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Method of recording brain activity could lead to mind-reading devices, Stanford scientists say

Method of recording brain activity could lead to mind-reading devices, Stanford scientists say | Amazing Science | Scoop.it

A brain region activated when people are asked to perform mathematical calculations in an experimental setting is similarly activated when they use numbers -- or even imprecise quantitative terms, such as "more than" -- in everyday conversation, according to a study by Stanford University School of Medicine scientists.

 

Using a novel method, the researchers collected the first solid evidence that the pattern of brain activity seen in someone performing a mathematical exercise under experimentally controlled conditions is very similar to that observed when the person engages in quantitative thought in the course of daily life.

 

"We're now able to eavesdrop on the brain in real life," said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford's Human Intracranial Cognitive Electrophysiology Program. Parvizi is the senior author of the study, published Oct. 15, 2013 in Nature Communications. The study's lead authors are postdoctoral scholar Mohammad Dastjerdi, MD, PhD, and graduate student Muge Ozker.

 

The finding could lead to "mind-reading" applications that, for example, would allow a patient who is rendered mute by a stroke to communicate via passive thinking. Conceivably, it could also lead to more dystopian outcomes: chip implants that spy on or even control people's thoughts.

 

"This is exciting, and a little scary," said Henry Greely, JD, the Deane F. and Kate Edelman Johnson Professor of Law and steering committee chair of the Stanford Center for Biomedical Ethics, who played no role in the study but is familiar with its contents and described himself as "very impressed" by the findings. "It demonstrates, first, that we can see when someone's dealing with numbers and, second, that we may conceivably someday be able to manipulate the brain to affect how someone deals with numbers."

 

The researchers monitored electrical activity in a region of the brain called the intraparietal sulcus, known to be important in attention and eye and hand motion. Previous studies have hinted that some nerve-cell clusters in this area are also involved in numerosity, the mathematical equivalent of literacy.

 

However, the techniques that previous studies have used, such as functional magnetic resonance imaging, are limited in their ability to study brain activity in real-life settings and to pinpoint the precise timing of nerve cells' firing patterns. These studies have focused on testing just one specific function in one specific brain region, and have tried to eliminate or otherwise account for every possible confounding factor. In addition, the experimental subjects would have to lie more or less motionless inside a dark, tubular chamber whose silence would be punctuated by constant, loud, mechanical, banging noises while images flashed on a computer screen.

 

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Comprehensive drug-gene database that matches thousands of disease genes with approved or experimental drugs

Comprehensive drug-gene database that matches thousands of disease genes with approved or experimental drugs | Amazing Science | Scoop.it

Researchers atWashington University School of Medicine in St. Louis have created a massive online database that matches thousands of genes linked to cancer and other diseases with drugs that target those genes. Some of the drugs are approved by the U.S. Food and Drug Administration, while others are in clinical trials or just entering the drug development pipeline.

 

The database was developed by identical twin brothers, Obi Griffith, PhD, and Malachi Griffith, PhD, whose interest in pairing drugs with genes is as much personal as it is scientific. Their mother died of breast cancer 17 years ago, just weeks before their high school graduation.

 

“We wanted to create a comprehensive database that is user-friendly, something along the lines of a Google search engine for disease genes,” explained Malachi Griffith, a research instructor in genetics. “As we move toward personalized medicine, there’s a lot of interest in knowing whether drugs can target mutated genes in particular patients or in certain diseases, like breast or lung cancer. But there hasn’t been an easy way to find that information.”

 

Details of the Drug Gene Interaction Database are reported online Oct. 13 inNature Methods. The database is weighted heavily toward cancer genes but also includes genes involved in Alzheimer’s disease, heart disease, diabetes and many other illnesses. The Griffiths created the database with a team of scientists at The Genome Institute at Washington University in St. Louis.

 

The database is easy to search and geared toward researchers and physician-scientists who want to know whether errors in disease genes – identified through genome sequencing or other methods – potentially could be targeted with existing drug therapies. Additional genes included in the database could be the focus of future drug development efforts because they belong to classes of genes that are thought to make promising drug targets.

 

“Developing the database was a labor of love for the Griffiths,” said senior author Richard K. Wilson, PhD, director of The Genome Institute. “There’s an amazing depth to this resource, which will be invaluable to researchers working to design better treatment options for patients.”

 

Wilson and his colleagues caution that the database is intended for research purposes and that it does not recommend treatments. The primary purpose of the database is to further clinical research aimed at treating diseases more effectively.

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Exploding Asteroids Pose Greater Threat Than Direct Hits

Exploding Asteroids Pose Greater Threat Than Direct Hits | Amazing Science | Scoop.it
Asteroid airbursts pose a greater-than-expected threat, cautions one impact expert, who calls for a new space warning scale.

 

An asteroid bursting apart in midair over a city poses a greater threat to humanity than a long-feared "planet buster" smacking into Earth, suggests one impact expert. He calls for a revised system of planetary defense focused on detecting smaller asteroids, instead of the big ones.

 

Earth orbits amid a shooting gallery of meteorites and asteroids; such shooting stars can be seen crossing the sky every 15 minutes on a typical night.

 

Sometimes those space visitors are larger, such as the February 15 fireball that exploded over Chelyabinsk, Russia, injuring some 1,500 people in six cities across the region, or the 1908 Tunguska event that flattened 830 square miles (2,150 square kilometers) of Siberian forest.

 

"The chances are virtually certain that we are going to be next hit by a little asteroid that is a 'city buster,' long before we are hit by a bigger one," said physicist Mark Boslough of Sandia National Laboratories in Albuquerque, New Mexico.

 

In an upcoming report in the Acta Astronautica journal, Boslough proposes a new "airbust" warning system for asteroids that blow apart in midair rather than blasting big holes in the ground.

 

"We really need to come up with a way to warn people," he said.

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One in 2000 people carry infectious cCJD prions in the UK

One in 2000 people carry infectious cCJD prions in the UK | Amazing Science | Scoop.it
Prevalence of vCJD prions is higher than previously shown, but questions remain over risk of clinical disease.

 

The prion protein which causes variant Creutzfeldt–Jakob disease destroys neurons in the brain but more easily infects the lymphoid system. As a new study in the British Medical Journal reveals that 1 in 2000 people in the UK may harbour the infectious prion protein which causes variant Creutzfeldt–Jakob disease (vCJD).


The usually fatal condition is the human form of bovine spongiform encepalpoathy — dubbed 'mad cow disease' in the UK after an outbreak of the disease in the 1980s. Both diseases are caused by misfolded proteins called prions, which induce other proteins in the brain to clump, eventually destoying neurons. Humans are thought to contract the disease by consuming beef containing infected bovine brain or other central nervous system tissue. But it also spreads through blood transfusions, and some worry that the prion disease is transmitted via contaminated surgical instruments .


The BSE outbreak in the 1980s and 1990s led to a surge in British vCJD cases, and a total of 177 have been detected in the UK to date, with just one in the last two years. Cases of vCJD peaked in 2000, leading some scientists to speculate that the disease takes about a decade to develop. Yet other studies of different forms of CJD suggest its incubation time could be much longer — indicating that many Britons may be carrying the infection without symtoms.

 

Studies have come to varying conclusions as to just how many people harbour the abnormal prion protein (PrP) that causes vCJD. Surveys of tens of thousands of appendices and tonsil, discarded after surgery, have come up with prevalence rates ranging from 1 in 4,000 to 1 in 10,000 to 0.


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Vloasis's curator insight, October 16, 2013 2:12 PM

Just trying to wrap my brain around the concept of prions is headache-worthy!

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First Fossil of Blood-Filled Mosquito Discovered

First Fossil of Blood-Filled Mosquito Discovered | Amazing Science | Scoop.it

Through a series of events that scientists themselves admit was “extremely improbable,” a mosquito that feasted on the blood of Eocene animals some 46 million years ago managed to die and become trapped in sediment, but remain in tact, all while carrying a belly full of blood — its last meal.

 

The result, recently discovered in some oil shale from northwestern Montana, is the first fossil of a mosquito found still engorged with ancient blood. According to the lead researcher of the study, Smithsonian Institution paleontologist Dale Greenwalt, this is only the fifth instance of blood-eating, or hematophagy, by any insect to be revealed in the fossil record, and it’s the first in a mosquito with traces of blood that his team calls “incontrovertible.”


Most fossils of blood-eating insects that have been found are of midges, a kind of biting fly, trapped in amber, the team points out. But since mosquitoes typically prefer open habitats near water, rather than forests full of sap-bearing trees, finding preserved remains of mosquitoes has been rare. Given all of these factors, Greenwalt’s team writes, “it is not surprising that a fossil of a blood-engorged mosquito has not been described [before]; this despite the popular misconception of dinosaur DNA recovery from blood-engorged mosquitoes in amber popularized by the 1993 movie Jurassic Park.”


Since they bring that up, it’s worth pointing out that the mosquito fossil dates to the Middle Eocene, some 19 million years after non-avian dinosaurs went extinct. DNA molecules are too complex and fragile to survive fossilization, the team says, so it’s impossible to tell what kind of animal the Montana mosquito took its final meal from.


But among the discoveries that this find has made possible is that other large molecules — like those large enough to denote the presence of blood — can still survive fossilization.

 

The team decided to investigate the fossil more closely after noticing the insect’s dark, distended abdomen, appearing much like a modern mosquito after drinking a big blood meal. Tests of the abdomen revealed very high levels of iron ions, a mineral in which animal blood is rich.


So the team analyzed the sample using mass spectroscopy to get a more precise chemical makeup of the insect’s gut contents. They found telltale organic compounds that are the “fingerprints” of a substance called heme, the molecule that allows hemoglobin in blood to carry oxygen, and that gives blood its red color.

 


 
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New Theory for Synapse Formation in the Brain

New Theory for Synapse Formation in the Brain | Amazing Science | Scoop.it
Jülich, 10 October 2013 – The human brain keeps changing throughout a person’s lifetime. New connections are continually created while synapses that are no longer in use degenerate.

 

To date, little is known about the mechanisms behind these processes. Jülich neuroinformatician Dr. Markus Butz has now been able to ascribe the formation of new neural networks in the visual cortex to a simple homeostatic rule that is also the basis of many other self-regulating processes in nature. With this explanation, he and his colleague Dr. Arjen van Ooyen from Amsterdam also provide a new theory on the plasticity of the brain – and a novel approach to understanding learning processes and treating brain injuries and diseases.


The brains of adult humans are by no means hard wired. Scientists have repeatedly established this fact over the last few years using different imaging techniques. This so-called neuroplasticity not only plays a key role in learning processes, it also enables the brain to recover from injuries and compensate for the loss of functions. Researchers only recently found out that even in the adult brain, not only do existing synapses adapt to new circumstances, but new connections are constantly formed and reorganized. However, it was not yet known how these natural rearrangement processes are controlled in the brain. In the open-access journal PLOS Computational Biology, Butz and van Ooyen now present a simple rule that explains how these new networks of neurons are formed.

 

"It’s very likely that the structural plasticity of the brain is the basis for long-term memory formation," says Markus Butz, who has been working at the recently established Simulation Laboratory Neuroscience at the Jülich Supercomputing Centre for the past few months. "And it’s not just about learning. Following the amputation of extremities, brain injury, the onset of neurodegenerative diseases, and strokes, huge numbers of new synapses are formed in order to adapt the brain to the lasting changes in the patterns of incoming stimuli."

 

These results show that the formation of new synapses is driven by the tendency of neurons to maintain a 'pre-set' electrical activity level. If the average electric activity falls below a certain threshold, the neurons begin to actively build new contact points. These are the basis for new synapses that deliver additional input – the neuron firing rate increases. This also works the other way round: as soon as the activity level exceeds an upper limit, the number of synaptic connections is reduced to prevent any overexcitation – the neuron firing rate falls. Similar forms of homeostasis frequently occur in nature, for example in the regulation of body temperature and blood sugar levels.

 

"It was previously assumed that structural plasticity also follows the principle of Hebbian plasticity. The findings suggest that structural plasticity is governed by the homeostatic principle instead, which was not taken into consideration before," says Prof. Abigail Morrison, head of the Simulation Laboratory Neuroscience at Jülich. Her team is already integrating the new rule into the freely accessible simulation software NEST, which is used by numerous scientists worldwide.

 

These findings are also of relevance for the Human Brain Project. Neuroscientists, medical scientists, computer scientists, physicists, and mathematicians in Europe are working hand in hand to simulate the entire human brain on high-performance computers of the next generation in order to better understand how it functions. “Due to the complex synaptic circuitry in the human brain, it’s not plausible that its fault tolerance and flexibility are achieved based on static connection rules. Models are therefore required for a self-organization process,” says Prof. Markus Diesmann from Jülich’s Institute of Neuroscience and Medicine, who is involved in the project. He heads Computational and Systems Neuroscience (INM-6), a subinstitute working at the interface between neuroscientific research and simulation technology.

 
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James J. Goldsmith's curator insight, July 28, 2014 3:22 PM

Some insights on a difficult, but important topic.  Recommended.

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New device harnesses sun and sewage to produce hydrogen fuel

New device harnesses sun and sewage to produce hydrogen fuel | Amazing Science | Scoop.it
A novel device that uses only sunlight and wastewater to produce hydrogen gas could provide a sustainable energy source while improving the efficiency of wastewater treatment.

 

A research team led by Yat Li, associate professor of chemistry at the University of California, Santa Cruz, developed the solar-microbial device and reported their results in a paper published in the American Chemical Society journal ACS Nano. The hybrid device combines a microbial fuel cell (MFC) and a type of solar cell called a photoelectrochemical cell (PEC). In the MFC component, bacteria degrade organic matter in the wastewater, generating electricity in the process. The biologically generated electricity is delivered to the PEC component to assist the solar-powered splitting of water (electrolysis) that generates hydrogen and oxygen.

 

Either a PEC or MFC device can be used alone to produce hydrogen gas. Both, however, require a small additional voltage (an "external bias") to overcome the thermodynamic energy barrier for proton reduction into hydrogen gas. The need to incorporate an additional electric power element adds significantly to the cost and complication of these types of energy conversion devices, especially at large scales. In comparison, Li's hybrid solar-microbial device is self-driven and self-sustained, because the combined energy from the organic matter (harvested by the MFC) and sunlight (captured by the PEC) is sufficient to drive electrolysis of water.

 

In effect, the MFC component can be regarded as a self-sustained "bio-battery" that provides extra voltage and energy to the PEC for hydrogen gas generation. "The only energy sources are wastewater and sunlight," Li said. "The successful demonstration of such a self-biased, sustainable microbial device for hydrogen generation could provide a new solution that can simultaneously address the need for wastewater treatment and the increasing demand for clean energy."

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Charged particles can be accelerated using light, leading the way for more compact particle accelerators

Charged particles can be accelerated using light, leading the way for more compact particle accelerators | Amazing Science | Scoop.it

Modern particle accelerators measure up to several kilometres in size and cost billions of euros. But thanks to a new method they could shrink to less than 10 meters and cost 10 times less in future. To this end, physicists at the Max Planck Institute of Quantum Optics in Garching accelerated electrons directly using a light wave. In the conventional procedure by contrast, particles are accelerated with microwaves. In their demonstration experiment, John Breuer and Peter Hommelhoff obtained an accelerating force that was equally as strong as the force achieved in current conventional particle accelerators. The unique feature of the Garching-based procedure is that it is modular and can be expanded into a multi-level system capable of accelerating charged particles – which could be protons or ions, as well as electrons – around 100 times faster than current systems, and therefore could be built to a much smaller scale. Developmental work is still necessary for this expansion, however.

Cost-effective, laboratory-scale particle accelerators measuring less than 10 meters would benefit the research community greatly. Many research groups regularly queue at the few linear accelerators in which a straight line of particles is accelerated almost to the speed of light. Smaller and less expensive accelerators, on the other hand, would be available in greater numbers and would lead to a growth in research and faster research results in areas such as nuclear physics, materials science and life sciences.

 

In order to be able to build more compact particle accelerators, the electric field driving the particles would have to be strengthened. This can be illustrated by a picture in which a car represents an electron, a street stands for the electric field and the gradient of the street corresponds to the strength of the field. A stronger electric field is then equivalent to a more steeply sloping street on which a rolling car gathers the same speed on a short stretch of road than it would on a long, flatter road. But it is almost impossible to increase the electric field with current technology. Metaphorically speaking, current accelerators are an incline with a limited gradient.

 

Breuer cites the easy scalability of the procedure as its most important advantage. This means that an accelerator can easily be expanded into a more high-performance system by concatenating multiple gratings. Another advantage is that the accelerated electron pulses can be controlled more precisely in terms of time. As the frequency of the driving light is significantly higher than that of microwaves, shorter electron pulses with higher frequencies can also be generated, stresses Breuer. According to the physicist, this effectively results in an extremely fast electron stroboscope which allows scientists to study rapid processes, such as changes in a crystal. "The method is also suitable for the construction of future, more cost-effective and more compact free electron lasers," adds Breuer. Such X-ray sources are also valuable research tools in materials science and biology.

 

However, even the accelerators or free electron lasers that are based on the new Garching method would have their limitations. They would generate a small flow of electrons and deliver a smaller beam diameter. The associated lower power of the X-ray light compared to today's conventional synchrotron sources can, however, be compensated for so that such innovative sources demonstrate better coherent properties – the light waves in their pulses vibrate more precisely in synchronisation than the waves of standard synchrotron radiation. This would enable scientists to conduct a whole range of new experiments, ranging from high-resolution tomography to the spectroscopy of atomic nuclei.

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Evidence for a new nuclear 'magic number'

Evidence for a new nuclear 'magic number' | Amazing Science | Scoop.it
Researchers have come one step closer to understanding unstable atomic nuclei.

 

The protons and neutrons in an atomic nucleus form distinct shells corresponding to large gaps between energy levels, rather like electrons orbiting in an atom. In stable, naturally occurring nuclei, fully occupied shells occur at proton or neutron numbers of 2, 8, 20, 28, 50, 82 or 126 — so-called magic numbers. In unstable nuclei in which a large imbalance of protons and neutrons exists, new shells can appear, others disappear and magic numbers can evolve. A spectroscopic study of the neutron-rich nucleus calcium-54 (20 protons and 34 neutrons) using proton knockout reactions from fast radioactive projectiles generated in RIKEN's Radioactive Isotope Beam Factory provides direct evidence that neutron number 34 is magic in this system. This result removes longstanding uncertainty about the existence of such a magic number, and establishes the 'doubly magic' (in neutron and proton number) nature of exotic calcium-54 isotopes.

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'Terminator arm' churned out of 3D printer

'Terminator arm' churned out of 3D printer | Amazing Science | Scoop.it

Transparent plastic arm shows how 3D printers can create strong structure, mobile joints and delicate sensors in one process.

 

It may look like a sci-fi movie prop, but it could be a glimpse at the future of prosthetics. 3D printing can render everyday artefacts in clear plastic, so we can see in unprecedented detail how they work – and this exquisite model of a prosthetic arm is a brilliant example. It is one of the highlights at the London Science Museum's 3D printing exhibition, which features more than 600 printed objects.


Designed by Richard Hague, director of the Additive Manufacturing and 3D Printing Research Group at the University of Nottingham, UK, and his students the arm shows how the printers can create strong structure, mobile joints and delicate sensors – like spiral-shaped metal touch-detectors – all in one process.

 

"It's a mock-up but it shows circuits that sense temperature, feel objects and control the arm's movement," says Hague. "3D printing gives us the freedom to make complex, optimised shapes, and our research aim is focused on printing-in electrical, optical or even biological functions."

 

Such techniques are also bringing prosthetics to people who previously could not afford them. For instance, the open-source "robohand" project, pioneered by South African carpenter Richard Van As, aims to print cheap, plastic customised prostheses for people who have lost fingers, or who were born with some digits missing or malformed. Some of his work – with the designs available online – is also on show at the Science Museum.

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Elon Musk’s Tesla Motors to Introduce Self-Driving Cars in Three Years

Elon Musk’s Tesla Motors to Introduce Self-Driving Cars in Three Years | Amazing Science | Scoop.it
Elon Musk and his companies have been a PR treasure trove of late. SpaceX continues to make strides in reusable rocket tech with its Grasshopper rocket. Musk showed off an Iron Man 3D design interface his engineers are building.

 

Then of course, there’s his hypothethical 700+ mph Hyperloop from SF to LA. Now, he’s pushing the envelope again. This time it’s robot cars—a hot topic any way you slice it.


Big automakers are stumbling over each other to forecast and commit to bold timelines. Earlier this year, BMW predicted we’d have highly automated cars by 2020 and the fully automated variety by 2025. More recently, Nissan upped the ante with their commitment to bring self-driving autos by 2020.

 

What’s Musk think about all this? In a Financial Times interview, he said his car company, Tesla Motors, would offer self-driving models three years from now. The project is still under wraps—Musk didn’t elaborate further, and there’s been nothing official from Tesla. But he said, “It’s not speculation.”

 

So what exactly did Musk promise? He thinks 90% of miles driven could be automated in three years. But full automation, that extra 10%, “may be a bridge too far.”

Musk has proven himself a businessman and engineer par excellence with a flare for showmanship and seemingly unflappable confidence.

 

In this case, his forecast isn’t too unreasonable. Tracking technology and smart algorithms are improving—and not just in the lab. You can purchase cars with significant levels of automation from Daimler, and Google’s autonomous cars are logging miles on public highways. Indeed, BMW’s i3 is an electric car capable of autonomous operation in city and highway traffic.

 

We don’t know how far along Tesla is in their plans to automate, but Musk’s firms tend to move fast and are defining or redefining the markets they’ve entered.

 

Tesla already makes the top high-end electric car on the market. SpaceX is a commercial space firm flying payloads to the International Space Station for a fraction of traditional costs. And whereas Google has no experience manufacturing cars—that’s exactly what Tesla does.

 

Regulatory agencies and legal professionals are already taking a look at automation in the US. And limited laws make it legal for Google to test its robot cars on public roads in California, Nevada, and Florida. Further, self-driving systems are gradually seeping into cars and becoming a trusted feature. As folks get used to the idea and become familiar with the systems, and as those systems prove robust, there’s no reason to believe regulatory and liability quandaries won’t be worked out.


Fewer accidents, a leading cause of death worldwide, would be a welcome benefit. Many traffic jams are caused by poor human decision-making—robot autos could adjust their speeds to ease snarls of traffic, maybe even by talking to one another. More consistent acceleration could improve gas mileage or better conserve charge.

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James Jandebeur's curator insight, October 12, 2013 10:53 AM

I'm not sure how comfortable I would be with a self-driving car, but perhaps they can do it right. As long as we can turn it off when we need to, and some people enjoy driving (and do it well).

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Genome-wide signatures of convergent evolution in echolocating mammals

Genome-wide signatures of convergent evolution in echolocating mammals | Amazing Science | Scoop.it
Evolution is typically thought to proceed through divergence of genes, proteins and ultimately phenotypes. However, similar traits might also evolve convergently in unrelated taxa owing to similar selection pressures.

 

Adaptive phenotypic convergence is widespread in nature, and recent results from several genes have suggested that this phenomenon is powerful enough to also drive recurrent evolution at the sequence level. Where homoplasious substitutions do occur these have long been considered the result of neutral processes. However, recent studies have demonstrated that adaptive convergent sequence evolution can be detected in vertebrates using statistical methods that model parallel evolution, although the extent to which sequence convergence between genera occurs across genomes is unknown.

 

A group of scientists recently analyzed genomic sequence data in mammals that have independently evolved echolocation and show that convergence is not a rare process restricted to several loci but is instead widespread, continuously distributed and commonly driven by natural selection acting on a small number of sites per locus.

 

Systematic analyses of convergent sequence evolution in 805,053 amino acids within 2,326 orthologous coding gene sequences compared across 22 mammals (including four newly sequenced bat genomes) revealed signatures consistent with convergence in nearly 200 loci. Strong and significant support for convergence among bats and the bottlenose dolphin was seen in numerous genes linked to hearing or deafness, consistent with an involvement in echolocation. Unexpectedly, we also found convergence in many genes linked to vision: the convergent signal of many sensory genes was robustly correlated with the strength of natural selection. 

 

23 ‘hearing loci’ were identified: TYR, SLC4A11, NECAP1, COCH, JAG1, HOXA1, GTF3C2, PROX1, GGA3, MKKS, SLC44A2, ITM2B, EDNRB, FBXO11, PI4KB, DISP1, ERCC3, HESX1, FZD6, BDNF, NF2, OPA1 and DFNB59, and 75 'vision' loci: PAX6, MED24, JMJD6, ATP6AP1, MCM2, TRAF4, GPC4, CIC, RDH8, IMPG2, CAD, RPGRIP1, HPS4, RABGGTA, RP2, CLN5, RPGRIP1L, VPS18, RP1, FZR1, GLI3, UNC119, GLRB, MYF5, COPZ1, MCM3, TTK, HMGCR, NPHP3, PDC, RPE65, PRPF3, ELOVL4, TGIF2, TCTN3, TGFBI, OPN4, ECD, NEUROD4, BBS2, PAICS, APC, LAMC1, SKIL, PDCL, RABGGTB, IFT172, BBS4, INTS7, LGSN, ZEB1, PELO, SMARCA5, KIT, CNNM4, GJD2, CCT3, RHO, RFC4, SLC45A2, VPS39, CTNNB1, STAT3, ADRA1B, GPRC5C, SP3, PRPF8, PVRL3, RRH, BCOR, SIX6, DRD1, NHS, TOPORS and LCAT.

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Timeline 1961-2013 — The Higgs Boson, From Theory to Reality

Timeline 1961-2013 — The Higgs Boson, From Theory to Reality | Amazing Science | Scoop.it

The long road to find the Higgs boson is littered with subatomic particle discoveries and canceled colliders, but it ends with a discovery and a theory validated nearly 50 years after the idea was born.

 

Two European scientists won the Nobel Prize in Physics for describing the Higgs boson, a theoretical particle that may explain where mass comes from and advances man’s understanding of how the world is constructed. Peter Higgs, 84, a retired professor of theoretical physics at the University of Edinburgh, and Francois Englert, 80, a retired professor at the Free University of Brussels, will share the 8 million-krona ($1.25 million) prize, the Royal Swedish Academy of Sciences said today inStockholm.

 

The particle is the final piece of the jigsaw puzzle in the Standard Model, a theory explaining how the universe is built, and its existence would help scientists gain a better understanding of how galaxies hold together.

 

“Some people have compared it to the discovery of DNA,” said Rolf-Dieter Heuer, the director-general at the European Organization for Nuclear Research, known as CERN. “It’s not so wrong. It’s one of the building blocks of our existence. It ranks pretty high in the discoveries of the past century.”

 

The boson is named after Higgs, one of six scientists who devised a working theory of how elemental particles achieve mass in a three-month period in 1964. Englert had been the first to publish the theory a month earlier, along with Robert Brout, a Belgian colleague who died two years ago and wasn’t eligible for Nobel recognition because it is limited to living recipients.

 

“I’m very, very happy to have the recognition of this extraordinary reward,” Englert said, speaking by phone to a press conference held at the science academy.

 

 

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Pandoraviruses: Virus particles more complex then primitive eukaryotic cells

Pandoraviruses: Virus particles more complex then primitive eukaryotic cells | Amazing Science | Scoop.it

With the discovery of Mimivirus ten years ago and, more recently, Megavirus chilensis , researchers thought they had reached the farthest corners of the viral world in terms of size and genetic complexity. With a diameter in the region of a micrometer and a genome incorporating more than 1,100 genes, these giant viruses, which infect amoebas of the Acanthamoeba genus, had already largely encroached on areas previously thought to be the exclusive domain of bacteria.

 

For the sake of comparison, common viruses such as the influenza or AIDS viruses, only contain around ten genes each.In the article published in Science, the researchers announced they had discovered two new giant viruses: (a) Pandoravirus salinus, on the coast of Chile; (b) Pandoravirus dulcis, in a freshwater pond in Melbourne, Australia.

 

Detailed analysis has shown that these first two Pandoraviruses have virtually nothing in common with previously characterized giant viruses. What's more, only a very small percentage (6%) of proteins encoded by Pandoravirus salinus are similar to those already identified in other viruses or cellular organisms. With a genome of this size, Pandoravirus salinus has just demonstrated that viruses can be more complex than some eukaryotic cells . Another unusual feature of Pandoraviruses is that they have no gene allowing them to build a protein like the capsid protein, which is the basic building block of traditional viruses.

 

Despite all these novel properties, Pandoraviruses display the essential characteristics of other viruses in that they contain no ribosome, produce no energy and do not divide.This groundbreaking research included an analysis of the Pandoravirus salinus proteome, which proved that the proteins making it up are consistent with those predicted by the virus’ genome sequence. Pandoraviruses thus use the universal genetic code shared by all living organisms on the planet. This shows just how much more there is to learn regarding microscopic biodiversity as soon as new environments are considered. The simultaneous discovery of two specimens of this new virus family in sediments located 15,000 km apart indicates that Pandoraviruses, which were completely unknown until now, are very likely not rare. It definitively bridges the gap between viruses and cells – a gap that was proclaimed as dogma at the very outset of modern virology back in the 1950s. It also suggests that cell life could have emerged with a far greater variety of pre-cellular forms than those conventionally considered, as the new giant virus has almost no equivalent among the three recognized domains of cellular life, namely eukaryota (or eukaryotes), eubacteria, and archaea.

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Beyond antibiotics: 'PPMOs' offer new approach to bacterial infection and other diseases

Beyond antibiotics: 'PPMOs' offer new approach to bacterial infection and other diseases | Amazing Science | Scoop.it

Researchers recently announced the successful use of a new type of antibacterial agent called a PPMO, which appears to function as well or better than an antibiotic, but may be more precise and also solve problems with antibiotic resistance.

 

"The mechanism that PPMOs use to kill bacteria is revolutionary," said Bruce Geller, a professor of microbiology in the OSU College of Science and lead author on the study. "They can be synthesized to target almost any gene, and in that way avoid the development of antibiotic resistance and the negative impacts sometimes associated with broad-spectrum antibiotics. "Molecular medicine," Geller said, "is the way of the future."

 

PPMO stands for a peptide-conjugated phosphorodiamidate morpholino oligomer -- a synthetic analog of DNA or RNA that has the ability to silence the expression of specific genes. Compared to conventional antibiotics, which are often found in nature, PPMOs are completely synthesized in the laboratory with a specific genetic target in mind.

 

In animal laboratory tests against A. baumannii, one of the most dangerous Acinetobacter strains, PPMOs were far more powerful than some conventional antibiotics like ampicillin, and comparable to the strongest antibiotics available today. They were also effective in cases where the bacteria were resistant to antibiotics.

 

PPMOs have not yet been tested in humans. However, their basic chemical structure, the PMO, has been extensively tested in humans and found safe. Although the addition of the peptide to the PPMO poses an uncertain risk of toxicity, the potency of PPMOs reduces the risk while greatly improving delivery of the PMOs into bacterial cells, Geller said.

 

Geller said research is being done with Acinetobacter in part because this pathogen has become a huge global problem, and is often spread in hospitals. It can cause respiratory infection, sepsis, and is a special concern to anyone whose immune system is compromised. Wounds in military battle conditions have led to numerous cases in veterans, and A. baumannii is now resistant to many antibiotics. "Urgent new approaches to therapeutics are needed," the scientists said in their report.

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Living Relatives of Iceman Ötzi Mummy Found in Tirol, Austria

Living Relatives of Iceman Ötzi Mummy Found in Tirol, Austria | Amazing Science | Scoop.it

Ötzi the Iceman has at least 19 living male relatives in the Austrian Tirol, according to a genetic study into the origins of the people who now inhabit the region.

 

Scientists from the Institute of Legal Medicine at Innsbruck Medical University analyzed DNA samples taken from 3,700 blood donors in the Tyrol region of Austria.

 

During their study, they discovered that 19 individuals share a particular genetic mutation with the 5,300-year-old mummy, whose full genome was published last year.  “These men and the Iceman had the same ancestors,” Walther Parson, the forensic scientist who carried out the study, told the Austrian Press Agency.


The researchers focused on parts of the human DNA which are generally inherited unchanged. “In men it is the Y chromosomes and in females the mitochondria. Eventual changes arise due to mutations, which are then inherited further,” Parson explained.


People with the same mutations are categorized in haplogroups. Designed with letters, haplogroups allow researchers to trace early migratory routes since they are often associated with defined populations and geographical regions.

 

Indeed, Ötzi’s haplogroup is very rare in Europe. “The Iceman had the halogroup G, sub category G-L91. In our research we found another 19 people with this genetic group and subgroup,” Parson said.

 
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Apes comfort each other 'like humans'

Apes comfort each other 'like humans' | Amazing Science | Scoop.it

Young bonobos that are more "socially competent" are more likely to cuddle and calm other apes that are in distress, research has revealed.

Scientists working at an African sanctuary found that bonobos that recovered quickly from an upsetting experience, such as a fight, were also more likely to comfort others.

 

This mirrors findings from studies in children, and suggests bonobos manage their emotions in a very similar way. The researchers captured footage showing "emotionally competent" young apes rushing to hug other juveniles that were screaming after being attacked.


Prof Frans de Waal from Yerkes National Primate Research Center at Emory University in Atlanta, said these new results revealed that their ability to console one another was part of this empathy. He added: "It's almost as if one first needs to have one's own emotional house in order before one is ready to visit the emotional house of another. "This is true for children, and apparently also for bonobos."


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Researchers Discover Innate Virus-killing Power in Mammals

Researchers Discover Innate Virus-killing Power in Mammals | Amazing Science | Scoop.it

Findings by UC Riverside's Shou-Wei Ding could help create vaccines against deadly infections, including SARS, West Nile, dengue, Hepatitis C and influenza.

 

Viruses have been outwitting that innate protection in our cells by using proteins to suppress our virus-killing mechanism. Remove the suppressor protein from the virus, Ding’s research discovered, and the subject’s body will quickly eliminate the virus using the RNAi process, which sends out small interfering RNAs (siRNAs) to kill the disease.

 

In their research on young mice, for instance, all the subjects died when they were infected with the Nodamura virus, but when Ding’s researchers removed the suppressor protein called B2 from the virus, the infected mice began producing huge armies of the virus-attacking siRNAs and lived, unaffected by the otherwise lethal infection.

 

“Many have tried to do this, that is, find the viral siRNAs in mammals, but they could not find the key,” said Ding. “The key was our prior knowledge of the B2 protein in the Nodamura virus, a virus few people know about. Other scientists asked me, ‘What is the Nodamura virus?’ They have been studying the more well-known human viruses, but Nodamura virus infection of mice proves to be the best model.”

 

How did Ding know where to look? The China native was partly acting on a hunch that started when he was a graduate student at the Australia National University in the late 1980s. There, during a lecture, he learned that the genomes of viruses infecting plants and animals are actually very similar, even though plants and animals are very different.

 

That, and further discussions with his mentor Adrian Gibbs, an expert on molecular evolution of viruses and a fellow of the Australian Academy of Sciences, “made me think there must be a common anti-viral mechanism in plants and animals to keep their viruses similar,” he said.

 

Ding produced the first evidence for that hypothesis while working with Bob Symons in the Waite Institute in South Australia, studying cucumber mosaic virus, a devastating, aphid-carried disease that infects more than 1,000 plant species, including many important crops.

 

Using computational analytical skills learned from Gibbs, Ding discovered a small gene in the virus other scientists had overlooked. He named the gene 2b and showed that it plays an essential role in helping the virus spread within the host plant. Based on his results, and published studies on the B2 protein of Flock house virus, an insect pathogen, Ding proposed in a 1995 paper that 2b and B2 proteins act by suppressing the host’s antiviral defense.

 

Fueled by that idea, Ding moved to Singapore in 1996 to set up his own laboratory in the Institute of Molecular Agrobiology. There, in collaboration with a British group led by RNAi-expert David Baulcombe, Ding’s group discovered that the 2b protein did indeed suppress the RNAi virus-fighting properties in plants. Further, the group found that the 2b proteins of the related viruses all have the suppressor activity even though they share limited sequence similarities.

 

Ding joined the faculty at UCR in December of 2000 to test the other half of his hypothesis: does the B2 protein of Flock house virus suppress RNAi in its animal host? Although RNAi was known as a major antiviral mechanism in plants by that time, few believed it was also true in the animal kingdom, which was known to fight viral infections by many other well-defined mechanisms. Over the next five years, Ding used Flock house virus to discover that fruit flies and C. elegans nematodes have the same RNAi virus-killing properties as plants, but the B2 in the virus stop their RNAi defenses from working. Remove the B2, and the hosts produce massive amounts of siRNAs and rapidly destroy the virus.

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Super resolution microscopy: Spinning-disk microscope offers window into cell

Super resolution microscopy: Spinning-disk microscope offers window into cell | Amazing Science | Scoop.it

Recent advances in optical physics have made it possible to use fluorescent microscopy to study complex structures smaller than 200 nanometres (nm) – around 500 times smaller than the width of a human hair. These methodologies are called super-resolution microscopy.


The drawback of such techniques is that they can only produce very clear images of structures that are at the bottom of the cell. Since the nucleus – the cell’s ‘control centre’ – is in the middle of the cell and bacterial and viral infections can happen anywhere in the cell, this technique has considerable limitations for biologists.

 

This study shows how these issues have been overcome with a newly developed imaging system, making it possible to image structures as small as 80nm or less anywhere in the cell. The Spinning Disk Statistical Imaging (SDSI) system was developed by Dr Neveen Hosny, a bioengineer working with Professor Martin Knight in the School of Engineering and Materials Science and Dr Ann Wheeler, Head of Imaging at Queen Mary’s Blizard Institute.

 

Dr Ann Wheeler said: “The spinning disk microscope produces focused images at high speed because it has a disk with an array of tiny holes in it which remove the out of focus light. We have combined this microscope with new fluorescent probes, which switch between a bright and dark state rapidly. This system is now allowing us to see structures three times smaller than could usually be seen using standard light microscopes.

 

“We have been able to visualise chromatin, which is the protein structure that controls DNA expression and the nuclear envelope. We have also used the method to get images of focal adhesions – sub-cellular macromolecules which the cell uses to attach to its environment.

 

“Although it was previously possible to see these structures, our method provides a greater degree of detail. It also allows us to look at protein complexes which are smaller than 200nm in the nucleus, which hasn't been done before.”

 

The microscope is housed in its own room with a carefully controlled environment to miminise vibrations.

 

Professor Knight added: “Super resolution microscopy is a major step forward and we are looking forward to using this technology in a wide range of applications from stem cell behaviour to understanding arthritis or the development of nanomedicine.”


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New material gives visible light an infinite wavelength

New material gives visible light an infinite wavelength | Amazing Science | Scoop.it
Researchers from the FOM Institute AMOLF and the University of Pennsylvania have fabricated a material which gives visible light a nearly infinite wavelength. The new metamaterial is made by stacking silver and silicon nitride nanolayers.

 

The phase velocity and group velocity of light dictate how light propagates in a material. The phase velocity determines how the peaks and valleys of the wave move in the material, whereas the group velocity describes the transport of energy. According to Einstein's laws, the transport of energy of light can never be faster than the speed of light. Therefore the group velocity is limited. There are however no physical limitations to the phase velocity. When the phase velocity becomes zero, there is no movement of the peaks and valleys of the wave; when it is infinite the wavelength diverges to very large values. In nature however, no materials with such special properties exist.

The research team now presents a metamaterial composed of a unit cell structure much smaller than the wavelength of light. By stacking nanoscale layers of silver and silicon nitride a new material is fabricated in which light 'feels' the optical properties of both layers.

 

The way light travels through matter is dependent on the material permittivity: the resistance of a material against the electric fields of light waves. Because the permittivity of silver is negative and that of silicon nitride is positive, the combined material has a permittivity which is effectively equal to zero. Therefore, it seems that the light experiences zero resistance, and propagates with an infinite phase velocity. The wavelength of the light is nearly infinite.

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Classification of cell death: How do cells die?

Classification of cell death: How do cells die? | Amazing Science | Scoop.it

Cell death can be classified according to its morphological appearance (which may be apoptotic, necrotic, autophagic or associated with mitosis), enzymological criteria (with and without the involvement of nucleases or of distinct classes of proteases, such as caspases, calpains, cathepsins and transglutaminases), functional aspects (programmed or accidental, physiological or pathological) or immunological characteristics (immunogenic or non-immunogenic).

 

The Nomenclature Committee on Cell Death (NCCD) has formulated a first round of recommendations in 2005, in Cell Death and Differentiation. Since then, the field of cell death research has continued its expansion, significant progress has been made and new putative cell death modalities have been described. The NCCD provides a forum in which names describing distinct modalities of cell death are critically evaluated and recommendations on their definition and use are formulated, hoping that a non-rigid, yet uniform, nomenclature will facilitate the communication among scientists and ultimately accelerate the pace of discovery.

 

As it stands now, three distinct routes of cellular catabolism can be defined according to morphological criteria, namely apoptosis, which is a form of cell death, autophagy, which causes the destruction of a part of the cytoplasm, but mostly avoids cell death, and necrosis, which is another form of cell death. Although frequently employed in the past, the use of Roman numerals (i.e., type I, type II and type III cell death, respectively) to indicate these catabolic processes should be abandoned.

 

Moreover, several critiques can be formulated against the clear-cut distinction of different cell types in the triad of apoptosis, autophagic cell death and necrosis. First, although this vocabulary was originally introduced based on observations of developing animals, it has rapidly been adopted to describe the results of in vitro studies performed on immortalized cell lines, which reflect very poorly the physiology of cell death in vivo. In tissues, indeed, dying cells are usually engulfed well before signs of advanced apoptosis or necrosis become detectable. Thus, it may be acceptable - if the irreversibility of these phenomena is demonstrated - to assess caspase activation and/or DNA fragmentation to diagnose apoptotic cell death in vivo.

 

Second, there are numerous examples in which cell death displays mixed features, for instance with signs of both apoptosis and necrosis, a fact that lead to the introduction of terms like ‘necroapoptosis’ and ‘aponecrosis’ (whose use is discouraged by the NCCD to avoid further confusion). Similarly, in the involuting D. melanogaster salivary gland, autophagic vacuolization is synchronized with signs of apoptosis, and results from genetic studies indicate that caspases and autophagy act in an additive manner to ensure cell death in this setting.  Altogether, these data argue against a clear-cut and absolute distinction between different forms of cell death based on morphological criteria.

 

Third and most importantly, it would be a desideratum to replace morphological aspects with biochemical/functional criteria to classify cell death modalities. Unfortunately, there is no clear equivalence between morphology and biochemistry, suggesting that the ancient morphological terms are doomed to disappear and to be replaced by truly biochemical definitions. In this context, ‘loss-of-function’ and ‘gain-of function’ genetic approaches (e.g., RNA interference, knockout models and plasmid-driven overexpression systems) represent invaluable tools to characterize cell death modes with more precision, but only if such interventions truly reduce/augment the rate of death, instead of changing its morphological appearance, as it is often the case.

 

Present cell death classifications are reminiscent of the categorization of tumors that has been elaborated by pathologists over the last one and a half centuries. As old morphological categorizations of tumors are being more and more supported and will presumably be replaced by molecular diagnostics, which allows for a more sophisticated stratification of cancer subtypes based on molecular criteria, the current catalog of cell death types is destined to lose its value as compared with biochemical / functional tests. In the end, such efforts of classification are only justified when they have a prognostic and/or predictive impact, allowing the matching of each individual cancer with the appropriate therapy.

 

Similarly, a cell death nomenclature will be considered useful only if it predicts the possibilities to pharmacologically/genetically modulate (induce or inhibit) cell death and/or if it predicts the consequences of cell death in vivo, with regard to inflammation and recognition by the immune system.

 

 

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Carbyne: A Material that could be Stronger than Diamond

Carbyne: A Material that could be Stronger than Diamond | Amazing Science | Scoop.it
According to scientists at Rice University, a material called carbyne will be the strongest material if and when anyone can make it in bulk.

 

Carbyne is a chain of carbon atoms held together by either double or alternating single and triple atomic bonds. That makes it a true one-dimensional material, unlike atom-thin sheets of graphene that have a top and a bottom or hollow nanotubes that have an inside and outside.

 

According to calculations reported in the journal ACS Nano, carbyne’s tensile strength – the ability to withstand stretching – surpasses that of any other known material and is double that of graphene.

 

It has twice the tensile stiffness of graphene and carbon nanotubes and nearly three times that of diamond. Stretching carbyne as little as 10 percent alters its electronic band gap significantly. The material is stable at room temperature, largely resisting crosslinks with nearby chains.

 

“You could look at it as an ultimately thin graphene ribbon, reduced to just one atom, or an ultimately thin nanotube. It could be useful for nanomechanical systems, in spintronic devices, as sensors, as strong and light materials for mechanical applications or for energy storage,” said study senior author Dr Boris Yakobson.

 

“Regardless of the applications, it’s very exciting to know the strongest possible assembly of atoms.”

 

“Based on the calculations, carbyne might be the highest energy state for stable carbon. People usually look for what is called the ‘ground state,’ the lowest possible energy configuration for atoms. For carbon, that would be graphite, followed by diamond, then nanotubes, then fullerenes. But nobody asks about the highest energy configuration. We think this may be it, a stable structure at the highest energy possible.”

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Stomach cells naturally revert to stem cells to repair damage from acid and digestive fluids

Stomach cells naturally revert to stem cells to repair damage from acid and digestive fluids | Amazing Science | Scoop.it

New research has shown that the stomach naturally produces more stem cells than previously realized, likely for repair of injuries from infections, digestive fluids and the foods we eat. 

 

Stem cells can make multiple kinds of specialized cells, and scientists have been working for years to use that ability to repair injuries throughout the body. But causing specialized adult cells to revert to stem cells and work on repairs has been challenging.

 

Scientists fromWashington University School of Medicine in St. Louis and Utrecht Medical Center in the Netherlands report in the new study that a class of specialized cells in the stomach reverts to stem cells more often than they thought.

 

“We already knew that these cells, which are called chief cells, can change back into stem cells to make temporary repairs in significant stomach injuries, such as a cut or damage from infection,” said Jason Mills, MD, PhD, associate professor of medicine at Washington University. “The fact that they’re making this transition more often, even in the absence of noticeable injuries, suggests that it may be easier than we realized to make some types of mature, specialized adult cells revert to stem cells.” The findings are published Oct. 10, 2013 in Cell.

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Learning in a digital age: From MOOCs to big data to crowd intelligence

Learning in a digital age: From MOOCs to big data to crowd intelligence | Amazing Science | Scoop.it

From massive open online courses (MOOCs) that are delivered to tens of thousands around the globe to adaptive digital tools that can improve outcomes by providing tailored learning experiences as well as mapping a student’s individual progress at every juncture, technology is transforming the 21st century student.

 

Classrooms haven't changed much in the past few centuries. Students attend class, take notes and do their homework. The teacher lectures and once in a while administers a test. Students get their grades and move on to the next topic. By and large, students—especially the most disadvantaged ones—attend the school or university closest to their home, regardless of its quality.

 

These routines are starting to change. In a small but growing number of schools, students watch lectures online and come to class prepared to tackle assignments and collaborate with teachers and peers. They interact with computer programs that allow them to work at their own pace, regardless of what the rest of the class is doing. Teachers rely on those same programs to grade tests and essays, allowing them to closely track more students at once. And local schools are no longer a pupil's only option. Start-ups and nonprofits make high-quality courses available online to anyone with an Internet connection.

 

What is driving this digital revolution? One factor is that schools and universities are under greater pressure than ever before. More and more students are pursuing higher levels of education at a time when budget-strapped principals and universities cannot hire the staff they need. At the same time, governments and institutions (prodded by employers) are raising standards for what students should know at every stage of school.

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Metal protein complexes help explain extreme survival of Deinococcaceae, tough enough for Mars

Metal protein complexes help explain extreme survival of Deinococcaceae, tough enough for Mars | Amazing Science | Scoop.it

Bacteria belonging to the family Deinococcaceae are some of the most radiation-resistant organisms yet discovered. Deinococcus (Micrococcus) radiodurans strain R1 (ATCC BAA-816) was first reported in 1956 by A. W. Anderson and coworkers of the Oregon Agricultural Experimental Station, Corvalis, Oregon. This obligate aerobic bacterium typically grows in rich medium as clusters of two cells (diplococci) in the early stages of growth, and as clusters of four cells (tetracocci) in the late stages of growth, is non-pathogenic, and best known for its ability to survive extremely high doses of acute ionizing radiation (10,000 Gy) without cell-killing. For comparison, 5 Gy is lethal to the average human, and 2,000 Gy can sterilize a culture of Escherichia coli. D. radiodurans is capable of growth under chronic radiation (60 Gy/hour) and resistant to other DNA damaging conditions including exposure to desiccation, ultraviolet (UV) light, and hydrogen peroxide. The genes and cellular pathways underlying the survival strategies of D. radiodurans are under investigation, and its resistance characteristics are being exploited in the development of bioremediation processes for cleanup of highly radioactive US Department of Energy waste sites, and in the development of radioprotectors.


The modern founding concept of radiation biology that deals with X-rays and g-rays is that ionizing radiation is dangerous because of its damaging effects on DNA. Mounting experimental evidence does not fit into this theoretical framework, instead supporting that radiation resistance is governed by protein damage. Recent studies from several independent labs implicate protein damage as the major probable cause of death in irradiated cells. Whereas DNA lesion-yields in cells exposed to a given dose of radiation appear to be fixed, protein-lesion yields are variable and closely related to survival. There are profound practical implications to this new view of radiation toxicity. Basically, if you want to survive radiation, protect your proteins! D. radiodurans has shown us how to protect proteins from radiation and other sources of reactive oxygen species (ROS). For the latest review see Michael J Daly (2011) Death by protein damage in irradiated cells. DNA Repair doi: 10.1016/j.dnarep.2011.10.024.

 

Early studies in bacteria incriminated DNA as the principal radiosensitive target, an assertion that remains central to modern radiation toxicity models. More recently, the emphasis has shifted to understanding why bacteria such as Deinococcus radiodurans are extremely resistant to ionizing radiation (IR), by focusing on DNA repair systems expressed during recovery from high doses of IR. Unfortunately, as key features of DNA-centric hypotheses of extreme resistance have grown weaker, the study of alternative cellular targets has lagged far behind, mostly because of their relative biological complexity. Recent studies have shown that extreme levels of bacterial IR resistance correlate with high intracellular Mn(II) concentrations, and resistant and sensitive bacteria are equally susceptible to IR-induced DNA damage (~0.005 DSB/Gy/haploid genome). Recent work has established a mechanistic link between the orthophosphate complex of Mn2+ and protection of proteins from radiation damage. In contrast to resistant bacteria, naturally sensitive bacteria are highly susceptible to IR-induced protein oxidation. Sensitive bacteria sustain lethal levels of protein damage at radiation doses that elicit relatively little DNA damage, and that extreme resistance in bacteria is dependent on protein protection.

 

This phenomenon can be exploited for vaccine development. A breakthrough application developed from Death by Protein Damage has been the preparation of ionizing radiation-sterilized whole-bacterial cell and whole-virus vaccines. A recent approach to protecting proteins at supra-lethal doses (25-40 kGy) has been successfully tested, where the epitopes of cells and viruses treated with reconstitutedDeinococcus Mn-peptide complexes (Cell Host & Microbe, 12(1):117-124, 2012) survive doses of gamma-radiation which obliterate their genomes. This approach has produced mouse-vaccines which are absolutely non-infective yet highly immunogenic and protective. The rapidity of vaccine development that is achieved by killing whole isolated pathogens makes this a powerful approach against bioterror threats and emerging infections caused by poorly characterized new or rapidly mutating agents, such as pandemic influenza and HIV.


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