The most recent supernova in our Galaxy has been discovered by tracking the rapid expansion of its remains. This result, using NASA’s Chandra X-ray Observatory and NRAO’s Very Large Array (VLA), has implications for understanding how often supernovas explode in the Milky Way galaxy.

The supernova explosion occurred about 140 years ago, making it the most recent supernova in the Milky Way as measured in Earth’s time frame. Previously, the last known galactic supernova occurred around 1680, based on studying the expansion of its remnant Cassiopeia A.

The recent supernova explosion was not seen in optical light about 140 years ago because it occurred close to the center of the Galaxy, and is embedded in a dense field of gas and dust. This made it about a trillion times fainter, in optical light, than an unobscured supernova. However, the supernova remnant it caused, G1.9+0.3, is now seen in X-ray and radio images.

“We can see some supernova explosions with optical telescopes across half of the Universe, but when they’re in this murk we can miss them in our own cosmic backyard,” said Stephen Reynolds of North Carolina State University, who led the Chandra study. “Fortunately, the expanding gas cloud from the explosion shines brightly in radio waves and X-rays for thousands of years. X-ray and radio telescopes can see through all that obscuration and show us what we’ve been missing.”

Astronomers regularly observe supernovas in other galaxies like ours, and based on those rates, estimate that about three should explode every century in our Milky Way, although these estimates have large margins of error.

“If the supernova rate estimates are correct, there should be the remnants of about 10 supernova explosions that are younger than Cassiopeia A,” said David Green of the University of Cambridge in the United Kingdom, who led the VLA study. “It’s great to finally track one of them down.”

The tracking of this source began in 1985 when astronomers, led by Green, used the VLA to identify G1.9+0.3 as the remnant of a supernova explosion near the center of our Galaxy. Based on its small size, it was thought to have resulted from a supernova that exploded about 400 to 1000 years ago.

Twenty two years later, Chandra observations of this object revealed that the remnant had expanded by a surprisingly large amount, about 16% since 1985. This indicates that the supernova remnant is much younger than previously thought.

The young age was confirmed when new radio observations from the VLA were made just within the past several weeks. This “apples to apples” comparison nails the age of the remnant to be about 140 years (less if it has been slowing down), making it the youngest on record in the Milky Way.

Finding such a recent, obscured supernova is a vital first step in making a better estimate of the supernova rate in our Galaxy. Knowing this rate is important because supernovas heat and redistribute large amounts of gas, pump large amounts of heavy elements out into their surroundings, and can trigger the formation of new stars, closing the cycle of stellar death and rebirth. The explosion may also leave behind, in addition to the expanding remnant, a central neutron star or black hole.

In addition to being a record holder for youth, G1.9+0.3 is of considerable interest for other reasons. The high expansion velocities and the extreme particle energies that have been generated are unprecedented and should stimulate deeper studies of this object with Chandra and the VLA.

“No other object in the Galaxy has properties like this,” said Reynolds. “Finding G1.9+0.3 is extremely important for learning more about how some stars explode and what happens in the aftermath.

Scientists can also use it to probe the environment into which it exploded. At perhaps only a few thousand light years from the center of the Galaxy, it appears to be embedded in the dense environment near the Milky Way’s supermassive black hole.

These results will appear in The Astrophysical Journal Letters. NASA’s Marshall Space Flight Center, Huntsville, Ala., manages the Chandra program for the agency’s Science Mission Directorate. The Smithsonian Astrophysical Observatory controls science and flight operations from the Chandra X-ray Center in Cambridge, Mass.

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Scientists at the Swedish medical university Karolinska Institutet have in two recent studies shown that a receptor called ALK7 plays important roles in the regulation of body fat deposition as well as the release of insulin from beta-cells in the pancreas. These findings have implications for the development of treatments against diabetes and obesity.

“We have shown in animal studies that removing the ALK7 receptor improves insulin release by beta-cells in the pancreas, and at the same time decreases fat deposition in situations of high caloric intake”, says Professor Carlos Ibáñez, who lead the two studies that are now published as back-to-back papers in the PNAS. “The well-known connections between diabetes and obesity make our combined findings quite exciting.”

Up to 6 per cent of the world population is estimated to suffer from some form of diabetes, either due to a reduced ability to produce insulin, or to insulin resistance. Insulin is a hormone required by cells in the body to absorb glucose from the blood, thereby providing them with energy. Obesity has been shown to increase the risk of developing diabetes, and as overweight becomes more prevalent in the human population, so do the cases of diabetes.

The research group led by Carlos Ibáñez studies how signaling by growth factors and their receptors regulate different physiological functions in the body. They have recently investigated the functions of one of these receptors, called ALK7, using mutant mice (knock-out mice) lacking this receptor. They found that in the absence of ALK7, mice developed abnormally high levels of insulin in the blood, which with age led to insulin resistance and liver steatosis, a pathological condition in which the liver enlarges and accumulates abnormally high levels of fat.

In collaboration with another research group at Karolinska Institutet, led by Professor Per-Olof Berggren, they also found that Calcium signaling in pancreatic beta-cells was reduced by the actions of the growth factor Activin B through the ALK7 receptor, and that blood glucose levels regulates the expression of both Activin B and ALK7. In agreement with these results, mice lacking Activin B also developed hyperinsulinemia to a similar extent as ALK7 mutants.

“In other words, our data revealed an unexpected negative feedback loop in the control of glucose-dependent insulin release, mediated the actions of Activin B on the ALK7 receptor”, says Carlos Ibáñez.

In the second study, the scientists found that mice lacking ALK7 accumulated less fat and gained less weight than their normal counterparts when fed on a high-fat diet. They discovered that another growth factor called GDF3 could also signal via the ALK7 receptor, and that mice lacking GDF3 showed similar defects in fat deposition and weight gain as the ALK7 mutants. Intriguingly, however, mutant mice consumed equal amounts of food as their normal counterparts during the experiment.

“These results show that lack of ALK7 or GDF3 improves energy balance in the body under regimes of high caloric intake”, says Carlos Ibáñez.

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Researchers at the University of British Columbia have discovered an anti-virulence factor in Salmonella, knowledge that could be used to design improved Salmonella vaccines.

Virulence factors allow a pathogen to thrive in the host and cause disease. An anti-virulence factor controls the degree of infectiveness.

Salmonella are bacteria that infect a variety of vertebrae hosts. Salmonellosis, infection from Salmonella, can lead to gastroenteritis or typhoid fever — a severe life-threatening systemic disease.

The finding, published in Public Library of Science, suggests that there is a distinct pathway in Salmonella that acts as an anti-virulence factor during salmonellosis. This pathway is also involved in fine-tuning the host-pathogen balance during salmonellosis.

The research demonstrates that the pathway is activated prior to ingestion and entry into the intestine and then shut off once Salmonella penetrates the intestine.

“When the anti-virulence factor is knocked out Salmonella becomes up to 10 times more virulent,” says Brett Finlay, Peter Wall Prof. of Microbiology and Biochemistry at UBC and senior investigator at the Michael Smith Laboratories. “The research also demonstrates that Salmonella has the ability to control its virulence even before it enters the host.”

“The pathway is designed to initially control the level of virulence and not kill the host immediately,” says Finlay. “Tapering the level of infectiveness allows Salmonella to establish itself in the host and then become more virulent.”

“This research will allow us to design improved salmonella vaccines,” says Finlay. “We will be able to better tailor the vaccine strain with the appropriate level of virulence.”

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