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Rett syndrome mutation in MeCP2 alters motor function in zebrafish

Rett syndrome mutation in MeCP2 alters motor function in zebrafish | Amazing Science |

Mutating the Rett syndrome gene in zebrafish allows researchers to investigate the disorder early in development, according to a study published 16 July  2913 in Frontiers in Neural Circuits.


Rett syndrome, which is primarily caused by mutations in the MeCP2 gene, is characterized by a loss of language and motor skills after 2 years of age. However, abnormal neuronal development may occur before the appearance of symptoms.


Researchers have modeled Rett syndrome in mice by deleting a single copy of the gene (which is on the X chromosome) in males. These mice have motor, learning and memory deficits, and clasp their paws together in a manner reminiscent of the hand flapping seen in Rett syndrome. They are also sterile and have significantly shortened lifespans.


In the new study, researchers introduced a mutation into one or both copies of the zebrafish MeCP2 gene that prevents production of the protein.

Zebrafish make for good models of neurological disorders because their transparent embryos allow researchers to monitor early brain development. They also breed readily, making them useful for large-scale drug-screening studies.


Unlike the Rett mice, the zebrafish lacking MeCP2 have only a slightly shortened lifespan and are fertile, the study found. This may be because zebrafish are able to make new neurons throughout life in certain brain regions, and so can better combat the effects of the mutation.


The zebrafish larvae show significant differences in motor function compared with controls, however. Zebrafish larvae often spontaneously contract their tails a single time and then rest. About 30 percent of the time, the larvae lacking MeCP2 instead contract their tails multiple times.


When normal zebrafish larvae are startled, they bend into a C-like shape and then swim away. The fish lacking MeCP2 spend longer in this bend after being tickled with an eyelash than do controls. When swimming freely around a circular space, the mutant larvae also spend most of their time in the middle, whereas controls hug the walls of the chamber. These deficits may indicate an imbalance between neurons that activate signals and those that inhibit them, the researchers say.

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Earth’s habitable lifetime: at least 1.75 billion years, say astrobiologists

Earth’s habitable lifetime: at least 1.75 billion years, say astrobiologists | Amazing Science |

If we can just hold out another 1.75 billion years, we’ll be fine — as long as we move to Mars by then, according to astrobiologists at the

University of East Anglia.


“We used the ‘habitable zone’ concept to make these estimates — this is the distance from a planet’s star at which temperatures are conducive to having liquid water on the surface,” said Andrew Rushby from UEA’s school of Environmental Sciences, who led the research.


“We used stellar evolution models to estimate the end of a planet’s habitable lifetime by determining when it will no longer be in the habitable zone.


“We estimate that Earth will cease to be habitable somewhere between 1.75 and 3.25 billion years from now. After this point, Earth will be in the ‘hot zone’ of the sun, with temperatures so high that the seas would evaporate. We would see a catastrophic and terminal extinction event for all life.


“Of course conditions for humans and other complex life will become impossible much sooner — and this is being accelerated by anthropogenic climate change,” the researchers suggest.


“Humans would be in trouble with even a small increase in temperature, and near the end, only microbes in niche environments would be able to endure the heat.”


If we ever needed to move to another planet, Mars is probably our best bet, said Rushby. “It’s very close and will remain in the habitable zone until the end of the Sun’s lifetime — six billion years from now.”


“Looking back a similar amount of time, we know that there was cellular life on earth. We had insects 400 million years ago, dinosaurs 300 million years ago and flowering plants 130 million years ago. Anatomically modern humans have only been around for the last 200,000 years — so you can see it takes a really long time for intelligent life to develop.

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Parasites make mice lose fear of cats permanently, even after Toxoplasma infection is cleared

Parasites make mice lose fear of cats permanently, even after Toxoplasma infection is cleared | Amazing Science |

Behavioral changes persist after Toxoplasma infection is cleared. A parasite that infects up to one-third of people around the world may have the ability to permanently alter a specific brain function in mice.

Toxoplasma gondii is known to remove rodents’ innate fear of cats. The new research shows that even months after infection, when parasites are no longer detectable, the effect remains. This raises the possibility that the microbe causes a permanent structural change in the brain. The microbe is a single-celled pathogen that infects most types of mammal and bird, causing a disease called toxoplasmosis. But its effects on rodents are unique; most flee cat odor, but infected ones are mildly attracted to it.

This is thought to be an evolutionary adaptation to help the parasite complete its life cycle: Toxoplasma can sexually reproduce only in the cat gut, and for it to get there, the pathogen's rodent host must be eaten.


In humans, studies have linked Toxoplasma infection with behavioral changes and schizophrenia. One work found an increased risk of traffic accidents in people infected with the parasite; another found changes in responses to cat odor. People with schizophrenia are more likely than the general population to have been infected with Toxoplasma, and medications used to treat schizophrenia may work in part by inhibiting the pathogen's replication.


Schizophrenia is thought to involve excess activity of the neurotransmitter dopamine in the brain. This has bolstered one possible explanation for Toxoplasma’s behavioral effect: the parasite establishes persistent infections by means of microscopic cysts that grow slowly in brain cells. It can increase those cells’ production of dopamine, which could significantly alter their function. Most other suggested mechanisms also rely on the presence of cysts.

Research on Toxoplasma has mainly used the North American Type II strain. Wendy Ingram, a molecular cell biologist at the University of California, Berkeley, and her colleagues investigated the effects of two other major strains, Type I and Type III, on mouse behavior. They found that within three weeks of infection with either strain, mice lost all fear of cat odor — showing that the behavioral shift is a general trait of Toxoplasma.


More surprising was the situation four months after infection. The Type I pathogen that the researchers used had been genetically modified to provoke an effective immune response, allowing the mice to overcome the infection. After four months, it was undetectable in the mouse brain, indicating that no more than 200 parasite cells remained. “We actually expected that Type I wouldn’t be able to form cysts, and therefore wouldn’t be able to cause the behavioral change,” explains Ingram.

But that was not the case: the mice remained as unperturbed by cat odour as they had been at three weeks. “Long after we lose the ability to see it in the brain, we still see its behavioral effect,” says geneticist Michael Eisen, also at Berkeley.


This suggests that the behavioral change could be due to a specific, hard-wired alteration in brain structure, which is generated before cysts form and cannot be reversed. The finding casts doubt on theories that cysts or dopamine cause the behavioral changes of Toxoplasma infections.

Becky Raines's comment, October 1, 2013 3:47 PM
That is so adorable. I was hoping that one day mice would stop being afraid and be sort of like friends, but that does mean that the cat has to agree as well. Cats like to chase mice so unless the cat agrees then it won't work out for either one animal.
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Single Molecule Label-Free Cancer Marker Detection

Single Molecule Label-Free Cancer Marker Detection | Amazing Science |

Just months after setting a record for detecting the smallest single virus in solution, researchers at the Polytechnic Institute of New York University (NYU-Poly) have announced a new breakthrough: They used a nano-enhanced version of their patented microcavity biosensor to detect a single cancer marker protein, which is one-sixth the size of the smallest virus, and even smaller molecules below the mass of all known markers. This achievement shatters the previous record, setting a new benchmark for the most sensitive limit of detection, and may significantly advance early disease diagnostics.  Unlike current technology, which attaches a fluorescent molecule, or label, to the antigen to allow it to be seen, the new process detects the antigen without an interfering label.

Stephen Arnold, university professor of applied physics and member of the Othmer-Jacobs Department of Chemical and Biomolecular Engineering, published details of the achievement in Nano Letters, a publication of the American Chemical Society.


In 2012, Arnold and his team were able to detect in solution the smallest known RNA virus, MS2, with a mass of 6 attograms. Now, with experimental work by postdoctoral fellow Venkata Dantham and former student David Keng, two proteins have been detected: a human cancer marker protein called Thyroglobulin, with a mass of just 1 attogram, and the bovine form of a common plasma protein, serum albumin, with a far smaller mass of 0.11 attogram. “An attogram is a millionth of a millionth of a millionth of a gram,” said Arnold, “and we believe that our new limit of detection may be smaller than 0.01 attogram.”


This latest milestone builds on a technique pioneered by Arnold and collaborators from NYU-Poly and Fordham University.  In 2012, the researchers set the first sizing record by treating a novel biosensor with plasmonic gold nano-receptors, enhancing the electric field of the sensor and allowing even the smallest shifts in resonant frequency to be detected. Their plan was to design a medical diagnostic device capable of identifying a single virus particle in a point-of-care setting, without the use of special assay preparations.


At the time, the notion of detecting a single protein—phenomenally smaller than a virus—was set forth as the ultimate goal. 


“Proteins run the body,” explained Arnold. “When the immune system encounters virus, it pumps out huge quantities of antibody proteins, and all cancers generate protein markers. A test capable of detecting a single protein would be the most sensitive diagnostic test imaginable.”


To the surprise of the researchers, examination of their nanoreceptor under a transmission electron microscope revealed that its gold shell surface was covered with random bumps roughly the size of a protein. Computer mapping and simulations created by Stephen Holler, once Arnold’s student and now assistant professor of physics at Fordham University, showed that these irregularities generate their own highly reactive local sensitivity field extending out several nanometers, amplifying the capabilities of the sensor far beyond original predictions. “A virus is far too large to be aided in detection by this field,” Arnold said. “Proteins are just a few nanometers across—exactly the right size to register in this space.”


The implications of single protein detection are significant and may lay the foundation for improved medical therapeutics.  Among other advances, Arnold and his colleagues posit that the ability to follow a signal in real time—to actually witness the detection of a single disease marker protein and track its movement—may yield new understanding of how proteins attach to antibodies.


Arnold named the novel method of label-free detection “whispering gallery-mode biosensing” because light waves in the system reminded him of the way that voices bounce around the whispering gallery under the dome of St. Paul’s Cathedral in London. A laser sends light through a glass fiber to a detector. When a microsphere is placed against the fiber, certain wavelengths of light detour into the sphere and bounce around inside, creating a dip in the light that the detector receives. When a molecule like a cancer marker clings to a gold nanoshell attached to the microsphere, the microsphere’s resonant frequency shifts by a measureable amount.

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Physicists spent a century puzzling over quantum theory; now a few of them are trying to reinvent it

Physicists spent a century puzzling over quantum theory; now a few of them are trying to reinvent it | Amazing Science |

If the truth be told, few physicists have ever really felt comfortable with quantum theory. Having lived with it now for more than a century, they have managed to forge a good working relationship; physicists now routinely use the mathematics of quantum behavior to make stunningly accurate calculations about molecular structure, high-energy particle collisions, semiconductor behavior, spectral emissions and much more.


But the interactions tend to be strictly formal. As soon as researchers try to get behind the mask and ask what the mathematics mean, they run straight into a seemingly impenetrable wall of paradoxes. Can something really be a particle and a wave at the same time? Is Schrödinger's cat really both alive and dead? Is it true that even the gentlest conceivable measurement can somehow have an effect on particles halfway across the Universe?


Many physicists respond to this inner weirdness by retreating into the 'Copenhagen interpretation' articulated by Niels Bohr, Werner Heisenberg and their colleagues as they were putting quantum theory into its modern form in the 1920s. The interpretation says that the weirdness reflects fundamental limits on what can be known about the world, and just has to be accepted as the way things are — or, as famously phrased by physicist David Mermin of Cornell University in Ithaca, New York, “shut up and calculate!”

But there have always been some who are not content to shut up — who are determined to get behind the mask and fathom quantum theory's meaning. “What is it about this world that forces us to navigate it with the help of such an abstract entity?” wonders physicist Maximilian Schlosshauer of the University of Portland in Oregon, referring to the uncertainty principle; the wave function that describes the probability of finding a system in various states; and all the other mathematical paraphernalia found in textbooks on quantum theory.


Over the past decade or so, a small community of these questioners have begun to argue that the only way forward is to demolish the abstract entity and start again. They are a diverse bunch, each with a different idea of how such a 'quantum reconstruction' should proceed. But they share a conviction that physicists have spent the past century looking at quantum theory from the wrong angle, making its shadow odd, spiky and hard to decode. If they could only find the right perspective, they believe, all would become clear, and long-standing mysteries such as the quantum nature of gravity might resolve themselves in some natural, obvious way — perhaps as an aspect of some generalized theory of probability.


“The very best quantum-foundational effort,” says Christopher Fuchs of the Perimeter Institute for Theoretical Physics in Waterloo, Canada, “will be the one that can write a story — literally a story, all in plain words — so compelling and so masterful in its imagery that the mathematics of quantum mechanics in all its exact technical detail will fall out as a matter of course”.

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Anti-Viral Drugs May Soon Be Available With DRACO

Anti-Viral Drugs May Soon Be Available With DRACO | Amazing Science |
By targeting virus-infected cells rather than the viruses themselves, researchers are closer than ever to developing treatments for a broad range of viruses from the common cold to deadly Ebola.


For many bacterial infections, antibiotic treatments such as penicillin are more than adequate. However, such drugs are useless against viral infections, including influenza, the common cold, and deadly hemorrhagic fevers such as Ebola.

Now, in a development that could transform how viral infections are treated, a team of researchers at MIT’s Lincoln Laboratory has designed a drug that can identify cells that have been infected by any type of virus, then kill those cells to terminate the infection.

In a recent paper, the researchers tested their drug against 15 viruses, and found it was effective against all of them — including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever. The drug works by targeting a type of RNA produced only in cells that have been infected by viruses. “In theory, it should work against all viruses,” says Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group who invented the new technology.

The concept for DRACO went like this: "It just occurred to me one day in the shower: oh, well, let's cross-wire these two to connect the successful detection of the long double-strand RNA with the successful final activation of suicide in the infected cells." Translated, Rider’s plan involved two parts. First, he knew that certain proteins could detect double-strand RNA, or dsRNA. The "D" in DRACO, dsRNA is found in almost all viruses (a strain of hantavirus is among those that don't), but not in healthy cells — it’s a near-perfect marker. But viruses shut down most responses to dsRNA; likewise, they disable another natural pathway inside cells, one that causes apoptosis, or cell death. Rider thought if he could combine the two, he’d have a viable method, one that detected dsRNA-containing cells and then caused them to commit cellular suicide.

Because the technology is so broad-spectrum, it could potentially also be used to combat outbreaks of new viruses, such as the 2003 SARS (severe acute respiratory syndrome) outbreak, Rider says.

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Amazing claim: UK scientists believe they have found life forms arriving to Earth's stratosphere from space

Amazing claim: UK scientists believe they have found life forms arriving to Earth's stratosphere from space | Amazing Science |

The team, led by Professor (Hon. Cardiff and Buckingham Universities) Milton Wainwright, from the University’s Department of Molecular Biology and Biotechnology found small organisms that could have come from space after sending a specially designed balloon to 27 km into the stratosphere during the recent Perseid meteor shower.


Professor Wainwright said: “Most people will assume that these biological particles must have just drifted up to the stratosphere from Earth, but it is generally accepted that a particle of the size found cannot be lifted from Earth to heights of, for example, 27km. The only known exception is by a violent volcanic eruption, none of which occurred within three years of the sampling trip.


“In the absence of a mechanism by which large particles like these can be transported to the stratosphere we can only conclude that the biological entities originated from space. Our conclusion then is that life is continually arriving to Earth from space, life is not restricted to this planet and it almost certainly did not originate here.”


Professor Wainwright said the results could be revolutionary: “If life does continue to arrive from space then we have to completely change our view of biology and evolution,” he added. “New textbooks will have to be written!”

The balloon, designed by Chris Rose and Alex Baker from the University of Sheffield’s Leonardo Centre for Tribology, was launched near Chester and carried microscope studs which were only exposed to the atmosphere when the balloon reached heights of between 22 and 27km. The balloon landed safely and intact near Wakefield. The scientists then discovered that they had captured a diatom fragment and some unusual biological entities from the stratosphere, all of which are too large to have come from Earth.


Professor Wainwright said stringent precautions had been taken against the possibility of contamination during sampling and processing, and said the group was confident that the biological organisms could only have come from the stratosphere.


The group’s findings have been published in the Journal of Cosmology and updated versions will appear in the same journal, a new version of which will be published in the near future. Professor Chandra Wickramasinghe of the Buckingham, University Centre for Astrobiology (of which Professor Wainwright is an Honorary Fellow) also gave a presentation of the group’s findings at a meeting of astronomers and astrobiologists in San Diego last month.


Professor Wainwright’s team is hoping to extend and confirm their results by carrying out the test again in October to coincide with the upcoming Haley’s Comet-associated meteorite shower when there will be large amounts of cosmic dust. It is hoped that more new, or unusual, organisms will be found.


Professor Wainwright added: “Of course it will be argued that there must be an, as yet, unknown mechanism for transferring large particles from Earth to the high stratosphere, but we stand by our conclusions. The absolutely crucial experiment will come when we do what is called ‘isotope fractionation’. We will take some of the samples which we have isolated from the stratosphere and introduce them into a complex machine – a button will be pressed. If the ratio of certain isotopes gives one number then our organisms are from Earth, if it gives another, then they are from space. The tension will obviously be almost impossible to live with!”

There have been a number of investigations showing that viable bacteria and fungi exist in both the lower and the upper stratosphere over the altitude range 20 km - 60 km. Since a number of different methodological approaches have been used in these studies, and a range of different microbes have been isolated from the stratosphere using a variety of approaches, there is little doubt that microbes do exist in the stratosphere. Such organisms are unlikely to grow in this “high cold biosphere” but survive instead in the dormant state as “extremodures”; the fact that bacteria and fungi can be grown on isolation media when returned to Earth shows however, that these stratospherederived microbes remain viable despite exposure to the extreme rigors of the stratosphere.

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Dinosaurs = Birds: First Dinosaur Feathers Found in Ancient Amber

Dinosaurs = Birds: First Dinosaur Feathers Found in Ancient Amber | Amazing Science |
Paleontologists have figured out what ancient dino feathers and fuzz looked like, including color.


Instead of digging through rocks and rubble to find fossils, a group of Canadian paleontologists decided to dig through museums’ amber collections instead. Their unique approach paid off when they discovered feathers and never-before-seen structures, which they think are something called dinofuzz.

The researchers combed through thousands of minuscule amber nuggets from nearly 80 million years ago. Among them they found 11 M&M-sized globules with traces of ancient feathers and fuzz. A number resembled modern feathers—some fit for flying and others designed to dive. And unlike fossils, the amber preserved colors too: white, gray, red and brown.


But a few hollow hair-like structures stumped researchers. The unidentifiable filaments weren’t plant fibers, fungus or fur, so the researchers surmise that they are protofeathers (thought to be the evolutionary precursors to feathers). The collection is among the first to reveal all major evolutionary stages of feather development in non-avian dinosaurs and birds.

The unusual find suggests a wide array of plumed creatures populated the time period—sporting everything from seemingly modern feathers to their filament-like forebears—and that even by this early date, feathers had become specialized, for example, for diving underwater.

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Better droplet condensation could boost worldwide production of electricity and clean water

Better droplet condensation could boost worldwide production of electricity and clean water | Amazing Science |

Steam condensation is key to the worldwide production of electricity and clean water: It is part of the power cycle that drives 85 percent of all electricity-generating plants and about half of all desalination plants globally, according to the United Nations and International Energy Agency. So anything that improves the efficiency of this process could have enormous impact on global energy use.

It has been known for years that making steam-condenser surfaces hydrophobic—that is, getting them to repel water—could improve the efficiency of condensation by causing the water to quickly form droplets. But most hydrophobic materials have limited durability, especially in steamy industrial settings. The new approach to coating condenser surfaces should overcome that problem, the MIT researchers say.

The findings are reported this week in the journal Advanced Materials by MIT professors Karen Gleason and Kripa Varanasi, graduate student Adam Paxson and postdoc Jose Yagüe. Tests of metal surfaces coated using the team's process show "a stark difference," Paxson says. In the tests, the material stood up well even when exposed to steam at 100 degrees Celsius in an accelerated endurance test. Typically, the steam in power-plant condensers would only be about 40 degrees Celsius, Varanasi says.

When materials currently used to make surfaces hydrophobic are exposed to 100 degrees Celsius steam, "after one minute, you start to see them degrade," Paxson says: The condensing water becomes "a film that covers the surface. It kills the hydrophobic surface, and degrades heat transfer by a factor of seven." By contrast, the new material shows no change in performance after prolonged endurance tests.


Varanasi and Paxson were part of a team that published research earlier this year on a different kind of durable hydrophobic material, a rare-earth ceramic. Varanasi says that the two approaches will likely both find useful applications, but in different situations: The ceramic material can withstand even higher temperatures, while the new coating should be less expensive and appropriate for use in existing power plants, he says. "Before, we had nothing, and we have two possible systems now," he says.


The new coating can easily be applied to conventional condenser materials—typically titanium, steel, copper or aluminum—in existing facilities, using a process called initiated chemical vapor deposition (iCVD).


Another advantage of the new coating is that it can be extremely thin—just one-thousandth of the thickness of conventional hydrophobic coatings. That means other properties of the underlying surface, such as its electrical or thermal conductivity, are hardly affected. "You can create ultrathin films, with no effect on thermal conductivity," Varanasi says, "so you're getting the best of all worlds here."

Elizabeth Oneil's comment, September 20, 2013 1:44 PM
VVX cool
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Gaming improves multitasking skills: Study reveals plasticity in age-related cognitive decline

Gaming improves multitasking skills: Study reveals plasticity in age-related cognitive decline | Amazing Science |

Commercial companies have claimed for years that computer games can make the user smarter, but have been criticized for failing to show that improved skills in the game translate into better performance in daily life. Now a study published this week in Nature convincingly shows that if a game is tailored to a precise cognitive deficit, in this case multitasking in older people, it can indeed be effective.

Led by neuroscientist Adam Gazzaley of the University of California, San Francisco, the study found that a game called NeuroRacer can help older people to improve their capacity to multitask — and the effect seems to carry over to tasks in everyday life and is still there after six months. The study also shows how patterns of brain activity change as those cognitive skills improve.


NeuroRacer is a three-dimensional video game in which players steer a car along a winding, hilly road with their left thumb, while keeping an eye out for signs that randomly pop up. If the sign is a particular shape and colour, players have to shoot it down using a finger on their right hand. This multitasking exercise, says Gazzaley, draws on a mix of cognitive skills just as real life does — such as attention focusing, task switching and working memory (the ability to temporarily hold multiple pieces of information in the mind).


Gazzaley and his colleagues first recruited around 30 participants for each of six decades of life, from the 20s to the 70s, and confirmed that multitasking skills as measured by the game deteriorated linearly with age. They then recruited 46 participants aged 60–85 and put them through a 4-week training period with a version of NeuroRacer that increased in difficulty as the player improved.


After training, subjects had improved so much that they achieved higher scores than untrained 20-year-olds, and the skill remained six months later without practice.

The scientists also conducted a battery of cognitive tests on the participants before and after training. Certain cognitive abilities that were not specifically targeted by the game improved and remained improved — such as working memory and sustained attention. Both skills are important for daily tasks, from reading a newspaper to cooking a meal.


That is significant, says Gazzaley. “Neuro­Racer doesn’t demand too much of those particular abilities — so it appears that the multitasking challenge may put pressure on the entire cognitive control system, raising the level of all of its components.”

The team also recorded brain activity using electroencephalography while participants played NeuroRacer. As their skills increased, so did activity in the prefrontal cortex of the brain, which is associated with cognitive control, in a manner that correlated with improvements in sustained-attention tasks. Activity also increased in a neural network linking the prefrontal cortex with the back of the brain.

But Gazzaley’s study confirms that cognitive function can be improved — if you design training methods properly, says Klingberg, who is a consultant for Cogmed, a company he founded in 1999 to market computer-based training methods, particularly for people with attention-deficit disorders.


Last year, Gazzaley also co-founded a company, called Akili, for which he is an adviser. It is developing a commercial product similar to NeuroRacer, which remains a research tool, and will seek approval from the US Food and Drug Administration to market it as a therapeutic agent. A ‘games’ approach might also help people with particular cognitive deficits, such as depression or schizophrenia, adds Daphne Bavelier, a cognitive neuroscientist at the University of Geneva in Switzerland, who develops computer games to improve brain function and who also advises Akili.


Gazzaley cautions against over-hyping: “Video games shouldn’t now be seen as a guaranteed panacea.” But Linsey, for her part, is happy with what the game did for her and about her own contribution. “It’s been exciting to discover the older brain can learn — and I’m glad my own brain helped make the discovery.”


JMS1 Group9's curator insight, September 30, 2013 7:53 AM

Not only is gaming a great leisure activity that can unwind stress and serve as an escapism, but now it has also been proven to help the gamer with muti-tasking and other skills.


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Older Brain Is Willing, but Too Full for New Memories

Older Brain Is Willing, but Too Full for New Memories | Amazing Science |
Studies in modified mice suggest that it is harder to make new long-term memories as we age because the brain is full of old ones that are hard to erase.


The N-methyl-d-aspartate receptor (NMDAR) is widely known to be the synaptic coincidence detector essential for controlling synaptic plasticity and gating memory formation . Together with the NR1 core subunit, the NR2A and NR2B subunits form the diheteromeric or triheteromeric complex of the NMDA receptor in the forebrain regions. Depending on ages or states of animals, dynamic changes in NR2A and NR2B can lead to the different mixture of NR1/NR2A, NR1/NR2B, and NR1/NR2A/NR2B receptors in the forebrain. There is a higher amount of NR2B expression in postnatal and juvenile brains, but NR2A gradually becomes more prevalent in adulthood and advanced ages.


Based on distinct biophysical properties of the NR2A and NR2B (such as longer channel opening duration with the NR2B subunit than the NR2A, etc.), it has been hypothesized that an increased NR2A:NR2B ratio in the sexually matured and/or aged brains may represent a major genetic factor underlying the age-dependent, gradual constraint on memory functions in comparison to that of juvenile or younger brains. However, it is difficult to test this NR2A:NR2B ratio hypothesis by directly comparing the young animals with the aged animals because there are significant differences in expression of many other genes between those two age groups. Moreover, the levels of NR2A or NR2B expression in the cortex and hippocampus can also be dynamically modulated by individual experiences (i.e. enriched environment, or social interactions).


A series of genetic studies have shown that global knockout of NR2A resulted in lesser CA1 long-term potentiation, a moderate deficiency in spatial reference memory and fear memory, and/or significant spatial working memory deficit. This suggests that the presence of NR2B in NR2A−/− mice largely preserves LTP and most long-term memories. On the other hand, genetic deletion of NR2B in the forebrain- or hippocampus-specific knockout of NR2B results in more profound memory deficits and impaired LTP. These experiments, by examining the extreme ends of the NR2A:NR2B ratio spectrum (without NR2A or NR2B), have provided fundamental insights into the roles of the pure NR2A- or NR2B-containing NMDA receptor population under the given test conditions.


The initial evidence for the concept that an increased NR2A:NR2B ratio may reduce synaptic plasticity and memory function in adulthood came from NR2B transgenic experiments. Research has shown that genetic overexpression of NR2B in the mouse forebrain can lead to larger hippocampal long-term potentiation (10–100 Hz range, without affecting LTD) and enhanced learning and memory function as tested in seven different memory tasks. Similar memory and LTP enhancement was also observed in NR2B overexpression transgenic rats, pointing to the conserved beneficial effects of NR2B in multiple animal species. Thus, these NR2B overexpression experiments, along with other studies, have provided important evidence that the increased NR2A:NR2B ratio can be detrimental to greater synaptic plasticity and memory function in the older brains.


In a recent study, scientists have directly tested this hypothesis and investigated the effects of increased NR2A:NR2B ratio in the adult mouse forebrain on synaptic plasticity and learning behaviors by producing CaMKII promoter-driven NR2A transgenic mice. They combined hippocampal slice electrophysiology and behavioral paradigms to investigate how such overexpression may alter synaptic plasticity and cognition, and showed that the high NR2A amount in the forebrain principal excitatory neurons can selectively affect long-term memory formation. But surprisingly, instead of the predicted smaller LTP in the CA1 region of the NR2A transgenic mice, the researchers found that NR2A overexpression selectively abolished 3–5 Hz frequency-induced LTD in the CA3-CA1 synapses without affecting 100 Hz LTP or 1 Hz LTD.


This results suggest a novel step by which long-term memory consolidation engages LTD-like process to sculpt, crystallize, and incorporate newly acquired information into long-term knowledge in the brain.

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Injectable sponge delivers drugs, cells, and structure

Injectable sponge delivers drugs, cells, and structure | Amazing Science |

Bioengineers at Harvard have developed a gel-based sponge that can be molded to any shape, loaded with drugs or stem cells, compressed to a fraction of its size, and delivered via injection. Once inside the body, it pops back to its original shape and gradually releases its cargo, before safely degrading.


The biocompatible technology, revealed this week in the Proceedings of the National Academy of Sciences, amounts to a prefabricated healing kit for a range of minimally invasive therapeutic applications, including regenerative medicine.


“What we’ve created is a three-dimensional structure that you could use to influence the cells in the tissue surrounding it and perhaps promote tissue formation,” explains principal investigator David J. Mooney, Robert P. Pinkas Family Professor of Bioengineering at the Harvard School of Engineering and Applied Sciences (SEAS) and a Core Faculty Member at the Wyss Institute for Biologically Inspired Engineering at Harvard.


“The simplest application is when you want bulking,” Mooney explains. “If you want to introduce some material into the body to replace tissue that’s been lost or that is deficient, this would be ideal. In other situations, you could use it to transplant stem cells if you’re trying to promote tissue regeneration, or you might want to transplant immune cells, if you’re looking at immunotherapy.”


Consisting primarily of alginate, a seaweed-based jelly, the injectable sponge contains networks of large pores, which allow liquids and large molecules to easily flow through it. Mooney and his research team demonstrated that live cells can be attached to the walls of this network and delivered intact along with the sponge, through a small-bore needle. Mooney’s team also demonstrated that the sponge can hold large and small proteins and drugs within the alginate jelly itself, which are gradually released as the biocompatible matrix starts to break down inside the body.


Normally, a scaffold like this would have to be implanted surgically. Gels can also be injected, but until now those gels would not have carried any inherent structure; they would simply flow to fill whatever space was available.

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Researchers engineer bacterium to hunt down and kill pathogens

Researchers engineer bacterium to hunt down and kill pathogens | Amazing Science |

Recent examples of new genetic circuits that enable cells to acquire biosynthetic capabilities, such as specific pathogen killing, present an attractive therapeutic application of synthetic biology. A team of researchers in Singapore has developed a technique for bioengineering a bacterium to seek out and kill targeted pathogens.


They demonstrate a novel genetic circuit that reprograms Escherichia coli to specifically recognize, migrate toward, and eradicate both dispersed and biofilm-encased pathogenic Pseudomonas aeruginosa cells. The reprogrammed E. coli degraded the mature biofilm matrix and killed the latent cells encapsulated within by expressing and secreting the antimicrobial peptide microcin S and the nuclease DNaseI upon the detection of quorum sensing molecules naturally secreted by P. aeruginosa. Furthermore, the reprogrammed E. coli exhibited directed motility toward the pathogen through regulated expression of CheZ in response to the quorum sensing molecules.

By integrating the pathogen-directed motility with the dual antimicrobial activity in E. coli, we achieved signifincantly improved killing activity against planktonic and mature biofilm cells due to target localization, thus creating an active pathogen seeking killer E. coli.

NCPbiology's curator insight, June 27, 2014 6:26 AM

Interesting extra reading?

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DNA damage may cause ALS (Lou Gehrig’s disease), involving SIRT1, HDAC1 and sarcoma breakpoint protein FUS

DNA damage may cause ALS (Lou Gehrig’s disease), involving SIRT1, HDAC1 and sarcoma breakpoint protein FUS | Amazing Science |

MIT neuroscientists have found new evidence that suggests that a failure to repair damaged DNA could underlie not only ALS, but also other neurodegenerative disorders such as Alzheimer’s disease. These findings imply that drugs that bolster neurons’ DNA-repair capacity could help ALS patients, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and senior author of a paper describing the ALS findings in the Sept. 15, 2013 issue of Nature Neuroscience.

Neurons are some of the longest-living cells in the human body. While other cells are frequently replaced, our neurons are generally retained throughout our lifetimes. Consequently, neurons can accrue a lot of DNA damage and are especially vulnerable to its effects. 

“Our genome is constantly under attack and DNA strand breaks are produced all the time. Fortunately, they are not a worry because we have the machinery to repair it right away. But if this repair machinery were to somehow become compromised, then it could be very devastating for neurons,” Tsai says.

Tsai’s group has been interested in understanding the importance of DNA repair in neurodegenerative processes for several years. In a study published in 2008, they reported that DNA double-strand breaks precede neuronal loss in a mouse model that undergoes Alzheimer’s disease-like neurodegeneration and identified a protein, HDAC1, which prevents neuronal loss under these conditions.  

HDAC1 is a histone deacetylase, an enzyme that regulates genes by modifying chromatin, which consists of DNA wrapped around a core of proteins called histones. HDAC1 activity normally causes DNA to wrap more tightly around histones, preventing gene expression. However, it turns out that cells, including neurons, also exploit HDAC1’s ability to tighten up chromatin to stabilize broken DNA ends and promote their repair. 

In a paper published earlier this year in Nature Neuroscience, Tsai’s team reported that HDAC1 works cooperatively with another deacetylase called SIRT1 to repair DNA and prevent the accumulation of damage that could promote neurodegeneration. 

When a neuron suffers double-strand breaks, SIRT1 migrates within seconds to the damaged sites, where it soon recruits HDAC1 and other repair factors. SIRT1 also stimulates the enzymatic activity of HDAC1, which allows the broken DNA ends to be resealed. 

SIRT1 itself has recently gained notoriety as the protein that promotes longevity and protects against diseases including diabetes and Alzheimer’s disease, and Tsai’s group believes that its role in DNA repair contributes significantly to the protective effects of SIRT1. 

In an attempt to further unveil other partners that work with HDAC1 to repair DNA, Tsai and colleagues stumbled upon a protein called Fused In Sarcoma (FUS). This finding was intriguing, Tsai says, because the FUS gene is one of the most common sites of mutations that cause inherited forms of ALS. 

The MIT team found that FUS appears at the scene of DNA damage very rapidly, suggesting that FUS is orchestrating the repair response. One of its roles is to recruit HDAC1 to the DNA damage site. Without it, HDAC1 does not appear and the necessary repair does not occur. Tsai believes that FUS may also be involved in sensing when DNA damage has occurred.

At least 50 mutations in the FUS gene have been found to cause ALS. The majority of these mutations occur in two sections of the FUS protein. The MIT team mapped the interactions between FUS and HDAC1 and found that these same two sections of the FUS protein bind to HDAC1. 

They also generated four FUS mutants that are most commonly seen in ALS patients. When they replaced the normal FUS with these mutants, they found that the interaction with HDAC1 was impaired and DNA damage was significantly increased. This suggests that those mutations prevent FUS from recruiting HDAC1 when DNA damage occurs, allowing damage to accumulate and eventually leading to ALS.

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Jetpack Moves a Step Closer to Reality, Possibly launched in 2014

Jetpack Moves a Step Closer to Reality, Possibly launched in 2014 | Amazing Science |

Talking non-traditional ways of flying, New Zealand's Martin Aircraft is making progress towards production of what it calls the first practical jetpack, with manned and unmanned flight tests of its latest prototype.

Manned flights of Martin's 12th prototype of the ducted-fan JetPack, the sporty-looking P12 (see image), are to resume later this year after modifications to reduce vibration from the 200hp V4 two-stroke engine, which is mounted vertically behind the standing pilot. 

P12 tests are planned to result in a pre-production design for Martin's first sellable JetPack, which will be aimed at first responders (such as fire services) and which is planned to be available in 2014. You will have to wait a bit longer for a personal JetPack.The JetPack is a serious design. Flight control is fly-by-wire and it comes as standard with a ballistic recovery parachute, linked to the engine so it deploys automatically if it malfunctions. The undercarriage and frame is impact-absorbing and there is a flotation device in case of a ditching. 

Martin is aiming for a maximum speed of 40kt and a 30kt cruise, 30km range and 30min endurance. In addition to first responders, the company says there is interest from the military and for uses ranging from border patrol and search-and-rescue to corporate events and "jetpack experience" thrill rides.

Adrian Rojas's comment, October 7, 2013 11:47 PM
The idea of the jet-pack is very old. But no one ever made one and if they did they didn't succeed in their attempt. But now would be the perfect time to build one. Because we are living in a time period where technology is very advanced. It would not surprise me if we could build it. The thought about making it is very simple all you need to make is something you can strap on your back and fly with.

Man has always wanted to fly but we are taking steps by steps. First we built a airplane then a hot air balloon and now it is time for us to make a jet-pack. It's never easy to build something as complex as a jet-pack because you would need a lot of money and you would need the knowledge of knowing where to put what. But I believe that soon we will have a jet-pack.
Gerome Tadeja's comment, October 13, 2013 1:51 PM
I thought this article was interesting to read because someone's idea for a jet pack is being tested to see if it would work
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Millimeter Wave Mobile Communications for 5G Cellular Networks: It Will Work!

Millimeter Wave Mobile Communications for 5G Cellular Networks: It Will Work! | Amazing Science |

The global bandwidth shortage facing wireless carriers has motivated the exploration of the underutilized millimeter wave (mm-wave) frequency spectrum for future broadband cellular communication networks. There is, however, little knowledge about cellular mm-wave propagation in densely populated indoor and outdoor environments. Obtaining this information is vital for the design and operation of future fifth generation cellular networks that use the mm-wave spectrum. In this paper, we present the motivation for new mm-wave cellular systems, methodology, and hardware for measurements and offer a variety of measurement results that show 28 and 38 GHz frequencies can be used when employing steerable directional antennas at base stations and mobile devices.

First generation cellular networks were basic analog systems designed for voice communications. A move to early data services and improved spectral efficiency was realized in 2G systems through the use of digital modulations and time division or code division multiple access. 3G introduced high-speed Internet access, highly improved video and audio streaming capabilities by using technologies such as Wideband Code Division Multiple Access (W-CDMA) and High Speed Packet Access (HSPA). HSPA is an amalgamation of two mobile telephony protocols, High Speed Downlink Packet Access (HSDPA) and High Speed Uplink Packet Access (HSUPA), which extends and improves the performance of existing 3G mobile telecommunication networks utilizing WCDMA protocols. An improved 3GPP (3rd Generation Partnership Project) standard, Evolved HSPA (also known as HSPA+), was released in late 2008 with subsequent worldwide utilization beginning in 2010. HSPA has been deployed in over 150 countries by more than 350 communications service providers (CSP) on multiple frequency bands and is now the most extensively sold radio technology worldwide, although LTE is closing the gap rapidly.


The International Mobile Telecommunications-Advanced (IMT-Advanced) standard is the next-generation of mobile communications technology defined by the ITU and includes capabilities outstripping those of IMT-2000 (3G) mobile communication. ITU refers to IMT-Advanced as a 4G mobile communications technology, although it should be noted that there is no universally accepted definition of the term 4G. LTE radio access technology has been developed by the 3GPP to offer a fully 4G-capable mobile broadband platform. LTE is an orthogonal frequency-division multiplexing (OFDM)-based radio access technology that supports a scalable transmission bandwidth up to 20 MHz and advanced multi-antenna transmission. As a key technology in supporting high data rates in 4G systems, Multiple-Input Multiple-Output (MIMO) enables multi-stream transmission for high spectrum efficiency, improved link quality, and adaptation of radiation patterns for signal gain and interference mitigation via adaptive beam-forming using antenna arrays. The coalescence of HSPA and LTE will increase the peak mobile data rates of the two systems, with data rates exceeding 100 Mbps, and will also allow for optimal dynamic load balancing between the two technologies.


As the demand for capacity in mobile broadband communications increases dramatically every year, wireless carriers must be prepared to support up to a thousand-fold increase in total mobile traffic by 2020, requiring researchers to seek greater capacity and to find new wireless spectrum beyond the 4G standard. To improve the existing LTE network, the wireless technology roadmap now extends to IMT-Advanced with LTE-Advanced defined to meet IMT-Advanced requirements, which will be theoretically capable of peak throughput rates that exceed 1 Gigabit per second (Gbps). LTE-Advanced supports heterogeneous networks with co-existing large macro, micro, and pico cells, and Wi-Fi access points. Low cost deployment will be realized by self-organizing features and repeaters/relays.


As fifth generation (5G) is developed and implemented, we believe the main differences compared to 4G will be the use of much greater spectrum allocations at untapped mm-wave frequency bands, highly directional beam-forming antennas at both the mobile device and base station, longer battery life, lower outage probability, much higher bit rates in larger portions of the coverage area, lower infrastructure costs, and higher aggregate capacity for many simultaneous users in both licensed and unlicensed spectrum (e.g., the convergence of Wi-Fi and cellular). The backbone networks of 5G will move from copper and fiber to mm-wave wireless connections, allowing rapid deployment and mesh-like connectivity with cooperation between base stations.


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Stem Cell Reprogramming Made Easier By Removing The MBD3 Block

Stem Cell Reprogramming Made Easier By Removing The MBD3 Block | Amazing Science |
The researchers showed that removing MBD3 from the adult cells can improve efficiency and speed the production of iPSCs by several orders of magnitude.


Embryonic stem cells have the enormous potential to treat and cure many medical problems. That is why the discovery that induced embryonic-like stem cells can be created from skin cells was rewarded with a Nobel Prize in 2012. But the process has remained frustratingly slow and inefficient, and the resulting stem cells are not yet ready for medical use. Research in the lab of the Weizmann Institute’s Dr. Yaqub Hanna,which appears Wednesday in Nature, dramatically changes that: He and his group revealed the “brake” that holds back the production of stem cells, and found that releasing this brake can both synchronize the process and increase its efficiency from around 1% or less today to 100%. These findings may help facilitate the production of stem cells for medical use, as well as advancing our understanding of the mysterious process by which adult cells can revert back into their original, embryonic state.

Embryonic stem cells are those that have not undergone any “specialization;” thus they can give rise to any type of cell in the body. This is what makes them so valuable: They can be used, among other things, to repair damaged tissue, treat autoimmune disease and even grow transplant organs. Using stem cells taken from embryos is problematic because of availability and ethical concerns, but the hopes for their use were renewed in 2006 when a team led by Shinya Yamanaka of Kyoto University discovered that it is possible to “reprogram” adult cells. The resulting cells, called “induced pluripotent stem cells” (iPSCs), are created by inserting four genes into their DNA. Despite this breakthrough, the reprograming process is fraught with difficulty: It can take up to four weeks; the timing is not coordinated among the cells; and less than one percent of the treated cells actually end up becoming stem cells. Hanna and his team asked: What is the main obstacle – or obstacles – that prevent successful reprograming in the majority of cells? In his postdoctoral research, Hanna had employed mathematical models to show that a single obstacle was responsible. Of course in biology, Hanna is the first to admit, experimental proof is required to back up the models. The present study not only provides the proof, it reveals the identity of that single obstacle and shows that removing it can dramatically improve reprograming.

Hanna’s group, led by Dr. Noa Novershtern, Yoach Rais, Asaf Zviran and Shay Geula of the Molecular Genetics Department, together with members of the genomics unit of the Institute’s Israel Structural Proteomics Center, looked at a certain protein, called MBD3, whose function was unknown. MBD3 had caught their attention because it is expressed in every cell in the body, at every stage of development. This is quite rare: In general, most types of proteins are produced in specific cells, at specific times, for specific functions. The team found that there is one exception to the rule of universal expression of this protein: the first three days after conception. These are exactly the three days in which the fertilized egg begins dividing, and the nascent embryo is a growing ball of pluripotent stem cells that will eventually supply all the cell types in the body. Starting on the fourth day, differentiation begins and the cells already start to lose their pluripotent status. And that is just when the MBD3 proteins first appear.

This finding has significant implications for the producing of iPSCs for medical use. Yamanaka used viruses to insert the four genes but, for safety reasons, these are not used in reprograming cells to be used in patients. This gives the process an even lower success rate of only around a tenth of a percent. The researchers showed that removing MBD3 from the adult cells can improve efficiency and speed the process by several orders of magnitude. The time needed to produce the stem cells was shortened from four weeks to eight days. As an added bonus, since the cells all underwent the reprograming at the same rate, the scientists will now be able, for the first time, to actually follow it step by step and reveal its mechanisms of operation. Hanna points out that his team’s achievement was based on research into the natural pathways of embryonic development: “Scientists investigating reprograming can benefit from a deeper understanding of how embryonic stem cells are produced in nature. After all, nature still makes them best, in the most efficient manner.”

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Anomalies in relic radiation: Universe may be curved, not flat

Anomalies in relic radiation: Universe may be curved, not flat | Amazing Science |

Anomalies in relic radiation could contradict the evidence for a level cosmos. 


We live in a lopsided universe: That has been a lesson that cosmologists have learned from examining the detailed structure of the radiation left over from the Big Bang. Now, two cosmologists show that the data are consistent with a Universe that is curved slightly, similarly to a saddle. If their model is correct, it would overturn the long-held belief that the cosmos is flat.


On a large scale, precision measurements of the cosmic microwave background (CMB) by NASA’s Wilkinson Microwave Anisotropy Probe provided the first hints of an asymmetry in 2004. Some experts wondered whether the finding was a systematic error that would be corrected when the NASA probe’s successor, the European Space Agency’s Planck spacecraft, mapped the CMB again with higher precision. But the Planck results, announced earlier this year, confirmed the anomaly.


To explain those results, Andrew Liddle and Marina Cortês, both at the University of Edinburgh, UK, have now proposed a model of cosmic inflation — a hypothetical period of rapid expansion right after the Big Bang in which the Universe grew by many orders of magnitude in a small fraction of a second.


The simplest theory of inflation holds that the Universe is flat and that its expansion is driven by a single quantum field called the inflaton. In this model the inflaton has two roles: it triggers hyperexpansion and generates the tiny density fluctuations that enlarged to become the seeds of galaxies.


But this version of inflation cannot account for the Universe’s lopsidedness except as a statistical fluke — similar to, for example, a fair coin that happens to come up heads many more times than tails over 1,000 flips. If the CMB anomalies are not flukes, they could offer an unprecedented window on the detailed structure of the early universe, says Liddle.


Like many theorists before them, Liddle and Cortês invoke a second quantum field — the curvaton — to set the primordial density fluctuations in the infant Universe, restricting the inflaton to driving the era of hyperexpansion only.

The researchers show that the curvaton field would generate the lopsided density fluctuations that have been observed if space had a slightly negative curvature on large scales. This means that if large triangles could be ‘drawn’ in space, their internal angles would add up to less than 180 degrees. In a flat Universe the angles would add up to 180 degrees exactly, and in a positively curved one they would add up to more than 180 degrees.


In Liddle and Cortês’s scenario, the asymmetry of the CMB would derive from a lack of uniformity on the very large scale of the Universe encoded in the curvaton field. In 2008, Erickcek and her colleagues proposed a similar mechanism. That model, however, did not invoke a negatively curved Universe.


Although numerous observations indicate that the cosmos is indeed flat, the deviations in the CMB data predicted by latest model — which the authors acknowledge is still speculative — could be small enough to fit within the limits imposed by measurements with the Planck satellite, says Liddle. Future experiments with measurements of improved precision however might determine who is right.

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Researchers decipher the 3D structure of telomerase

As seen in the 2013 article, "The architecture of Tetrahymena telomerase holoenzyme" published in Nature.


Telomerase adds telomeric repeats to chromosome ends using an internal RNA template and a specialized telomerase reverse transcriptase (TERT), thereby maintaining genome integrity. Little is known about the physical relationships among protein and RNA subunits within a biologically functional holoenzyme. Here we describe the architecture of Tetrahymena thermophila telomerase holoenzyme determined by electron microscopy.


Six of the seven proteins and the TERT-binding regions of telomerase RNA (TER) have been localized by affinity labelling. Fitting with high-resolution structures reveals the organization of TERT, TER and p65 in the ribonucleoprotein (RNP) catalytic core. p50 has an unanticipated role as a hub between the RNP catalytic core, p75–p19–p45 subcomplex, and the DNA-binding Teb1. A complete in vitro holoenzyme reconstitution assigns function to these interactions in processive telomeric repeat synthesis. These studies provide the first view of the extensive network of subunit associations necessary for telomerase holoenzyme assembly and physiological function.

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40 years after ban, pesticide DDT is still killing California condors

40 years after ban, pesticide DDT is still killing California condors | Amazing Science |

The U.S. banned the use of DDT (dichlorodiphenyltrichloroethane) back in 1972 after studies linked it to the thinning of eggs in bald eagles, peregrine falcons and other species. The pesticide has also been linked to other health hazards in wildlife and humans. But even though it is no longer employed in this country, DDT persists for a long time in the environment, and its effects are still being felt today.


The Ventana Wildlife Society (VWS), which manages the California condor (Gymnogyps californianus) reintroduction program in the coastal Big Sur region, first began to suspect in 2006 that DDT was affecting the big birds. Two captive-born condors successfully nested in the wild then for the first time in that region. The birds mated and laid eggs, but they soon cracked and the nest failed. An examination revealed that the shells were so thin that they didn’t even resemble normal condor eggs.


Since that time many more eggs have been laid in the region but 12 out of 16 condor nest sites failed between 2007 and 2009. Fragments of shells—all visibly thin—were recovered from those sites. Meanwhile, the condors released 650 kilometers farther south have enjoyed a 70 to 80 percent hatching success rate.


Now, research pending publication in the journal The Condor reveals that the egg fragments recovered in the Big Sur region were 34 percent thinner than eggs laid at the same time in the southern reintroduction zone. Many of the latter shells lacked a normal external crystalline layer. The researchers link the thinness and malformations to DDT and the compound DDE (dichloro diphenyldichloroethylene), which is formed when the pesticide breaks down.


How did the condors end up with DDT and DDE in their systems? The birds in Big Sur have been observed dining on the carcasses of sea lions, sea otters and other marine mammals, animals the inland southern population lacks the opportunity to eat. Previous research into California sea lions (Zalophus californianus) from 1994 to 2006 found high levels of DDT and related compounds in their blubber, especially in the males. The marine mammals live near the 54-hectare Palos Verdes Shelf Superfund site, an underwater region contaminated by an estimated 1,540 metric tons of DDT discharged by the Montrose Chemical Corp. DDT manufacturing plant between the 1950s and 1970s. Earlier this year new tests estimated that the DDT at the site had somehow shrunk to just 12.7 metric tons; it is not yet known what happened to all of those missing chemicals.

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Dual Action Virolytic Entry Inhibitor ("DAVEI") neutralizes HIV virus by making it think it's attached to a cell

Dual Action Virolytic Entry Inhibitor ("DAVEI") neutralizes HIV virus by making it think it's attached to a cell | Amazing Science |

Pinning down an effective way to combat the spread of the human immunodeficiency virus, the viral precursor to AIDS, has long been a challenge for scientists and physicians, because the virus is an elusive one that mutates frequently and, as a result, quickly becomes immune to medication. A team of Drexel University researchers is trying to get one step ahead of the virus with a microbicide they’ve created that can trick HIV into “popping” itself into oblivion.


Its name is DAVEI - which stands for “Dual Action Virolytic Entry Inhibitor”- and it can pull a fast one on HIV. DAVEI was invented and tested by scientists from Drexel’s College of Engineering; School of Biomedical Engineering, Science and Health Systems; and College of Medicine, and is the latest in a new generation of HIV treatments that function by specifically destroying the virus without harming healthy cells.


“While several molecules that destroy HIV have recently been announced, DAVEI is unique among them by virtue of its design, specificity and high potency,” said Dr. Cameron Abrams, a professor in Drexel’s College of Engineering and a primary investigator of the project.


A team co-led by Abrams and Dr. Irwin Chaiken in the Department of Biochemistry and Molecular Biology in Drexel’s College of Medicine, and including Dr. Mark Contarino and doctoral students Arangassery Rosemary Bastian and R. V. Kalyana Sundaram, developed the chimeric recombinantly engineered protein – that is, a molecule assembled from pieces of other molecules and engineered for a specific purpose, in this case to fight HIV. Their research will be published in the October edition of the American Society for Microbiology’s Antimicrobial Agents and Chemotherapy.


The idea behind DAVEI was to design a molecule that hijacks the virus’s fusion machinery, the tools it uses to attach to and attack a healthy cell, and tricks the virus into destroying itself. HIV invades a healthy cell by first attaching via protein “spikes” that then collapse to pull viral and cell membranes together, fusing them and allowing the genetic contents of the virus to enter the healthy cell. The cell is rewired by the viral genetic material into producing more viruses instead of performing its normal function, which, in the case of cells infected by HIV, involves normal immunity. AIDS is the result.


“We hypothesized that an important role of the fusion machinery is to open the viral membrane when triggered, and it follows that a trigger didn't necessarily have to be a doomed cell,” Abrams said. “So we envisioned particular ways the components of the viral fusion machinery work and designed a molecule that would trigger it prematurely,” Abrams said.


The team designed DAVEI from two main ingredients. One piece, called the Membrane Proximal External Region (MPER), is itself a small piece of the fusion machinery and interacts strongly with viral membranes. The other piece, called cyanovirin, binds to the sugar coating of the protein spike.


Working together, the MPER and cyanovirin in DAVEI “tweak” the fusion machinery in a way that mimics the forces it feels when attached to a cell.    

“For lack of a better term, DAVEI 'tricks' the virus into 'thinking' it is about to infect a healthy cell, when, in fact, there is nothing there for it to infect,” Abrams said. “Instead, it releases its genetic payload harmlessly and dies.”

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Time Magazine Wonders "Can Google Solve Death?"

Time Magazine Wonders "Can Google Solve Death?" | Amazing Science |
Time magazine's new cover story is the about the ultimate tech company cage match: GOOGLE VS. DEATH. In Silicon Valley parlance, this mortal coil is a bug, not a feature, and Time gives GOOG pretty generous odds.


It’s worth pointing out that there is no other company in Silicon Valley that could plausibly make such an announcement. Smaller outfits don’t have the money; larger ones don’t have the bones. Apple may have set the standard for surprise unveilings but, excepting a major new product every few years, these mostly qualify as short-term. Google’s modus operandi, in comparison, is gonzo airdrops into deep “Wait, really?” territory. Last week Apple announced a gold iPhone; what did you do this week, Google? Oh, we founded a company that might one day defeat death itself.


Also worth pointing out? No company can plausibly claim to defeat death. It's de facto implausible! "Might," doesn't quite cover it. Probably. "One day." Outlook hazy, but hey, it gives Time and Google an excuse to talk about "moon shots," Larry Page's pet phrasefor outlandish, presumably genius ideas. Page, who helped found Singularity University, has had a life-extension fetish for a while. Last year, the company hired transhumanist cheerleader Ray Kurzweil to build "the ultimate AI."


The death-curing company Time is referring to is Calico. According to a press release put out at the same time as the article, Calico "will focus on health and well-being, in particular the challenge of aging and associated diseases." Calico's CEO and founding investor is Arthur D. Levinson, the former CEO of Genentech, the biotech corporation. Even with this new role to alter the basic nature of human existence, Levinson "will remain Chairman of Genentech and a director of Hoffmann-La Roche, as well as Chairman of Apple."


Medicine is well on its way to becoming an information science: doctors and researchers are now able to harvest and mine massive quantities of data from patients. And Google is very, very good with large data sets. While the company is holding its cards about Calico close to the vest, expect it to use its core data-handling skills to shed new light on familiar age-related maladies. Sources close to the project suggest it will start small and focus entirely on researching new technologies.


What’s certain is that looking at medical problems through the lens of data and statistics, rather than simply attempting to bring drugs to market, can produce startlingly counterintuitive opinions. “Are people really focused on the right things?” Page muses. “One of the things I thought was amazing is that if you solve cancer, you’d add about three years to people’s average life expectancy. We think of solving cancer as this huge thing that’ll totally change the world. But when you really take a step back and look at it, yeah, there are many, many tragic cases of cancer, and it’s very, very sad, but in the aggregate, it’s not as big an advance as you might think.”Page, in other words, is a man for whom solving—not curing—cancer may not be a big enough task.


Solving death over curing cancer is a pretty high class problem. But before we start working ourselves into a frenzy about who has access to Google's "solution"—decrying some dystopian double feature of Elysiumand In Time, where only the poor die young—consider the hubris of Page's claims.


The fact that Time is laundering that belief is a bubble indicator. How do you know when everyone is too intoxicated on the phantom power of pampered billionaires? When they tell you they can solve death and you believe them.


Steve Kingsley's comment, September 20, 2013 11:56 AM
Pampered billioners? Larry Page works harder than the writer of this article and 10 of like him together!
Elizabeth Oneil's comment, September 20, 2013 1:42 PM
VVX cool
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EPFL is developing a tiny, personal blood testing laboratory that implants under your skin

EPFL is developing a tiny, personal blood testing laboratory that implants under your skin | Amazing Science |

EPFL scientists have developed a tiny, portable personal blood testing laboratory: a minuscule device implanted just under the skin provides an immediate analysis of substances in the body, and a radio module transmits the results to a doctor over the cellular phone network. This feat of miniaturization has many potential applications, including monitoring patients undergoing chemotherapy.


Humans are veritable chemical factories - we manufacture thousands of substances and transport them, via our blood, throughout our bodies. Some of these substances can be used as indicators of our health status. A team of EPFL scientists has developed a tiny device that can analyze the concentration of these substances in the blood. Implanted just beneath the skin, it can detect up to five proteins and organic acids simultaneously, and then transmit the results directly to a doctor’s computer. This method will allow a much more personalized level of care than traditional blood tests can provide. Health care providers will be better able to monitor patients, particularly those with chronic illness or those undergoing chemotherapy. The prototype, still in the experimental stages, has demonstrated that it can reliably detect several commonly traced substances.

The device was developed by a team led by EPFL scientists Giovanni de Micheli and Sandro Carrara. The implant, a real gem of concentrated technology, is only a few cubic millimeters in volume but includes five sensors, a radio transmitter and a power delivery system. Outside the body, a battery patch provides 1/10 watt of power, through the patient’s skin – thus there’s no need to operate every time the battery needs changing.


Information is routed through a series of stages, from the patient’s body to the doctor’s computer screen. The implant emits radio waves over a safe frequency. The patch collects the data and transmits them via Bluetooth to a mobile phone, which then sends them to the doctor over the cellular network.


Great care was taken in developing the sensors. To capture the targeted substance in the body – such as lactate, glucose, or ATP – each sensor’s surface is covered with an enzyme. “Potentially, we could detect just about anything,” explains De Micheli. “But the enzymes have a limited lifespan, and we have to design them to last as long as possible.” The enzymes currently being tested are good for about a month and a half; that’s already long enough for many applications. “In addition, it’s very easy to remove and replace the implant, since it’s so small.”


The electronics were a considerable challenge as well. “It was not easy to get a system like this to work on just a tenth of a watt,” de Micheli explains. The researchers also struggled to design the minuscule electrical coil that receives the power from the patch.


The prototype has already been tested in the laboratory for five different substances, and proved as reliable as traditional analysis methods. The project brought together eletronics experts, computer scientists, doctors and biologists from EPFL, the Istituto di Ricerca di Bellinzona, EMPA and ETHZ. It is part of the Swiss Nano-Tera program, whose goal is to encourage interdisciplinary research in the environmental and medical fields. Researchers hope the system will be commercially available within 4 years.


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Patricia Nicoll's curator insight, October 6, 2013 9:46 PM

Instantaneous sampling and blood results

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Novel type of lens combines human and insect vision to focus wide-angle views

Novel type of lens combines human and insect vision to focus wide-angle views | Amazing Science |

Multi-part lens expands and contracts to change focus. A lens invented at The Ohio State University combines the focusing ability of a human eye with the wide-angle view of an insect eye to capture images with depth.

The results could be smartphones that rival the photo quality of digital cameras, and surgical imaging that enables doctors to see inside the human body like never before.


Engineers described the patent-pending lens in the Technical Digest of the 25th IEEE International Conference on Micro Electro Mechanical Systems.

"Our eye can change focus. An insect eye is made of many small optical components that can't change focus but give a wide view. We can combine the two," explained Yi Zhao, associate professor of biomedical engineering and ophthalmology at Ohio State. "What we get is a wide-angle lens with depth of field."


That is to say, the lens shows a wide view, but still offers a sense of human-like depth perception: as close objects come into focus, far away objects look blurry.


Zhao's prototype lens is made of a flexible transparent polymer filled with a gelatinous fluid similar to fluid inside the human eye. It's actually a composite of several separate dome-shaped fluid pockets, with small domes sitting atop one larger dome. Each dome is adjustable, so that as fluid is pumped into and out of the lens, different parts of it expand and contract to change the overall shape-and thus, the direction and focus-of the lens.


This shape-changing strategy is somewhat similar to the way muscles in the human eye change the shape of the lens tissue in order to focus. It differs dramatically from the way typical cameras and microscopes focus, which involves moving separate glass lenses back and forth along the line of sight.

The shape-changing lens could potentially offer the same focusing capability as multiple moving lenses in a single stationary lens, which would make for smaller and lighter cameras and microscopes.


In particular, Zhao is interested in using the lens in confocal microscopes, which use a system of moving glass lenses and a laser to scan three-dimensional images of tiny objects.


"We believe that it is possible to make a confocal microscope with no moving parts," he said.

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WIRED: NASA's Plutonium Problem Could End Deep-Space Exploration - Earth's Reserves Almost Ran Out

WIRED: NASA's Plutonium Problem Could End Deep-Space Exploration - Earth's Reserves Almost Ran Out | Amazing Science |

In 1977, the Voyager 1 spacecraft left Earth on a five-year mission to explore Jupiter and Saturn. Thirty-six years later, the car-size probe is still exploring, still sending its findings home. It has now put more than 19 billion kilometers between itself and the sun. Last week NASA announced that Voyager 1 had become the first man-made object to reach interstellar space.


The distance this craft has covered is almost incomprehensible. It’s so far away that it takes more than 17 hours for its signals to reach Earth. Along the way, Voyager 1 gave scientists their first close-up looks at Saturn, took the first images of Jupiter’s rings, discovered many of the moons circling those planets and revealed that Jupiter’s moon Io has active volcanoes. Now the spacecraft is discovering what the edge of the solar system is like, piercing the heliosheath where the last vestiges of the sun’s influence are felt and traversing the heliopause where cosmic currents overcome the solar wind. Voyager 1 is expected to keep working until 2025 when it will finally run out of power.


None of this would be possible without the spacecraft’s three batteries filled with plutonium-238. In fact, Most of what humanity knows about the outer planets came back to Earth on plutonium power. Cassini’s ongoing exploration of Saturn, Galileo’s trip to Jupiter, Curiosity’s exploration of the surface of Mars, and the 2015 flyby of Pluto by the New Horizons spacecraft are all fueled by the stuff. The characteristics of this metal’s radioactive decay make it a super-fuel. More importantly, there is no other viable option. Solar power is too weak, chemical batteries don’t last, nuclear fission systems are too heavy. So, we depend on plutonium-238, a fuel largely acquired as by-product of making nuclear weapons.


But there’s a problem: We’ve almost run out. “We’ve got enough to last to the end of this decade. That’s it,” said Steve Johnson, a nuclear chemist at Idaho National Laboratory. And it’s not just the U.S. reserves that are in jeopardy. The entire planet’s stores are nearly depleted.

The country’s scientific stockpile has dwindled to around 36 pounds. To put that in perspective, the battery that powers NASA’s Curiosity rover, which is currently studying the surface of Mars, contains roughly 10 pounds of plutonium, and what’s left has already been spoken for and then some. The implications for space exploration are dire: No more plutonium-238 means not exploring perhaps 99 percent of the solar system. In effect, much of NASA’s $1.5 billion-a-year (and shrinking) planetary science program is running out of time. The nuclear crisis is so bad that affected researchers know it simply as “The Problem.”


But it doesn’t have to be that way. The required materials, reactors, and infrastructure are all in place to create plutonium-238. In fact, the U.S. government recently approved spending about $10 million a year to reconstitute production capabilities the nation shuttered almost two decades ago. In March, the DOE even produced a tiny amount of fresh plutonium inside a nuclear reactor in Tennessee.

The only natural supplies of plutonium-238 vanished eons before the Earth formed some 4.6 billion years ago. Exploding stars forge the silvery metal, but its half-life, or time required for 50 percent to disappear through decay, is just under 88 years.


Fortunately, we figured out how to produce it ourselves — and to harness it to create a remarkably persistent source of energy. Like other radioactive materials, plutonium-238 decays because its atomic structure is unstable. When an atom’s nucleus spontaneously decays, it fires off a helium core at high speed while leaving behind a uranium atom. These helium bullets, called alpha radiation, collide en masse with nearby atoms within a lump of plutonium — a material twice as dense as lead. The energy can cook a puck of plutonium-238 to nearly 1,260 degrees Celsius. To turn that into usable power, you wrap the puck with thermoelectrics that convert heat to electricity. Voila: You’ve got a battery that can power a spacecraft for decades.

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