by the British government. Warble flies lay their eggs in a cow’s skin, causing health problems and reducing the value of cow hides. To combat this heavy doses of organophosphate insecticides were used. These were poured along the spinal column of cows to be absorbed into the cow’s body. They exert their toxic effect by entering the central nervous system and deforming the molecular shape of various nerve proteins. Organophosphates were developed by Nazi chemists during the course of World War II as a biological weapon. The effects of organophosphates can be made more severe because they remove copper from the body leaving the door open for manganese or similar metals to replace the copper in the prion protein. This creates a condition akin to the occupational disease known as “Manganese Madness.” The “informational” disease caused in humans by BSE is called variant Crueutzfeldt-Jakob Disease (vCJD)s. In addition to CJD and vCJD, could other degenerative ailments in humans, such as Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease involve abnormal changes in the shapes of proteins caused by environmental factors that affect us directly or indirectly via our food supply?
“Confusingly, researchers also recognized that some prion diseases, such as GSS, were inherited. The pattern of inheritance was recognized as being autosomal and dominant, meaning that if a parent developed GSS, there was a 50 percent chance that a child of either sex would also develop the disease. Any explanation for the cause of a prion disease therefore has to account for random, inherited and transmitted variants of the disease.
“Although there is not yet a universally accepted explanation of this puzzle, progress is being made. We now know that a normal cellular protein, called PrP ( for proteinaceous infectious particle) and which is found in all of us, is centrally involved in the spread of prion diseases. This protein consists of about 250 amino acids.
“Some researchers believe that the prions are formed when PrP associates with a foreign pathogenic nucleic acid. This is called the virino hypothesis. (Viruses consist of proteins and nucleic acids that are specified by the virus genome. A virino would also consist of proteins and nucleic acids, but the protein component is specified by the host genome, not the pathogen genome). In support of the virino hypothesis is the existence of different strains of prions that cause differing patterns of disease and breed true; the existence of strains in pathogens is usually the result of changes in the nucleic acid sequence of the infectious agent. Scientists have not found any nucleic acid associated with a prion, however, despite intensive efforts in many laboratories. Furthermore, prions appear to remain infectious even after being exposed to treatments that destroy nucleic acids.
“This evidence has led to the now widely accepted prion theory, which states that the cellular protein PrP is the sole causative agent of prion diseases; there is no nucleic acid involved. The theory holds that PrP is normally in a stable shape (pN) that does not cause disease. The protein can be flipped, however, into an abnormal shape (pD) that does cause disease. pD is infectious because it can associate with pN and convert it to pD, in an exponential process–each pD can convert more pN to pD.
“Prions can be transmitted, possibly by eating and certainly by inoculation either directly into the brain or into skin and muscle tissue. Exponential amplification of the prion (converting pN into pD in the body) would then result in disease. Occasional, sporadic cases of prion diseases arise in middle or old age, presumably because there is a very small but real chance that pN can spontaneously flip to pD; the cumulative likelihood of such a flip grows over the years. Inherited cases of CJD and GSS may result from mutations in the PrP gene, which gives rise to changes in the amino acid sequence of the PrP protein. This change would increase the probability of pN transforming into pD, so that the disease would almost certainly occur.

Scientific Research

300px-R7_prion“Physical analysis of the structure of PrP provides some direct evidence for the existence of two different (normal and aberrant) shapes. Recently the structure of the core part of the PrP protein was determined by magnetic resonance image analysis. Mutations that cause prion disease are clustered within or adjacent to key structural elements in the protein, so it is easy to imagine that mutations destabilize the structure of pN and cause it to reconfigure into pD.
“The prion theory has not been proved correct, but much evidence now supports it. We do not yet know why the pD structure of a prion would result in neurodegeneration, but we do know that prion protein accumulates in brain tissue. One part of the prion protein can cause apoptosis, or programmed cell death; perhaps this mechanism explains the pattern of the disease.
“Prions have long intrigued scientists because of their unusual properties. Recently the general public has become interested in them as well because of the epidemic of BSE, more dramatically known as mad cow disease. Hundreds of thousands of infected animals have been eaten by Europeans and particularly the British over the past 10 years. The latest research suggests that the infected meat may pose a threat to human health, but the significance of that threat may not become apparent for years. Although it is generally considered a British problem, BSE is almost certainly a natural disease of cattle, so it is undoubtedly found in other countries as well. The normal incidence of BSE is vanishingly small, however. The U.S. Department of Agriculture claims that BSE has not been identified in any U.S. cattle.

Could Alzheimer’s and Parkinson’s be infectious?

The archetypal prion-based disease is kuru, which spread through cannibalistic rituals in the Eastern Highlands of Papua New Guinea.

Kuru affected mostly women and children of the Fore tribe, who ate brains and spinal cords of deceased relatives, and subsequently developed body tremors, balance problems and slurred speech. There’s no cure for kuru and sufferers always died. But it no longer strikes as cannibalism in the region has been eliminated.
Other prion diseases include scrapie in sheep and goats and bovine spongiform encephalopathy (BSE) in cows. When transmitted to humans during the “mad cow disease” outbreak in Europe, BSE resulted in variant CJD (vCJD).
The newly described addition to the prion disease canon, Shy-Drager syndrome (SDS) or multiple system atrophy (MSA), was first recognised in the early 1960s and has many features in common with Parkinson’s disease.
The most important of these is that a protein known as α-synuclein (α-syn) accumulates in the brain, in both Parkinson’s and SDS/MSA. This accumulation is very similar to what happens in CJD, where the prion protein (PrP) accumulates, and also in Alzheimer’s disease and other dementias, where two types of proteins, known as amyloid beta (Aβ-amyloid) and tau, build up in the brain.

1223_NID_CJD_Disease_1280

Infected with prions, the brain of a vCJD victim reveals spongy areas (yellow).

The clumps and tangles of these various aggregated proteins cause neurons to degenerate and die. This is a cumulative process which takes between months and decades to manifest as overt disease.
In fact, many of the neurodegenerative diseases of the ageing brain are associated with the accumulation and deposition of specific proteins. It has long been suspected that neurodegenerative diseases in general may all ultimately be caused by this process of proteins getting caught in the wrong process, and misfolding.
This misfolding sets off a cascade of events: the proteins oligomerise (a number of identical molecules join together); accumulate; nucleate (form a nucleus or centre); polymerise (combine to build a structure with its components); self-replicate; and eventually, propagate and spread throughout the brain. Many of these protein changes also occur in the usual food cooking process (aggregation of proteins caused by heating) or food preparation (the solidification of proteins in the refrigerator).
Finally, some but not all of these misfolded proteins gain the ability to be transmitted between people and animals. In fact, the word “prion” was coined by Prusiner in 1982 to describe this property of a pro_teinaceous in_fectious particle. And we don’t yet know of ways to easily “dis-infect” or kill these proteins. All kinds of chemicals that kill bacteria and viruses do not harm prions.
Infectious Proteins
Scientists have always kept – and still do – an open mind about whether Alzheimer’s disease and other neurodegenerative conditions are transmissible. We’ve known since the early 1960s that amyloid fibrils – the accumulations of Aβ-amyloid in the brain – are self-propagating entities.
In diseases involving amyloid protein, the “amyloid enhancing factor”, which causes the disease to progress, is thought to be amyloid itself. In other words, the amyloid is self-replicating and makes copies of itself exponentially.

We know that the Alzheimer’s disease-causing human Aβ-amyloid can cross-seed Aβ-amyloid accumulation in genetically susceptible rodents. Mice carrying an unstable and genetically modified human protein can then be “infected” by giving them a dose of the human abnormal protein. But there’s still no direct evidence that Alzheimer’s disease is transmissible between people.
Working out whether SDS/MSA is transmissible, at least from humans to genetically susceptible transgenic cell and rodents, is the first step in testing if it’s transmissible from humans to primates, or indeed among people.
As a precautionary measure, the authors of the paper warn we should now take additional safety precautions in the neurosurgical clinics where deep brain stimulation is used to control the tremors caused by Parkinson’s disease. Because of the overlap in symptoms and signs of Parkinson’s with SDS/MSA, it’s likely that some people with the newly described disease have been treated by deep brain stimulation.
It’s important to ensure that cross-contamination of neurosurgical equipment doesn’t occur because we don’t want to inadvertently transmit a disease between humans. Using disposable stimulation electrodes, for instance, will be mandatory in the future. Similar concerns have already been raised about other neurodegenerative illnesses, such as diseases involving misfolded tau protein, which cause frontotemporal dementia.
With the publication of this paper, the spectrum of prion diseases has been enlarged, perhaps considerably. But until it becomes possible to evaluate the role of intra-species transmission, SDS/MSA will have to remain in the category of “hypothetically transmissible to a genetically susceptible recipient”.
It’s premature to classify it as being the same as CJD, which is clearly transmissible within and between species. That has been made apparent by the mad cow saga, which still has years to run due to the long latency from prion infection to overt disease.

The impact on the future

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Some have come up with the idea that on a long term view, the existence of prions and their devastating consequences in living organisms together with their way of transmission will definitely change human nutrition habits.
“Science is trying to find a prevention and a solution for the phenomenon of prions”, says Dr. Peter Weiler, who was formerly teaching at the German university in Potsdam. “However, they come in a variety of forms and spread in a way that doesn’t follow any known pattern. Always more species are being discovered to develop prion-based disease. Meat-eating from animals that were once alive might become a deadly danger one day – or a luxury not affordable for everybody.”
So will meat-eaters soon have to give up on their preferred dishes?
Weiler thinks that meat will be created from cell cultures on day.
“Nature won’t be able to cope with the current habits of a human population that increases at such a high rate,” he says.
To the question whether prions might be the answer of nature to human behavior, we only receive an enigmatic smile.

 

Sources:

iflscience.com

livescience.com

Foundation for Mind-being Research

American Scientific

You may also want to read:

Mad cow disease remains a threat. New blood tests could detect it

Cultured beef

Is the future of beef animal-free?

 

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Passing Beyond

What if Death Were Not the End?

Part I: Near Death Experience and Dreams

Written by LLS

A friend of mine recently died – unexpectedly and much too early. His death left a deep void for many of his friends. It left an empty space in my life as well, and like so many times before I hoped he would in any way contact me, or leave me a sign. But like all other times, nothing happened, and again I thought about what may happen after death. As someone who studied psychology and neurology but also loves to go beyond scholarship, I have investigated the subject in its different aspects and had long planned to write an article about this. The death of my friend finally made me sit down and do it.

I’ll present three different approaches to the subject which come to different conclusions. At the end, there will be a more likely and a less likely outcome for the readers. I leave the conclusion to each of them.

Quo vadis?

afterlife

NDE experience: the tunnel of light

The questions are probably as old as mankind itself: what happens after we’re biologically dead? Is there life after death? Is there an Otherworld? Will we be reborn? Or is there just nothing after we close our eyes forever?

The different cultures have found different solutions for this question. For some cultures that have still shamanic background, the dead continue to exist in a world that continuously touches ours, is as real as our world and can be accessed by breaking through the thin membrane between the two realities.

In antiquity, the dead often had to undertake a long journey to another world far away and needed therefore supplies to have a safe trip and a good status in the Otherworld.

Today’s world religions don’t agree with each other concerning this question, either. In Hinduism and Buddhism exists the concept of reincarnation; Judaism, Christianity and Islam divide the souls in good and bad ones and the Otherworld in Heaven and hell.

Modern science doesn’t conceive any further existence after death at all. Western societies educate their members with the idea of life that happens by chance, with no hope for another reality. Dead is dead and there’s no doubt that everything is over for the one who passes through that doorway. This happens majorly because modern science refuses the idea of a god, of a reality beyond matter. Only what we can experience is real – all the rest is fantasy. For those who die, the world ceases to exist. Innumerable people have therefore tried to find the sense of life and got lost in the desperation of not finding a deeper meaning to their existence.

However, in the last decades, scientists have started to ponder the question whether an existence after death might be actually a possibility. As quantum physics naturally trespassed the rigid frontiers of positivism – the type of science that denies anything we have no proof for – also the concept of existence started shifting. The fact that people who had been clinically dead and were reanimated all reported the same experiences of leaving their physical bodies, entering tunnels of light and feeling extreme happiness and freedom, triggered a whole bunch of investigations that would try to scientifically explain what was actually happening.

Perception and the brain: a doorway to the explanation of near death experience?

brain_12

Enhanced brain activity

A recently published study focuses on the aspect of perception. The scientists think that the near death experiences are based on neurological processes that provoke particular pseudo-experiences when we die. When we’re about to die, we reach a state that doctors call “clinical death”. That is when the heart stops beating. Scientists observed that in the first  30 seconds after clinical death, there was strongly synchronized brain gamma-wave brain activity, similar to the moment when the brain is highly stimulated. They concluded that the reduction of sugar and oxygen supply can enhance the brain’s activity. This, so the scientists, is the reason why many people have the feeling to pass through a tunnel of light. However, they say, after that light it’s really over. The clinical death is followed by the biological death. All functions of organs and cells are finally terminated.

So far the commonly accepted scientific theory concerning near death experiences.

However, inevitably the question arises: if so, and if all near death experiences are based on mere brain stimulation given by the lack of sugar and oxygen, how come all NDE reports are the same?

Let’s compare the described situation to our dreams. Basically, we’re in front of a similar phenomenon, only that it’s not based on the lack of any vital substances. So let’s have a look at the brain.

gene-linking-brain-structure-to-intelligence-discovered

Depiction of the human brain

Our brain consists of several parts. Much of the size of the human brain comes from the cerebral cortex, especially the frontal lobes, which are associated with executive functions such as self-controlplanningreasoning, and abstract thought. The human cerebral cortex is a layer of neural tissue that covers the two cerebral hemispheres that make up most of the brain. (Wikipedia) The two hemispheres which have different tasks are interconnected by a small organ called pons (lat. “bridge”).  The pons is part of the brainstem, and in humans and other bipeds lies between the midbrain (above) and the medulla oblongata (below) and in front of the cerebellum. This region of the brainstem includes neural pathways or tracts that conduct signals from the brain down to the cerebellum and medulla, and tracts that carry the sensory signals up into the thalamus. In the research about dreams, scientists have observed that during sleep electric impulses are being fired on the cortex, coming from the area of the pons. They came to the conclusion that the pictures of our dreams are being triggered by the area of the cortex where the impulses arrive. However, the discussion between behaviorists and depth psychologists has never stopped as the depth psychologists sustain that the pictures aren’t created by chance but have something to do with the psychological situation of the dreaming individual. However it is, one thing is for sure: when we sleep, impulses reach the cortex where entire movies are being created, and whether they have a deeper psychological meaning or not, we all know that our all dreams are far from being only slightly similar. Our dreams are as individual as we are. So why should our all brains create the almost identical pictures in a situation when again our brains experience stimulation – in the moments after our clinical death? This seems illogical. A group of doctors has therefore performed an in-depth research on people who were clinically dead and could be reanimated. They came to very different conclusions.

(To be continued: NDE and Afterlife experiments)

Tissue regeneration: Researchers create gel that regrows tooth enamel

…and eliminates pain associated with tooth decay

Our article “How to Heal Cavities Naturally” has triggered an ongoing discussion ever since it was posted.

However, science has developed a new technique that holds the promise of tooth regrowth.

Researchers say tooth gel will regrow enamel and cover painful blemishes.

Dual discoveries in tissue regeneration at the University of Southern California propose a promising method to regrow nonliving hard tissue, lessening or even eliminating pain associated with tooth decay, which the National Institutes of Health calls the most prevalent chronic disease.

newly-grown-enamel-jpg-scale-large

Nearly grown enamel

Janet Moradian-Oldak, a dentistry professor at the Herman Ostrow School of Dentistry of USC, has investigated methods to regrow tooth enamel for the past two decades. The process is especially tricky because unlike bone, mature enamel cannot rejuvenate. Tooth enamel is a nonliving tissue.

The a-ha moment came October 22 when, in collaboration with lead author Sauma Prajapati of USC and other colleagues, she published a study in the Biomaterials journal saying matrix metalloproteinase-20, an enzyme found only in teeth, chops up amelogenin proteins, which facilitate organized enamel crystal formation. MMP-20 clears the way for hard material to usurp vacated space.

Her team is the first to define the function of an enzyme for preventing protein occlusion inside a crystal, she said.

“MMP-20 is released at a very early stage of enamel formation,” said Moradian-Oldak, the study’s senior author. “MMP-20 chops up proteins during the crystallization of enamel. Together with other enzymes, it gets rid of ‘sludge’ so the enamel making cells in the body can add more mineral and make enamel, the hardest bioceramic in the human body.”

Repairing tooth decay
Moradian-Oldak will marry the MMP-20 discovery with another study published Nov. 2 in the Journal of Biomedical Engineering and Informatics, which concluded an amelogenin-chitosan hydrogel could repair early tooth decay by growing an enamel-like layer that reduces lesions by up to 70%.

“Recognizing MMP-20’s function in biomineralization is one of the first steps to learning how dental enamel forms in nature,” said Qichao Ruan, lead author of the hydrogel study and a postdoctoral research associate in the Center for Craniofacial Molecular Biology at USC. “The findings regarding MMP-20 not only help us to further understand the mechanisms of enamel formation but also can be applied in the design of novel biomaterials for future clinical applications in dental restoration or repair.”

The Food and Drug Administration has not yet approved any type of enamel regrowing gel. USC is in preclinical trials. Moradian-Oldak said one day people may be able to use an overnight mouth guard or teeth strips saturated with hydrogel to regrow enamel-like substances and reduce teeth sensitivity.

Finding the right fix
Products such as toothpaste and mouthwash containing fluoride and casein phosphopeptide-amorphous calcium phosphate promote remineralization of initial enamel lesions; however, they need to be used regularly and are more of a tire patch than a real solution, Moradian-Oldak said. It plugs up the problem so people don’t feel pain. The gel, however, fills the cracks and holes with an enamel-like substance.

In the United States, 92% of adults aged 20 to 64 have had dental decay in their permanent teeth, Moradian-Oldak said. Grinding teeth at night, gum recession, and the disappearance of enamel over a lifetime due to demineralizing acidic food and drink are all common problems people everywhere face.

When tested in an environment that mimics an oral cavity’s biochemical processes, the gel created a robust attachment, eliminating the threat of secondary cavities in the same spot, Ruan said. The gel could be more effective than traditional crowns, whose adhesion weakens over time, he added.

“Besides biocompatibility and biodegradability, the gel has unique antimicrobial and adhesion properties that are important for dental applications,” Ruan said.

MMP-20 carves out proteins that decrease enamel strength
USC researchers tested their theory using wild type mice and MMP-20 null mice. The MMP-20 null mice had inconsistent enamel hydroxyapatite crystals that were shorter, wider, and thinner than those found in the wild type mice.

Some 31% of the enamel nanocrystals area isolated from MMP-20 mice were imperfect, whereas only 10% of the area was imperfect in crystals from wild type mice.

The gel that produces enamel-like growth
In preparation for a possible human study, USC researchers used human molars without any lesions. They sliced teeth into three or four blocks, created artificial tooth decay, then cycled the samples in artificial saliva with pH 4.6, 7.0, and 6.5.

Normal salivary pH is between 6 to 7 but could quickly fluctuate between 5.3 to 7.8 based on food and beverage intake.

A sample of supersaturated calcium and phosphate ions in a remineralization solution produced an enamel-like substance; however, it created a disorganized structure with irregular crystals. In contrast, the hydrogel grew oriented crystals, reducing the depth of the lesions by 50% to 70% after seven days of hydrogel application. It is a big improvement over other methods, Ruan said.

“In one study, it was reported that only about 24% of tooth decay was recovered after 12 days of pH cycling with sodium fluoride treatment,” he said.

The next step is to alter the gel recipe using MMP-20 to create a stronger enamel-like seal, Moradian-Oldak said.

“We create a protective cover on enamel,” she said. “We restore the structure of enamel, and it will prevent decay from progressing.”

The studies were funded by grants from the National Institutes of Health’s National Institute of Dental and Craniofacial Research (DE-13414 and DE-020099) and USC Coulter Translational Research Partnership Program via the Wallace Coulter Foundation (WCF/GRZYWACZ/2011).

 

Source: Dentistry IQ

Beyond Angkor: How lasers revealed a lost city

_77664683_angkorwat624

Deep in the Cambodian jungle lie the remains of a vast medieval city, which was hidden for centuries. New archaeological techniques are now revealing its secrets – including an elaborate network of temples and boulevards, and sophisticated engineering.

In April 1858 a young French explorer, Henri Mouhot, sailed from London to south-east Asia. For the next three years he travelled widely, discovering exotic jungle insects that still bear his name.

Today he would be all but forgotten were it not for his journal, published in 1863, two years after he died of fever in Laos, aged just 35.

Mouhot’s account captured the public imagination, but not because of the beetles and spiders he found.

Readers were gripped by his vivid descriptions of vast temples consumed by the jungle: Mouhot introduced the world to the lost medieval city of Angkor in Cambodia and its romantic, awe-inspiring splendour.

“One of these temples, a rival to that of Solomon, and erected by some ancient Michelangelo, might take an honourable place beside our most beautiful buildings. It is grander than anything left to us by Greece or Rome,” he wrote.

 

His descriptions firmly established in popular culture the beguiling fantasy of swashbuckling explorers finding forgotten temples.

Today Cambodia is famous for these buildings. The largest, Angkor Wat, constructed around 1150, remains the biggest religious complex on Earth, covering an area four times larger than Vatican City.

It attracts two million tourists a year and takes pride of place on Cambodia’s flag.

But back in the 1860s Angkor Wat was virtually unheard of beyond local monks and villagers. The notion that this great temple was once surrounded by a city of nearly a million people was entirely unknown.

It took over a century of gruelling archaeological fieldwork to fill in the map. The lost city of Angkor slowly began to reappear, street by street. But even then significant blanks remained.

Then, last year, archaeologists announced a series of new discoveries – about Angkor, and an even older city hidden deep in the jungle beyond.

An international team, led by the University of Sydney’s Dr Damian Evans, had mapped 370 sq km around Angkor in unprecedented detail – no mean feat given the density of the jungle and the prevalence of landmines from Cambodia’s civil war. Yet the entire survey took less than two weeks.

Their secret?

Lidar – a sophisticated remote sensing technology that is revolutionising archaeology, especially in the tropics.

Mounted on a helicopter criss-crossing the countryside, the team’s lidar device fired a million laser beams every four seconds through the jungle canopy, recording minute variations in ground surface topography.

The findings were staggering.

Lidar technology has revealed the original city of Angkor - red lines indicate modern features including roads and canals

Lidar technology has revealed the original city of Angkor – red lines indicate modern features including roads and canals

The archaeologists found undocumented cityscapes etched on to the forest floor, with temples, highways and elaborate waterways spreading across the landscape.

“You have this kind of sudden eureka moment where you bring the data up on screen the first time and there it is – this ancient city very clearly in front of you,” says Dr Evans.

These new discoveries have profoundly transformed our understanding of Angkor, the greatest medieval city on Earth.

Phra Sav Ling Povn, palace of the leprous king, near Angkor Wat, circa 1930

Phra Sav Ling Povn, palace of the leprous king, near Angkor Wat, circa 1930

At its peak, in the late 12th Century, Angkor was a bustling metropolis covering 1,000 sq km. (It would be another 700 years before London reached a similar size.)

Angkor was once the capital of the mighty Khmer empire which, ruled by warrior kings, dominated the region for centuries – covering all of present-day Cambodia and much of Vietnam, Laos, Thailand and Myanmar. But its origins and birthplace have long been shrouded in mystery.

A few meagre inscriptions suggested the empire was founded in the early 9th Century by a great king, Jayavarman II, and that his original capital, Mahendraparvata, was somewhere in the Kulen hills, a forested plateau north-east of the site on which Angkor would later be built.

But no-one knew for sure – until the lidar team arrived.

The lidar survey of the hills revealed ghostly outlines on the forest floor of unknown temples and an elaborate and utterly unexpected grid of ceremonial boulevards, dykes and man-made ponds – a lost city, found.

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Most striking of all was evidence of large-scale hydraulic engineering, the defining signature of the Khmer empire.

By the time the royal capital moved south to Angkor around the end of the 9th Century, Khmer engineers were storing and distributing vast quantities of precious seasonal monsoon water using a complex network of huge canals and reservoirs.

Harnessing the monsoon provided food security – and made the ruling elite fantastically rich. For the next three centuries they channelled their wealth into the greatest concentration of temples on Earth.

One temple, Preah Khan, constructed in 1191, contained 60t of gold. Its value today would be about £2bn ($3.3bn).

But despite the city’s immense wealth, trouble was brewing.

At the same time that Angkor’s temple-building programme peaked, its vital hydraulic network was falling into disrepair – at the worst possible moment.

The end of the medieval period saw dramatic shifts in climate across south-east Asia.

Tree ring samples record sudden fluctuations between extreme dry and wet conditions – and the lidar map reveals catastrophic flood damage to the city’s vital water network.

With this lifeline in tatters, Angkor entered a spiral of decline from which it never recovered.

In the 15th Century, the Khmer kings abandoned their city and moved to the coast. They built a new city, Phnom Penh, the present-day capital of Cambodia.

Life in Angkor slowly ebbed away.

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When Mouhot arrived he found only the great stone temples, many of them in a perilous state of disrepair.

Nearly everything else – from common houses to royal palaces, all of which were constructed of wood – had rotted away.

The vast metropolis that once surrounded the temples had been all but devoured by the jungle.

 

Source: BBC

Image credit: David Lazar

Cassini Watches Mysterious Feature Evolve in Titan Sea

pia18430-640

September 29, 2014

NASA’s Cassini spacecraft is monitoring the evolution of a mysterious feature in a large hydrocarbon sea on Saturn’s moon Titan. The feature covers an area of about 100 square miles (260 square kilometers) in Ligeia Mare, one of the largest seas on Titan. It has now been observed twice by Cassini’s radar experiment, but its appearance changed between the two apparitions.

Images of the feature taken during the Cassini flybys are available at:

http://photojournal.jpl.nasa.gov/catalog/PIA18430

The mysterious feature, which appears bright in radar images against the dark background of the liquid sea, was first spotted during Cassini’s July 2013 Titan flyby. Previous observations showed no sign of bright features in that part of Ligeia Mare. Scientists were perplexed to find the feature had vanished when they looked again, over several months, with low-resolution radar and Cassini’s infrared imager. This led some team members to suggest it might have been a transient feature. But during Cassini’s flyby on August 21, 2014, the feature was again visible, and its appearance had changed during the 11 months since it was last seen.

Scientists on the radar team are confident that the feature is not an artifact, or flaw, in their data, which would have been one of the simplest explanations. They also do not see evidence that its appearance results from evaporation in the sea, as the overall shoreline of Ligeia Mare has not changed noticeably.

The team has suggested the feature could be surface waves, rising bubbles, floating solids, solids suspended just below the surface, or perhaps something more exotic.

The researchers suspect that the appearance of this feature could be related to changing seasons on Titan, as summer draws near in the moon’s northern hemisphere. Monitoring such changes is a major goal for Cassini’s current extended mission.

“Science loves a mystery, and with this enigmatic feature, we have a thrilling example of ongoing change on Titan,” said Stephen Wall, the deputy team lead of Cassini’s radar team, based at NASA’s Jet Propulsion Laboratory in Pasadena, California. “We’re hopeful that we’ll be able to continue watching the changes unfold and gain insights about what’s going on in that alien sea.”

The Cassini-Huygens mission is a cooperative project of NASA, the European Space Agency and ASI, the Italian Space Agency. JPL, a division of the California Institute of Technology in Pasadena, manages the mission for NASA’s Science Mission Directorate, Washington. The radar instrument was built by JPL and the Italian Space Agency, working with team members from the United States and several European countries.

For more information about Cassini and its mission, visit:

http://www.nasa.gov/cassini

http://saturn.jpl.nasa.gov

Source: NASA news

Gigantic Ocean Vortices Seen From Space Could Change Climate Models

By  – 06.26.14

The weather is a dance between an odd couple: the frantic atmosphere and the staid sea. The atmosphere changes quickly, as when a strong wind suddenly starts to blow or a cyclone careens ashore. The ocean seems more sedate. Its wide gyres trace the edges of continents, carrying sun-warmed water from the equator out towards the poles. Even the rough storms that terrorize sailors are more the sky’s fault than the sea’s. The waves that toss a ship are whipped up by the wind.

But it turns out that the ocean makes its own gestures; it just makes them very slowly. Enormous vortices of water, measuring 60 miles across, spin their way across the sea at a deliberate pace—3 miles per day. Oceanographers have dubbed them mesoscale eddies for their middle size, larger than a wake formed by an aircraft carrier and smaller than a gyre. Each one is like an upside down mountain of water, held together by its own rotation and extending about 3,000 feet beneath the surface. In the video above, eddies show up as red and blue dots dancing around. (Red ones spin clockwise, blue ones counterclockwise.) Just how much water gets carried around by all these eddies? The total is staggering: more than 30 times the amount dumped by all the world’s rivers into the ocean, according to a paper published today in Science. Other stuff gets caught in the vortices and taken along for the ride. This huge network of eddies may be shipping packets of pollutants, organic nutrients, and dissolved carbon all around the world.

These eddies are almost invisible unless you look from space. For decades, oceanographers have been tracking eddies using NASA satellites. By bouncing a pulse of radar off the surface of the water and recording the time it takes to return, the satellites can measure their distance from the water to within less than an inch. This astounding accuracy turns out to be necessary, since unlike the deep ship-swallowing whirlpools of Greek mythology, the depression at the center of an eddy is a mere 20 inches.

Enormous ocean eddies are measured using satellites (height map, top layer) and submersibles (vorticity map, bottom layers). Ocean University of China

Enormous ocean eddies are measured using satellites (height map, top layer) and submersibles (vorticity map, bottom layers).
Ocean University of China

To reconstruct the 3-D structure of the eddies and find their volume, a team of oceanographers led by Bo Qiu of the University of Hawaii used data from underwater floats. More than 3,000 ARGO submersibles are scattered around the globe, lurking under the surface. Each comes to the surface every 10 days to report the water temperature, salt content, density, and velocity. An eddy, once born, might travel for months or years before dissipating. By combining a decade of satellite and submersible data, the researchers were able to track the incredible mass of water collectively moved by eddies across the entire world. Qiu’s calculations surprised even him.

“We didn’t expect the number to be that high,” he said. “We know they propagate westward, and there are a lot of eddies. But the mass… there’s an order of magnitude more than we expected.”

Previously, it was thought that the steady currents like the Gulf Stream were almost entirely responsible for moving stuff through the ocean. The ocean transports trash, nutrients, radioactive waste, dissolved carbon dioxide and heat all around the world, and the latter two are especially important for understanding climate change. Qiu’s study raises the possibility that eddies also make a substantial contribution to these transports.

This paper will kick off a wave of research among climate modelers, says Ryan Abernathey, who studies the impact of ocean circulation on climate at Columbia University.  “The volume estimate is really surprising,” he said. “This is an important effect. The next question is how leaky the eddy is.” The eddy is made of water, after all, and the difference between inside and outside is not precise. If, say, the dissolved carbon caught in an eddy slowly slips out, then after a year of meandering an eddy may have left its original contents an ocean away. But if the eddies hold their cargo tightly, they might be shipping enormous packages of carbon, salt, and pollutants from Australia to Africa and from Europe to America. Scientists are now trying to figure out how the packages effect local ecosystems and the planet’s climate.

 

Originally posted on: Wired.com

Consciousness On And Off?

Consciousness on-off switch discovered deep in brain

20140704-114540.jpgONE moment you’re conscious, the next you’re not. For the first time, researchers have switched off consciousness by electrically stimulating a single brain area.

Scientists have been probing individual regions of the brain for over a century, exploring their function by zapping them with electricity and temporarily putting them out of action. Despite this, they have never been able to turn off consciousness – until now.

Although only tested in one person, the discovery suggests that a single area – the claustrum – might be integral to combining disparate brain activity into a seamless package of thoughts, sensations and emotions. It takes us a step closer to answering a problem that has confounded scientists and philosophers for millennia – namely how our conscious awareness arises.

Many theories abound but most agree that consciousness has to involve the integration of activity from several brain networks, allowing us to perceive our surroundings as one single unifying experience rather than isolated sensory perceptions.

One proponent of this idea was Francis Crick, a pioneering neuroscientist who earlier in his career had identified the structure of DNA. Just days before he died in July 2004, Crick was working on a paper that suggested our consciousness needs something akin to an orchestra conductor to bind all of our different external and internal perceptions together.

With his colleague Christof Koch, at the Allen Institute for Brain Science in Seattle, he hypothesised that this conductor would need to rapidly integrate information across distinct regions of the brain and bind together information arriving at different times. For example, information about the smell and colour of a rose, its name, and a memory of its relevance, can be bound into one conscious experience of being handed a rose on Valentine’s day.

The pair suggested that the claustrum – a thin, sheet-like structure that lies hidden deep inside the brain – is perfectly suited to this job (Philosophical Transactions of The Royal Society B, doi.org/djjw5m).

It now looks as if Crick and Koch were on to something. In a study published last week, Mohamad Koubeissi at the George Washington University in Washington DC and his colleagues describe how they managed to switch a woman’s consciousness off and on by stimulating her claustrum. The woman has epilepsy so the team were using deep brain electrodes to record signals from different brain regions to work out where her seizures originate. One electrode was positioned next to the claustrum, an area that had never been stimulated before.

When the team zapped the area with high frequency electrical impulses, the woman lost consciousness. She stopped reading and stared blankly into space, she didn’t respond to auditory or visual commands and her breathing slowed. As soon as the stimulation stopped, she immediately regained consciousness with no memory of the event. The same thing happened every time the area was stimulated during two days of experiments (Epilepsy and Behavior, doi.org/tgn).

To confirm that they were affecting the woman’s consciousness rather than just her ability to speak or move, the team asked her to repeat the word “house” or snap her fingers before the stimulation began. If the stimulation was disrupting a brain region responsible for movement or language she would have stopped moving or talking almost immediately. Instead, she gradually spoke more quietly or moved less and less until she drifted into unconsciousness. Since there was no sign of epileptic brain activity during or after the stimulation, the team is sure that it wasn’t a side effect of a seizure.

Koubeissi thinks that the results do indeed suggest that the claustrum plays a vital role in triggering conscious experience. “I would liken it to a car,” he says. “A car on the road has many parts that facilitate its movement – the gas, the transmission, the engine – but there’s only one spot where you turn the key and it all switches on and works together. So while consciousness is a complicated process created via many structures and networks – we may have found the key.”

Awake but unconscious

Counter-intuitively, Koubeissi’s team found that the woman’s loss of consciousness was associated with increased synchrony of electrical activity, or brainwaves, in the frontal and parietal regions of the brain that participate in conscious awareness. Although different areas of the brain are thought to synchronise activity to bind different aspects of an experience together, too much synchronisation seems to be bad. The brain can’t distinguish one aspect from another, stopping a cohesive experience emerging.

Since similar brainwaves occur during an epileptic seizure, Koubeissi’s team now plans to investigate whether lower frequency stimulation of the claustrum could jolt them back to normal. It may even be worth trying for people in a minimally conscious state, he says. “Perhaps we could try to stimulate this region in an attempt to push them out of this state.”

Anil Seth, who studies consciousness at the University of Sussex, UK, warns that we have to be cautious when interpreting behaviour from a single case study. The woman was missing part of her hippocampus, which was removed to treat her epilepsy, so she doesn’t represent a “normal” brain, he says.

However, he points out that the interesting thing about this study is that the person was still awake. “Normally when we look at conscious states we are looking at awake versus sleep, or coma versus vegetative state, or anaesthesia.” Most of these involve changes of wakefulness as well as consciousness but not this time, says Seth. “So even though it’s a single case study, it’s potentially quite informative about what’s happening when you selectively modulate consciousness alone.”

“Francis would have been pleased as punch,” says Koch, who was told by Crick’s wife that on his deathbed, Crick was hallucinating an argument with Koch about the claustrum and its connection to consciousness.

“Ultimately, if we know how consciousness is created and which parts of the brain are involved then we can understand who has it and who doesn’t,” says Koch. “Do robots have it? Do fetuses? Does a cat or dog or worm? This study is incredibly intriguing but it is one brick in a large edifice of consciousness that we’re trying to build.”

Source: New Scientist

This article appeared in print under the headline “Consciousness – we hit its sweet spot”

NASA Reports Mysterious Signal From Outer Space

By:

NASA has detected a mysterious signal from deep outer space. The signal was detected using the agency’s Chandra X-ray Observatory and ESA’s XMM-Newton. One intriguing possibility is that the X-rays are produced by the decay of sterile neutrinos, a type of particle that has been proposed as a candidate for dark matter.

“We know that the dark matter explanation is a long shot, but the pay-off would be huge if we’re right,” said Esra Bulbul of the Harvard-Smithsonian Center for Astrophysics (CfA) in Cambridge, Mass. who led the study. “So we’re going to keep testing this interpretation and see where it takes us.”

While the NASA X-ray mysterious signal holds exciting potential, these results must be confirmed with additional data to rule out other explanations and determine whether it is plausible that dark matter has been observed.

Astronomers think dark matter constitutes 85% of the matter in the Universe, but does not emit or absorb light like “normal” matter such as protons, neutrons and electrons that make up the familiar elements observed in planets, stars, and galaxies. Because of this, scientists must use indirect methods to search for clues about dark matter.

NASA’s latest mysterious signal results from Chandra and XMM-Newton consist of an unidentified X-ray emission line, that is, a spike of intensity at a very specific wavelength of X-ray light. Astronomers detected this emission line in the Perseus galaxy cluster using both Chandra and XMM-Newton. They also found the line in a combined study of 73 other galaxy clusters with XMM-Newton.

The authors suggest this emission line could be a signature from the decay of a “sterile neutrino.” Sterile neutrinos are a hypothetical type of neutrino that is predicted to interact with normal matter only via gravity. Some scientists have proposed that sterile neutrinos may at least partially explain dark matter.

“We have a lot of work to do before we can claim, with any confidence, that we’ve found sterile neutrinos,” said Maxim Markevitch, a co-author from NASA’s Goddard Space Flight Center in Greenbelt, Maryland. “But just the possibility of finding them has us very excited.”

NASA says the mysterious signal has one source of uncertainty. The detection of this emission line is pushing the capabilities of the two observatories in terms of sensitivity. Also, there may be explanations other than sterile neutrinos if this X-ray emission line is deemed to be real.

There are ways that normal matter in the cluster could have produced the line, although the team’s analysis suggested that all of these would involve unlikely changes to our understanding of physical conditions in the galaxy cluster or the details of the atomic physics of extremely hot gases.

The NASA authors of this mysterious signal note that even if the sterile neutrino interpretation is correct, their detection does not necessarily imply that all of dark matter is composed of these particles. As previously reported by NewsOXY, scientists found a newly discovered water planet in 2012. It is located in the right distance from its sun to hold life.

Source: Newsoxy.com

‘Time Crystals’ Could Upend Physicists’ Theory of Time

By Natalie Wolchover, Simons Science News

 

In February 2012, the Nobel Prize-winning physicist Frank Wilczek decided to go public with a strange and, he worried, somewhat embarrassing idea. Impossible as it seemed, Wilczek had developed an apparent proof of “time crystals” — physical structures that move in a repeating pattern, like minute hands rounding clocks, without expending energy or ever winding down. Unlike clocks or any other known objects, time crystals derive their movement not from stored energy but from a break in the symmetry of time, enabling a special form of perpetual motion.

“Most research in physics is continuations of things that have gone before,” said Wilczek, a professor at the Massachusetts Institute of Technology. This, he said, was “kind of outside the box.”

Wilczek’s idea met with a muted response from physicists. Here was a brilliant professor known for developing exotic theories that later entered the mainstream, including the existence of particles called axions and anyons, and discovering a property of nuclear forces known as asymptotic freedom (for which he shared the Nobel Prize in physics in 2004).But perpetual motion, deemed impossible by the fundamental laws of physics, was hard to swallow. Did the work constitute a major breakthrough or faulty logic? Jakub Zakrzewski, a professor of physics and head of atomic optics at Jagiellonian University in Poland who wrote a perspective on the research that accompanied Wilczek’s publication, says: “I simply don’t know.”

Now, a technological advance has made it possible for physicists to test the idea. They plan to build a time crystal, not in the hope that this perpetuum mobile will generate an endless supply of energy (as inventors have striven in vain to do for more than a thousand years) but that it will yield a better theory of time itself.

A Crazy Concept

The idea came to Wilczek while he was preparing a class lecture in 2010. “I was thinking about the classification of crystals, and then it just occurred to me that it’s natural to think about space and time together,” he said. “So if you think about crystals in space, it’s very natural also to think about the classification of crystalline behavior in time.”

When matter crystallizes, its atoms spontaneously organize themselves into the rows, columns and stacks of a three-dimensional lattice. An atom occupies each “lattice point,” but the balance of forces between the atoms prevents them from inhabiting the space between. Because the atoms suddenly have a discrete, rather than continuous, set of choices for where to exist, crystals are said to break the spatial symmetry of nature — the usual rule that all places in space are equivalent. But what about the temporal symmetry of nature — the rule that stable objects stay the same throughout time?

Wilczek mulled over the possibility for months. Eventually, his equations indicated that atoms could indeed form a regularly repeating lattice in time, returning to their initial arrangement only after discrete (rather than continuous) intervals, thereby breaking time symmetry. Without consuming or producing energy, time crystals would be stable, in what physicists call their “ground state,” despite cyclical variations in structure that scientists say can be interpreted as perpetual motion.

“For a physicist, this is really a crazy concept to think of a ground state which is time-dependent,” said Hartmut Häffner, a quantum physicist at the University of California, Berkeley. “The definition of a ground state is that this is energy-zero. But if the state is time-dependent, that implies that the energy changes or something is changing. Something is moving around.”

How can something move, and keep moving forever, without expending energy? It seemed an absurd idea — a major break from the accepted laws of physics. But Wilczek’s papers on quantum and classical time crystals (the latter co-authored by Alfred Shapere of the University of Kentucky) survived a panel of expert reviewers and were published in Physical Review Letters in October 2012. Wilczek didn’t claim to know whether objects that break the symmetry of time exist in nature, but he wanted experimentalists to try to make one.

“It’s like you draw targets and wait for arrows to hit them,” he said. “If there’s no logical barrier to this behavior being realized, then I expect it will be realized.”

The Big Test

In June, a group of physicists led by Xiang Zhang, a nanoengineer at Berkeley, and Tongcang Li, a physicist and postdoctoral researcher in Zhang’s group, proposed creating a time crystal in the form of a persistently rotating ring of charged atoms, or ions. (Li said he had been contemplating the idea before reading Wilczek’s papers.) The group’s article was published with Wilczek’s in Physical Review Letters.

Since then, a single critic — Patrick Bruno, a theoretical physicist at the European Synchrotron Radiation Facility in France — has voiced dissent in the academic literature. Bruno thinks Wilczek and company mistakenly identified time-dependent behavior of objects in excited energetic states, rather than their ground states. There is nothing surprising about objects with surplus energy moving in a cyclical fashion, with the motion decaying as the energy dissipates. To be a time crystal, an object must exhibit perpetual motion in its ground state.

Bruno’s comment and Wilczek’s reply appeared in Physical Review Letters in March 2013. Bruno demonstrated that a lower energy state is possible in a model system that Wilczek had proposed as a hypothetical example of a quantum time crystal. Wilczek said that although the example is not a time crystal, he doesn’t think the error “calls into question the basic concepts.”

“I proved that example is not correct,” Bruno said. “But I have no general proof — so far, at least.”

The debate will probably not be settled on theoretical grounds. “The ball is really in the hands of our very clever experimental colleagues,” Zakrzewski said.

An international team led by Berkeley scientists is preparing an elaborate lab experiment, although it may take “anywhere between three and infinity years” to complete, depending on funding or unforeseen technical difficulties, said Häffner, who is co-principal investigator with Zhang. The hope is that time crystals will push physics beyond the precise but seemingly imperfect laws of quantum mechanics and lead the way to a grander theory.

“I’m very interested in seeing if I can make a new contribution following Einstein,” Li said. “He said that quantum mechanics is not complete.”

Read full article here