The LHC Has Discovered Its First New Particle

And no, it's not the Higgs boson

By Clay Dillow

Big Smash: Atlas's eight giant superconducting magnets, together powerful enough to crush a bus CERN

Though researchers think the Higgs boson is running out of places to hide, the LHC has yet to provide conclusive proof of its existence. But the ATLAS experiment at the LHC--one of the two main experiments taking precise measurements of particle collisions--has found what is thought to be the first observation of a new particle at the world’s largest science experiment. Known as c_b(3P)--or Chi-b (3P)--observations of the particle should yield new insights into the strong force that holds atomic nuclei together.

The c_b(3P) particle is a newly observed means of combing what’s known as a beauty quark with its antiquark equivalent. It’s considered a boson like the Higgs, and like the Higgs it has long been thought to be there, theoretically speaking. It’s a more excited state of Chi particles already witnessed in previous collider experiments. But no one had actually seen it until now.

The as-yet unpublished research should be a jumping off point toward a greater understanding of what holds the universe together. The Higgs gets a lot of air time, as it has proven the most elusive of the Standard Model puzzle pieces and is thought to be the particle that gives all others mass. But once a theory establishes how the universe got mass, it still has to demonstrate how that mass is held together at the fundamental level. That means understanding the strong force and the roles of particles like c_b(3P).

Geek out on some hard physics over at arXiv.

[University of Birmingham]

Self-Healing Electronics Use Liquid Metal to Fix Broken Circuits

Video: Self-Healing Electronics Use Liquid Metal to Fix Broken Circuits

By Rebecca Boyle

Self-Healing Circuit Microcapsules full of liquid metal sit atop a gold circuit. When the circuit is broken, the microcapsules rupture, filling in the crack and restoring the circuit. Scott White/University of Illinois

Over the weekend, faced with the dreaded Yellow Light of Death, I ripped apart a PlayStation 3 and blasted it with a 500-degree heat gun to re-flow the GPU and CPU. It was pretty fun and it worked, much to the delight of the member of my household who was this close to finishing “Batman: Arkham City.” Next time, this new self-healing circuit compound could make our work unnecessary.

Broken circuits could fix themselves using an emergency capsule of liquid metal, invented by researchers at the University of Illinois. As a crack propagates in a circuit, a microcapsule breaks open, spilling liquid metal into the gap and restoring electrical flow. The circuit would only be broken for a few microseconds, just as long as it takes for the capsule to fill in the cracks. During tests, 90 percent of the circuit samples healed to 99 percent of original conductivity, even when only a small amount of microcapsules were used, according to the U of I. Watch White explain the system in the video below.

Illinois professors Nancy Sottos, Scott White and Jeffrey Moore had already done lots of work on self-healing polymers and other types of structural repairs, but this is the first time anyone has tried self-healing conductivity. It works automatically and only at the point of a circuit failure. It’s so simple, you wonder why no one has thought of this before.

The method could replace some of the redundancies in complex circuits, perhaps making electronics cheaper, lighter and more sustainable. The researchers even hope it could be used to improve battery performance. The work was published in the journal Advanced Materials.

[University of Illinois via The Verge]

Eco-Friendly Battery Runs on Old Newspapers

By Dan Nosowitz

Paper-Powered Battery Sony

I'll start you guys off with a quote here: In talking about Sony's new battery technology, which uses old cellulose product like newspapers and cardboard to generate electricity, the BBC says: "Their work builds on a previous project in which they used fruit juice to power a Walkman music player." Thank you, crazy Sony recycling-engineers.

This new tech relies on turning cellulose products (including, lest we forget, the paper greeting cards all you Earth-hating monsters are exchanging this time of year) into glucose sugar. That's done by introducing the old paper products to a solution of water and cellulase, an enzyme found in nature, and, um, shaking it. The cellulase solution decomposes the cellulose to form that necessary glucose, which is in turn combined with oxygen and some other unnamed enzymes, producing electrons and hydrogen ions, the former of which is fed into batteries to charge them.

If you're wondering where in nature this wood-eating cellulase enzyme is found, look no further than the termite. Cellulase is naturally occurring in the wood-eating species, and in fact the Sony researchers involved in the project actually compared their technique to that of a termite.

As with all new battery tech, especially in the early stages like this one is, the battery isn't powerful enough to run high-demand gear. A portable music player, like the Walkman™, is about all it can handle at the moment. But as the byproducts are basically harmless (water and gluconolactone, a neutral product often used in anti-aging cosmetics), it's definitely a tech we'd like to see improve and become viable.

[BBC]

Video: Plasma Torch Toothbrush Successfully Used In Human Mouth

By Dan Nosowitz

Plasma Brush on Dentist Missouri University

Attentive followers of dentistry developments that we are, we've been following the story of theplasma brush for awhile now. And it seems like it's making some serious progress: human clinical trials are supposed to begin in early 2012, and there's also a video (below) of the World's Bravest Dentist shooting a plasma beam into his own mouth.

Some background, for anyone who doesn't subscribe to Dentistry Illustrated Weekly: the plasma brush isn't a toothbrush, but actually a tool dentists are hoping to use for two primary situations. The first is breaking up plaque; the plasma torch, though it's no hotter than room temperature, is excellent at breaking the bonds that adhere plaque to a tooth. The second is as a sort of primer for filling cavities.

There are certain kinds of cavities, according to Hao Li, associate professor of mechanical and aerospace engineering in the Missouri University College of Engineering, that need to be refilled every five or seven years using current technology--and they can only be refilled a few times before having to be pulled. The plasma brush can prime a cavity for filling in sort of the same way pavers create those divots in roads before filling them in with new asphalt: it provides more surface area for the filling to stick to, and the research team claims plasma-assisted fillings could be 60% stronger than traditional fillings.

Human clinical trials are due to begin early next year at the University of Tennessee at Memphis, with the team hoping the tool could be approved by the FDA and available to dentists by 2013.

Study uncovers clues to what makes anesthetics work

Physicians use inhalation anesthetics in a way that is incredibly safe for patients, but very little is known about the intricacies of how these drugs actually work in children and adults. Now, researchers have uncovered what cells respond to anesthesia in an organism known as the C. elegans, according to a new study from the Seattle Children's Research Institute. C. elegans is a transparent roundworm used often in research. The study, "Optical reversal of halothane-induced immobility in C. elegans," is published in the December 20, 2011 issue of Current Biology.

"Our findings tell us what cells and channels are important in making the anesthetic work," said lead author Phil Morgan, MD, researcher at Seattle Children's Research Institute and University of Washington professor of anesthesiology and pain medicine. "The scientific community has attempted to uncover the secrets of how anesthetics work since the 1860s, and we now have at least part of the answer." Margaret Sedensky, MD, Seattle Children's Research Institute and a UW professor of anesthesiology and pain medicine, and Vinod Singaram, graduate student, Case Western Reserve University, are co-lead authors of the study.

The team studied the roundworm after inserting a pigment or protein typically found in the retina of a human eye — called a retinal-dependent rhodopsin channel — into its cells. The proteins in cell membranes act as channels to help movement. Researchers then used a blue light, activating channels in the roundworm that allowed the immediate reversal of anesthetics, and resulting in the roundworm waking up and seemingly swimming off the slide.

This video is not supported by your browser at this time.

A roundworm (known as C. elegans) is under anesthesia in the first part of the video. At 17 seconds, a blue light is turned on, with the effect of reversing the anesthesia.

The team's findings won't immediately translate into a discovery that would be available for humans, cautioned Dr. Morgan, who has been working in this field for some 25 years. "But it tells us what function we have to treat to try to do so," he said.

"We believe that there is a class of potassium channels in humans that are crucial in this process of how anesthetics work and that they are perhaps the ones that are sensitive to potential anesthesia reversal. There are drugs for blocking these channels and with these same drugs, maybe we can eventually reverse anesthesia." Potassium channels are found in all living organisms and in most cell types, and they control a wide variety of cell functions.

Anesthesia medications are used in both children and adults, but many are used more often in kids. Dr. Morgan and his colleagues plan to replicate the study in other animal models, starting with a mouse.

More information: The study "Optical reversal of halothane-induced immobility in C. elegans," in Current Biology can be found here:http://www.cell.co … 0960-9822(11

 

)01203-6

Provided by Seattle Children's

"Study uncovers clues to what makes anesthetics work." December 22nd, 2011. http://www.physorg.com/news/2011-12-uncovers-clues-anesthetics.html

 

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Robert Karl Stonjek

Neuroscientists identify a master controller of memory

Yingxi Lin, a member of the McGovern Institute for Brain Research and the the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences.
Photo courtesy Kent Dayton

When you experience a new event, your brain encodes a memory of it by altering the connections between neurons. This requires turning on many genes in those neurons. Now, MIT neuroscientists have identified what may be a master gene that controls this complex process.

The findings, described in the Dec. 23 issue of Science, not only reveal some of the molecular underpinnings of memory formation — they may also help neuroscientists pinpoint the exact locations of memories in the brain.

The research team, led by Yingxi Lin, a member of the McGovern Institute for Brain Research at MIT, focused on the Npas4 gene, which previous studies have shown is turned on immediately following new experiences. The gene is particularly active in the hippocampus, a brain structure known to be critical in forming long-term memories.

Lin and her colleagues found that Npas4 turns on a series of other genes that modify the brain’s internal wiring by adjusting the strength of synapses, or connections between neurons. “This is a gene that can connect from experience to the eventual changing of the circuit,” says Lin, the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences.

To investigate the genetic mechanisms of memory formation, the researchers studied a type of learning known as contextual fear conditioning: Mice receive a mild electric shock when they enter a specific chamber. Within minutes, the mice learn to fear the chamber, and the next time they enter it, they freeze.

The researchers showed that Npas4 is turned on very early during this conditioning. “This sets Npas4 apart from many other activity-regulated genes,” Lin says. “A lot of them are ubiquitously induced by all these different kinds of stimulations; they are not really learning-specific.”

Furthermore, Npas4 activation occurs primarily in the CA3 region of the hippocampus, which is already known to be required for fast learning.

“We think of Npas4 as the initial trigger that comes on, and then in turn, in the right spot in the brain, it activates all these other downstream targets. Eventually they’re going to modify synapses in a way that’s likely changing synaptic inhibition or some other process that we’re trying to figure out,” says Kartik Ramamoorthi, a graduate student in Lin’s lab and lead author of the paper.

Genetic regulation

So far, the researchers have identified only a few of the genes regulated by Npas4, but they suspect there could be hundreds more. Npas4 is a transcription factor, meaning it controls the copying of other genes into messenger RNA — the genetic material that carries protein-building instructions from the nucleus to the rest of the cell. The MIT experiments showed that Npas4 binds to the activation sites of specific genes and directs an enzyme called RNA polymerase II to start copying them.

“Npas4 is providing this instructive signal,” Ramamoorthi says. “It’s telling the polymerase to land at certain genes, and without it, the polymerase doesn’t know where to go. It’s just floating around in the nucleus.”

When the researchers knocked out the gene for Npas4, they found that mice could not remember their fearful conditioning. They also found that this effect could be produced by knocking out the gene just in the CA3 region of the hippocampus. Knocking it out in other parts of the hippocampus, however, had no effect. Though they focused on contextual fear conditioning, the researchers believe that Npas4 will also prove critical for other types of learning.

Gleb Shumyatsky, an assistant professor of genetics at Rutgers University, says that an important next step is to identify more of the genes controlled by Npas4, which should reveal more of its role in memory formation. “It’s definitely one of the major players,” says Shumyatsky, who was not involved in this research. “Future experiments will show how major a player it is.”

The MIT team also plans to investigate whether the same neurons that turn on Npas4 when memories are formed also turn it on when memories are retrieved. This could help them pinpoint the exact neurons that are storing particular memories.

“We’re hunting for the memory, and we think we can use Npas4 to mark where it is,” Ramamoorthi says. “That’s because it’s turned on specifically and now we can label the cells and maybe fish out where in the brain the memory is sitting.”

More information: Npas4 Regulates a Transcriptional Program in CA3 Required for Contextual Memory Formation, Science, 23 December 2011: 
Vol. 334 no. 6063 pp. 1669-1675. DOI: 10.1126/science.1208049

 

Provided by Massachusetts Institute of Technology

This story is republished courtesy of MIT News (http://web.mit.edu/newsoffice/

 

), a popular site that covers news about MIT research, innovation and teaching.

"Neuroscientists identify a master controller of memory." December 22nd, 2011. http://medicalxpress.com/news/2011-12-neuroscientists-master-memory.html

 

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Robert Karl Stonjek

How skin is wired for touch

 

Compared to our other senses, scientists don't know much about how our skin is wired for the sensation of touch. Now, research reported in the December 23rd issue of the journal Cell provides the first picture of how specialized neurons feel light touches, like a brush of movement or a vibration, are organized in hairy skin.

Looking at these neurons in the hairy skin of mice, the researchers observed remarkably orderly patterns, suggesting that each type of hair follicle works like a distinct sensory organ, each tuned to register different types of touches. Each hair follicle sends out one wire-like projection that joins with others in the spinal cord, where the information they carry can be integrated into impulses sent to the brain. This network of neurons in our own skin allows us to perceive important differences in our surroundings: a raindrop versus a mosquito, a soft fingertip versus a hard stick.

"We can now begin to appreciate how these hair follicles and associated neurons are organized relative to one another and that organization enables us to think about how mechanosensory information is integrated and processed for the perception of touch," says David Ginty of The Johns Hopkins University School of Medicine.

Mice have several types of hair follicles with three in particular that make up their coats. Ginty's team made a technical breakthrough by coming up with a way to label distinct populations of known low-threshold mechanoreceptors (LTMRs). Before this study, there was no way to visualize LTMRs in their natural state. The neurons are tricky to study in part because they extend from the spinal cord all the way out to the skin. The feeling in the tips of our toes depends on cells that are more than one meter long.

The images show something unexpected and fascinating, Ginty says. Each hair follicle type includes a distinct combination of mechanosensory endings. Those sensory follicles are also organized in a repeating and stereotypical pattern in mouse skin.

The neurons found in adjacent hair follicles stretch to a part of the spinal cord that receives sensory inputs, forming narrow columns. Ginty says there are probably thousands of those columns in the spinal cord, each gathering inputs from a particular region of the skin and its patch of 100 or so hairs.

Of course, we don't have hair like a mouse, and it's not yet clear whether some of these mechanosensory neurons depend on the hairs themselves to pick up on sensations and whether others are primarily important as scaffolds for the underlying neural structures. They don't know either how these inputs are integrated in the spinal cord and brain to give rise to perceptions, but now they have the genetic access they need to tinker with each LTMR subtype one by one, turning them on or off at will and seeing what happens to the brain and to behavior. Intriguingly, one of the LTMR types under study is implicated as "pleasure neurons" in people, Ginty notes.

At this point, he says they have no clue how these neurons manage to set themselves up in this way during development. The neurons that form this sensory network are born at different times, controlled by different growth factors, and "yet they assemble in these remarkable patterns." And for Ginty that leads to a simple if daunting question to answer: "How does one end of the sensory neuron know what the other end is doing?"

More information: Online paper: DOI:10.1016/j.cell.2011.11.027

 

Provided by Cell Press

"How skin is wired for touch." December 22nd, 2011. http://medicalxpress.com/news/2011-12-skin-wired.html

 

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Young children understand the benefits of positive thinking

Even kindergarteners know that thinking positively will make you feel better. And parents' own feelings of optimism may play a role in whether their children understand how thoughts influence emotions.

Those are the findings of a new study by researchers at Jacksonville University and the University of California, Davis. The study appears in the journal Child Development.

In the study, researchers looked at 90 mostly White children ages 5 to 10. The children listened to six illustrated stories in which two characters feel the same emotion after experiencing something positive (getting a new puppy), negative (spilling milk), or ambiguous (meeting a new teacher). Following each experience, one character has a separate optimistic thought, framing the event in a positive light, and the other has a separate pessimistic thought, putting the event in a negative light. Researchers described the subsequent thoughts verbally, then asked the children to judge each character's emotions and provide an explanation for those emotions. They were most interested in the degree to which children predicted different emotions for two characters in the same situation.

The researchers also had the children and their parents complete surveys to measure their individual levels of hope and optimism.

Children as young as 5 predicted that people would feel better after thinking positive thoughts than they would after thinking negative thoughts. They showed the strongest insight about the influence of positive versus negative thoughts on emotions in ambiguous situations. And there was significant development in the children's understanding about the emotion-feeling link as they grew older.

The study also found that children had the most difficulty understanding how positive thinking could boost someone's spirits in situations that involved negative events—such as falling down and getting hurt. In these coping situations, children's levels of hope and optimism played a role in their ability to understand the power of positive thinking, but parents' views on the topic played an even larger part.

"The strongest predictor of children's knowledge about the benefits of positive thinking—besides age—was not the child's own level of hope and optimism, but their parents'," reports Christi Bamford, assistant professor of psychology at Jacksonville University, who led the study when she was at the University of California, Davis.

The findings point to parents' role in helping children learn how to use positive thinking to feel better when things get tough, Bamford notes. "In short, parents should consider modeling how to look on the bright side."

Provided by Society for Research in Child Development

"Young children understand the benefits of positive thinking." December 22nd, 2011. http://medicalxpress.com/news/2011-12-young-children-benefits-positive.html

 

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Study points to long-term recall of very early experiences

Most adults can't recall events that took place before they were 3 or 4 years old—a phenomenon called childhood amnesia. While some people can remember what happened at an earlier age, the veracity of their memories is often questioned. Now a new longitudinal study has found that events experienced by children as young as 2 can be recalled after long delays.

The study, by researchers at the University of Otago (in New Zealand), appears in the journal Child Development.

To determine at what age our earliest memories occur, the researchers looked at about 50 children and their parents. The children played a unique game when they were 2- to 4-year-olds. In the game, children placed a large object in a hole at the top of a machine and turned a handle on the side. When a bell rang, a small but otherwise identical object was delivered through a door at the bottom of the machine.

Six years later, the researchers interviewed the children and their parents to determine how well they remembered playing the game. Only about a fifth of the children recalled the event, including two children who were under 3 years old when they played the game. About half of the parents remembered the event. Parents and children who recalled the event provided very similar reports about the game.

Although the researchers couldn't predict children's long-term recall on the basis of the youngsters' general memory and language skills, they found evidence that talking about the event soon after it occurred may have helped preserve it in the memories of those who remembered it.

"Our results are consistent with theories that suggest that basic capacity for remembering our own experiences may be in place by 2 years of age," according to Fiona Jack, postdoctoral fellow at the University of Otago, who led the study. "The study has implications in clinical and legal settings, where it is often important to know how likely it is that a particular memory of an early experience is in fact genuine."

Provided by Society for Research in Child Development

"Study points to long-term recall of very early experiences." December 22nd, 2011. http://medicalxpress.com/news/2011-12-long-term-recall-early.html

 

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Robert Karl Stonjek