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For the first time, researchers have managed to capture images of individual potassium atoms distributed on an optical lattice, providing them with a unique opportunity to see how they interact with one another.

While capturing these images is a feat in itself, the technique could help researchers to better understand the conditions needed for individual atoms to come together and form exotic states of matter like superfluids and superconductors.

“Learning from this atomic model, we can understand what’s really going on in these superconductors, and what one should do to make higher-temperature superconductors, approaching hopefully room temperature,” team member Martin Zwierlein from MIT said in a statement.

To capture the images, the team took potassium gas, and cooled it only a few nanokelvins - just above absolute zero. To put that into perspective, 1 nanokelvin is -273 degrees Celsius (-460 degrees Fahrenheit).

At this extremely cold temperature, the potassium atoms slow to a crawl, which allowed the team to trap some of them inside a two-dimensional optical lattice - a complex series of overlapping lasers that can trap individual atoms inside different intensity waves.

Ability to turn off genes in brain crucial for learning, memory

Every time you play a game of basketball, make a cup of coffee or flick on a light switch, you are turning on genes in your brain. These same genes typically are turned off when the activity ceases – but when that doesn’t happen, damaging consequences can occur.

A study in mice at Washington University School of Medicine in St. Louis shows how such genes stuck in the “on” position can lead to faulty brain wiring that affects learning and memory.

“We’ve shown in mice that genes don’t just shut off by themselves; there’s an active mechanism to turn off genes after they’re turned on,” said Azad Bonni, MD, PhD, the Edison Professor of Neuroscience and head of the Department of Neuroscience. “If that mechanism is disrupted in the brain, you see serious consequences for learning and memory.”

The study was published July 15 in Science.

Genes in living cells constantly are being turned on and off in response to signals as diverse as physical activity, hormones and microbial infection. Decades of research have gone into understanding how and why genes turn on, but how genes turn off has consistently received less attention.

Bonni, Yue Yang, PhD, Tomoko Yamada, PhD, and colleagues decided to investigate how genes turn off in the brain. In doing so, they found that the inability to turn off such genes leads to faulty brain wiring.

The researchers studied genes in the cerebellum of mice – the part of the brain responsible for motor functions such as walking – that turn on when the mice are physically active.

They found that a large enzyme is bound to the genes that are turned on when the mice move about, but not to the genes that are not switched on by movement. The enzyme, known as the nucleosome remodeling and deacetylase (NuRD) complex, appears to be critical to turning off genes. Mice that lack the enzyme are unable to turn off the genes after physical activity ceased.

The enzyme, the scientists found, turns off genes by switching out one kind of a DNA-associated protein for another. These proteins, called histones, serve as spools around which the DNA thread is wound, in some places tightly and other places loosely. By switching out one kind of histone for another, the enzyme causes the DNA to be more tightly wound, shutting off any genes in that section of DNA.

“Turning on and off genes is a fundamental property of cell biology, and this is the first epigenetic mechanism that explains how you turn off genes after they’re turned on,” Bonni said. “I think we’ll find that this mechanism turns off genes in many different contexts.”

Epigenetics refers to factors apart from the DNA sequence itself that affect whether genes are on or off.

“We think that the NuRD complex has the potential to rapidly turn off thousands of genes,” said Yamada, co-lead author on the study and an assistant professor of medicine at the University of Tsukuba in Japan.

During development, neurons form many connections with each other and then prune back all but the most important ones. Neurons in the cerebellum of mice lacking the enzyme do not prune, leaving abnormal connections in place.

“We were surprised to discover that failure to prune connections caused abnormal responses of the neurons to the environment,” said Yang, a postdoctoral researcher and co-lead author on the study. “Our study reveals the importance of eliminating the excess connections formed in early development.”

Such connections did not affect the mice’s ability to walk but did affect their ability to learn motor skills as adults. In people, learning a motor skill would include learning how to play the piano or ride a bicycle.

Adult mice lacking the enzyme were unable to learn how to walk on a rotating rod that gradually sped up, a task other mice could do easily.

“They’re walking normally, they’re coordinated, but they are really profoundly impaired in learning,” Bonni said. “What’s really surprising is that these deficits are due not to failure to activate genes but to failure to turn them off.”

Bonni and colleagues are working on figuring out the mechanism by which changes in gene activity lead to changes in brain cell activity.

Hydrogen is often considered a fuel for the future, in the form of fuel cells to power electric motors or burned in internal combustion engines. But finding a practical, inexpensive and nontoxic way to produce large amounts of hydrogen gas – especially by splitting water into its component parts, hydrogen and oxygen – has been a challenge.

A team of researchers from the University of Houston and the California Institute of Technology has reported a more efficient catalyst, using molybdenum sulfoselenide particles on three-dimensional porous nickel diselenide foam to increase catalytic activity.

The foam, made using commercially available nickel foam, significantly improved catalytic performance because it exposed more edge sites, where catalytic activity is higher than it is on flat surfaces, said Zhifeng Ren, MD Anderson Professor of physics at UH.

They are the toughest known animals on Earth and now the secret to one of their superpowers – resistance to radiation – is out.

Tardigrades, also known as water bears or moss piglets, are tiny, eight-legged creatures that live in small bodies of water in habitats such as moss across the planet and are renowned for their extreme survival skills.

They can survive in the vacuum of outer space, withstand temperatures ranging from close to absolute zero to nearly 100°C, cope with pressures six times greater than those at the bottom of the deepest ocean and survive dehydration and being frozen for years on end.

They can also defy hefty amounts of radiation that would be lethal to most other life on the planet – and now we know how they do it.

It is mainly down to a bizarre protective protein they evolved that somehow shields their DNA from radiation damage. Short for “Damage suppressor”, Dsup appears to work by physically cuddling up to DNA and cocooning it from harm, but without disrupting its normal functions.

It may also help by somehow mopping up DNA-damaging agents called reactive oxygen species.

“We guess that Dsup binds densely to DNA to provide a shield against environmental stress, somehow making DNA inaccessible to any damaging agents,” says Takekazu Kunieda at the University of Tokyo. “To our knowledge, this is the first identification of a DNA-associating protein which confers DNA protection and improved tolerance to radioactivity in animal cells.”