Today, stars and planetary bodies bear traces of these elements, having formed from the gas enriched by these supernovas over time. For the past 50 years, scientists have been analyzing stars of various ages, looking to chart the evolution of chemical elements in the universe and to identify the astrophysical phenomena that created them.

Now a team of researchers from institutions including MIT has detected the element tellurium for the first time in three ancient stars. The researchers found traces of this brittle, semiconducting element -- which is very rare on Earth -- in stars that are nearly 12 billion years old. The finding supports the theory that tellurium, along with even heavier elements in the periodic table, likely originated from a very rare type of supernova during a rapid process of nuclear fusion. The researchers published their findings online in Astrophysical Journal Letters.

"We want to understand the evolution of tellurium -- and by extension any other element -- from the Big Bang to today," says Anna Frebel, an assistant professor of astrophysics at MIT and a co-author on the paper. "Here on Earth, everything's made from carbon and various other elements, and we want to understand how tellurium on Earth came about."..........

It's scenes like this that neurosurgeon Jason Huang, M.D., confronts every day. Severe damage to nerves is one of the most challenging wounds to treat for Huang and colleagues. It's a type of wound suffered by people who are the victims of gunshots or stabbings, by those who have been involved in car accidents -- or by soldiers injured on the battlefield, like those whom Huang treated in Iraq.

Now, back in his university laboratory, Huang and his team have taken a step forward toward the goal of repairing nerves in such patients more effectively. In a paper published in the journal PLoS ONE, Huang and colleagues at the University of Rochester Medical Center report that a surprising set of cells may hold potential for nerve transplants.

In a study in rats, Huang's group found that dorsal root ganglion neurons, or DRG cells, help create thick, healthy nerves, without provoking unwanted attention from the immune system.

The finding is one step toward better treatment for the more than 350,000 patients each year in the United States who have serious injuries to their peripheral nerves. Huang's laboratory is one of a handful developing new technologies to treat such wounds.

"These are very serious injuries, and patients really suffer, many for a very long time," said Huang, associate professor of Neurosurgery and chief of Neurosurgery at Highland Hospital, an affiliate of the University of Rochester Medical Center. "There are a variety of options, but none of them is ideal.

"Our long-term goal is to grow living nerves in the laboratory, then transplant them into patients and cut down the amount of time it takes for those nerves to work," added Huang, whose project was funded by the National Institute of Neurological Disorders and Stroke and by the University of Rochester Medical Center.

For a damaged nerve to repair itself, the two disconnected but healthy portions of the nerve must somehow find each other through a maze of tissue and connect together. This happens naturally for a very small wound -- much like our skin grows back over a small cut -- but for some nerve injuries, the gap is simply too large, and the nerve won't grow back without intervention.

For surgeons like Huang, the preferred option is to transplant nerve tissue from elsewhere in the patient's own body -- for instance, a section of a nerve in the leg -- into the wounded area. The transplanted nerve serves as scaffolding, a guide of sorts for a new nerve to grow and bridge the gap. Since the tissue comes from the patient, the body accepts the new nerve and doesn't attack it.

But for many patients, this treatment isn't an option. They might have severe wounds to other parts of the body, so that extra nerve tissue isn't available. Alternatives can include a nerve transplant from a cadaver or an animal, but those bring other challenges, such as the lifelong need for powerful immunosuppressant drugs, and are rarely used.

One technology used by Huang and other neurosurgeons is the NeuraGen Nerve Guide, a hollow, absorbable collagen tube through which nerve fibers can grow and find each other. The technology is often used to repair nerve damage over short distances less than half an inch long.

In the PLoS One study, Huang's team compared several methods to try to bridge a nerve gap of about half an inch in rats. The team transplanted nerve cells from a different type of rat into the wound site and compared results when the NeuraGen technology was was used alone or when it was paired with DRG cells or with other cells known as Schwann cells.

After four months, the team found that the tubes equipped with either DRG or Schwann cells helped bring about healthier nerves. In addition, the DRG cells provoked less unwanted attention from the immune system than the Schwann cells, which attracted twice as many macrophages and more of the immune compound interferon gamma.

While both Schwann and DRG cells are known players in nerve regeneration, Schwann cells have been considered more often as potential partners in the nerve transplantation process, even though they pose considerable challenges because of the immune system's response to them.

"The conventional wisdom has been that Schwann cells play a critical role in the regenerative process," said Huang, who is a scientist in the Center for Neural Development and Disease. "While we know this is true, we have shown that DRG cells can play an important role also. We think DRG cells could be a rich resource for nerve regeneration."

In a related line of research, Huang along with colleagues in the laboratory of Douglas H. Smith, M.D. , at the University of Pennsylvania are creating DRG cells in the laboratory by stretching them, which coaxes them to grow about one inch every three weeks. The idea is to grow nerves several inches long in the laboratory, then transplant them into the patient, instead of waiting months after surgery for the nerve endings to travel that distance within the patient to ultimately hook up.

For the first time, a team led by Carnegie Mellon University neuroscientists has identified how different neural regions communicate to determine what to visually pay attention to and what to ignore. This finding is a major discovery for visual cognition and will guide future research into visual and attention deficit disorders.

The study, published in the Journal of Neuroscience, used various brain imaging techniques to show exactly how the visual cortex and parietal cortex send direct information to each other through white matter connections in order to specifically pick out the information that you want to see.

"We have demonstrated that attention is a process in which there is one-to-one mapping between the first place visual information comes from the eyes into the brain and beyond to other parts of the brain," said Adam S. Greenberg, postdoctoral fellow in the Dietrich College of Humanities and Social Sciences' Department of Psychology and lead author of the study.

"With so much information in the visual world, it's dramatic to think that you have an entire system behind knowing what to pay attention to," said Marlene Behrmann, professor of psychology at CMU and an expert in using brain imaging to study the visual perception system. "The mechanisms show that you can actually drive the visual system -- you are guiding your own sensory system in an intelligent and smart fashion that helps facilitate your actions in the world."

For the study, the research team conducted two sets of experiments with five adults. They first used several different functional brain scans to identify regions in the brain responsible for visual processing and attention. One task had the participants look at a dot in the center of the screen while six stimuli danced around the dot. The second task asked the participants to respond to the stimuli one at a time. These scans determined the regions in both the visual and parietal cortices. The researchers could then look for connectivity between these regions.

The second part of the experiment collected anatomical data of the brain's white matter connectivity while the participants had their brains scanned without performing any tasks. Then, the researchers combined the results with those from the functional experiments to show how white matter fibers tracked from the regions determined previously, the visual cortex and the parietal cortex. The results demonstrated that the white matter connections are mapped systematically, meaning that direct connections exist between corresponding visual field locations in visual cortex and parietal cortex.

The researchers used a technique called "diffusion spectrum imaging," a new procedure pioneered at Carnegie Mellon and the University of Pittsburgh to generate the fiber tracts of the white matter connectivity. This method was combined with high-resolution tractography and provides scientists with better estimates of the hard-wired connections between brain regions and increased accuracy over conventional tractography methods, such as those typically used with diffusion tensor imaging.

"The work done in collaboration with the University of Pittsburgh researchers exploits a very new, precise and cutting edge methodology," Behrmann said.

"Because we know that training can alter white matter, it might be possible, through training, that the ability to filter out irrelevant or unwanted information could be improved," Greenberg said.

In a report in the journal Nature, an international consortium of researchers that includes Case Western Reserve University School of Medicine in Cleveland and Baylor College of Medicine explains the molecular linkage between the circadian clock and the deadly heart rhythms that lead to sudden death.

The answer begins with a controller of the circadian clock -- krüppel-like factor 15 (Klf15), which has been a long-time target of the laboratory of Dr. Mukesh Jain of Case Western, said Dr. Xander Wehrens, professor of molecular physiology and biophysics and cardiology at BCM, also an author.

Klf15, in turn, controls the level of a potassium channel-interacting protein (KChIP2), which affects how potassium flows out of heart muscle cells called cardiac myocytes.

Changes affect potassium current

Because the level of this KChIP2 protein fluctuates during the circadian or daily cycle, it can change the size of the potassium current in cardiac myocytes. Changes in this subunit or Klf15 can affect the potassium current that governs repolarization of the cardiac myocyte. Overall, this can shorten or lengthen the time the heart muscle has to empty the heart's pumping chamber (ventricle) of blood. This time interval for repolarization is critical. Too much or too little can result in abnormal heart rhythms called arrhythmias. As the heart loses the regularity of the beat, it cannot pump blood efficiently.

Studies of mice that lacked Klf15 and mice with a genetic change that caused them to make more Klf15 than normal increased the risk of deadly arrhythmias.

This was a proof of principle, said Wehrens.

"It is the first example of a molecular mechanism for the circadian change in susceptibility to cardiac arrhythmias," he said.

"If there was too much Klf15 or none, the mice were at risk for developing the arrhythmias," he said.

Long QT or Short QT

Because Klf15 is regulated by the circadian "clock," the rate of flow through the potassium channel goes up and down and if disrupted, can lead to a change that results in one of two known heart problems linked to sudden death -- long QT or short QT syndrome. (QT refers to an interval measured from an electrocardiogram or ECG, which corresponds to the electrical recovery time of heart.)

Wehrens credits Jain's laboratory with accomplishing much of the work. His laboratory performed the electrophysiology experiments with the mice that lacked Klf15 and those who produced too much, he said.

Much of the BCM work was done by Dr. Mark McCauley, a cardiology fellow who was a post-doctoral fellow in the laboratory at the time, said Wehrens.