"For the first time, we have evidence on the environment, and thus the origin, of this middle-weight black hole," said Mathieu Servillat, who worked at the Harvard-Smithsonian Center for Astrophysics when this research was conducted.

Astronomers know how massive stars collapse to form stellar-mass black holes (which weigh about 10 times the mass of our sun), but it's not clear how supermassive black holes (like the four million solar-mass monster at the center of the Milky Way) form in the cores of galaxies. One idea is that supermassive black holes may build up through the merger of smaller, intermediate-mass black holes weighing hundreds to thousands of suns.

Lead author Sean Farrell, of the Sydney Institute for Astronomy in Australia, discovered this unusual black hole in 2009 using the European Space Agency's XMM-Newton X-ray space telescope. Known as HLX-1 (Hyper-Luminous X-ray source 1), the black hole weighs in at 20,000 solar masses and lies towards the edge of the galaxy ESO 243-49, which is 290 million light-years from Earth.

Farrell and his team then observed HLX-1 simultaneously with NASA's Swift observatory in X-ray and Hubble in near-infrared, optical, and ultraviolet wavelengths. The intensity and the color of the light shows a cluster of young stars, 250 light-years across, encircling the black hole. Hubble can't resolve the stars individually because the suspected cluster is too far away. The brightness and color are consistent with other clusters of young stars seen in other galaxies.

Farrell's team detected blue light from hot gas in the accretion disk swirling around the black hole. However, they also detected red light produced by much cooler gas, which would most likely come from stars. Computer models suggested the presence of a young, massive cluster of stars encircling the black hole.

"What we can definitely say with our Hubble data is that we require both emission from an accretion disk and emission from a stellar population to explain the colors we see," said Farrell.

Such young clusters of stars are commonly seen in nearby galaxies, but not outside the flattened starry disk, as found with HLX-1. The best explanation is that the HLX-1 black hole was the central black hole in a dwarf galaxy. The larger host galaxy then captured the dwarf. Most of the dwarf's stars were stripped away through the collision between the galaxies. At the same time, new young stars were formed in the encounter. The interaction that compressed the gas around the black hole also triggered star formation.

Farrell and Servillat found that the star cluster must be less than 200 million years old. This means that the bulk of the stars were formed following the dwarf's collision with the larger galaxy. The age of the stars tells how long ago the two galaxies crashed into each other.

The future of the black hole is uncertain at this stage. It depends on its trajectory, which is currently unknown. It's possible the black hole may spiral in to the center of the big galaxy and eventually merge with the supermassive black hole there. Alternately, the black hole could settle into a stable orbit around the galaxy. Either way, it's likely to fade away in X-rays as it depletes its supply of gas.

"This black hole is unique in that it's the only intermediate-mass black hole we've found so far. Its rarity suggests that these black holes are only visible for a short time," said Servillat.

More observations are planned this year to track the history of the interaction between the two galaxies.

"A rise of 2 degrees centigrade of water temperature will likely have a devastating impact on this Antarctic fish lineage, which is so well adapted to water at freezing temperatures," said Thomas Near, associate professor of ecology and evolutionary biology and lead author of the study published online the week of Feb. 13 in the Proceedings of the National Academy of Sciences.

The successful origin and diversification into 100 species of fish, collectively called notothenioids, is a textbook case of how evolution operates. A period of rapid cooling led to mass extinction of fish acclimated to a warmer Southern Ocean. The acquisition of so-called antifreeze glycoproteins enabled notothenioids to survive in seas with frigid temperatures. As they adapted to vacant ecological niches, new species of notothenioids arose and contributed to the rich biodiversity of marine life found today in the waters of Antarctica.

The three species of fish are an example of the diversity this lineage achieved when it expanded into niches left by fish decimated by cold water environment.

Notothenioids account for the bulk of the fish diversity and are a major food source for larger predators, including penguins, toothed whales, and seals.*

However, the new study suggests the acquisition of the antifreeze glycoproteins 22 to 42 million years ago was not the only reason for the successful adaptation of the Antarctic notothenioids. The largest radiation of notothenioid fish species into new habitats occurred at least 10 million years after the first appearance of glycoproteins, the study found.

"The evolution of antifreeze was often thought of as a 'smoking gun,' triggering the diversification of these fishes, but we found evidence that this adaptive radiation is not linked to a single trait, but to a combination of factors," Near said.

This evolutionary success story is threatened by climate change that has made the Southern Ocean around Antarctica one of the fastest-warming regions on Earth. The same traits that enabled the fish to survive and thrive on a cooling earth make them particularly susceptible to a warming one, notes Near.

"Given their strong polar adaptations and their inability to acclimate to warmer water temperatures, climate change could devastate this most interesting lineage of fish with a unique evolutionary history," Near said.

*Yale's Peabody Museum of Natural History has one of the most important collections of these specimens in the world. Yale-affliated authors of the study are Alex Dornburg, Kristen L. Kuhn, and Jillian N. Pennington.

A team of researchers led by McGill neuroscientist Terence Coderre, who is also affiliated with the Research Institute of the McGill University Health Centre, has found the key to understanding how memories of pain are stored in the brain. More importantly, the researchers are also able to suggest how these memories can be erased, making it possible to ease chronic pain.

It has long been known that the central nervous system "remembers" painful experiences, that they leave a memory trace of pain. And when there is new sensory input, the pain memory trace in the brain magnifies the feeling so that even a gentle touch can be excruciating.

"Perhaps the best example of a pain memory trace is found with phantom limb pain," suggests Coderre. "Patients may have a limb amputated because of gangrene, and because the limb was painful before it was amputated, even though the limb is gone, the patients continue to feel they are suffering from pain in the absent limb. That's because the brain remembers the pain. In fact, there's evidence that any pain that lasts more than a few minutes will leave a trace in the nervous system." It's this memory of pain, which exists at the neuronal level, that is critical to the development of chronic pain. But until now, it was not known how these pain memories were stored at the level of the neurons.

Recent work has shown that the protein kinase PKMzeta plays a crucial role in building and maintaining memory by strengthening the connections between neurons. Now Coderre and his colleagues have discovered that PKMzeta is also the key to understanding how the memory of pain is stored in the neurons. They were able to show that after painful stimulation, the level of PKMzeta increases persistently in the central nervous system (CNS).

Even more importantly, the researchers found that by blocking the activity of PKMzeta at the neuronal level, they could reverse the hypersensitivity to pain that neurons developed after irritating the skin by applying capsaicin -- the active ingredient in hot peppers. Moreover, erasing this pain memory trace was found to reduce both persistent pain and heightened sensitivity to touch.

Coderre and his colleagues believe that building on this study to devise ways to target PKMzeta in pain pathways could have a significant effect for patients with chronic pain. "Many pain medications target pain at the peripheral level, by reducing inflammation, or by activating analgesia systems in the brain to reduce the feeling of pain," says Coderre. "This is the first time that we can foresee medications that will target an established pain memory trace as a way of reducing pain hypersensitivity. We believe it's an avenue that may offer new hope to those suffering from chronic pain."

Other contributing researchers on this study include Andre Laferrière, Mark H Pitcher, Anne Haldane, Yue Huang, Virginia Cornea, Naresh Kumar, Fernando Cervero (all from the Alan Edwards Centre for Research on Pain at McGill) and co-author Todd C Sacktor (State University of New York Downstate Medical Center).

This research was supported by grants from Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, National Institutes of Health (NIH) and an Astra-Zeneca/AECRP fellowship

The system is far from foolproof. Cancer cells can undergo unchecked proliferation, producing self-antigens that are tolerated by the immune system, rather than being targeted for destruction. At the opposite extreme, a range of so-called autoimmune disorders can result when healthy cells in the body are misidentified as hazards. The immune system has developed a further line of protection against such autoimmune responses in order to limit the pathology that can result. Essentially, the immune system is programmed to 'turn itself off' after prolonged recognition of an antigen.

In a new study appearing in the current issue of the journal Science, Dr. Joseph Blattman, a researcher at Arizona State University's Biodesign Institute examines how CD8 T cells -- critical weapons in the body's defensive arsenal -- are regulated when they transition from this tolerant state to an activated state and back."We have previously shown that prolonged stimulation of T cells in disseminated cancers or chronic viral infections results in a tolerant state to the tumor or pathogen. It was never clear if this 'immune exhaustion' was a reversible fate or if 'resting' the T cells by removing them from the cancer or infection environment could restore their function" said Dr. Blattman. "These results show that even if you can temporarily rescue a tolerant T cell, it is hard-wired to become tolerant again."

Lymphocytes or white blood cells are central players in the immune systems of all vertebrates, and come in various types. Large granular lymphocytes include natural killer cells (NK cells), while small lymphocytes consist of T cells and B cells. Cytotoxic T cells (also called CD8 T cells) take their name from their place of maturation in the thymus gland and the CD8 glycoprotein adorning their surfaces. These cells help the immune system identify infected or malignant cells and are the main cells responsible for eliminating them.

In the thymus, T cells undergo both positive and negative selection. In this process, T cells that bind too weakly or too strongly to self-antigens are weeded out, undergoing cell death. The first group would result in a deficient immune response to foreign invasion while the latter would tend to overreact to self proteins, leading to autoimmunity. Only about 2 percent of these developing T cells or thymocytes will survive. This dual process of selection generally produces cells capable of recognizing foreign threats while maintaining a tolerance for self-antigens.

However, some self-reactive CD8 T cells do make it out of the thymus and are exposed to self-antigen. In order to avoid causing autoimmune disease, the stimulation by self cells results in T cell tolerance. This could be for a number of reasons including lack of costimulation, the presence of regulatory T cells that inhibit CD8 T cell responses, or continuous stimulation by self antigens. This essential safeguard however can become an Achilles' heel, causing unresponsiveness in CD8 T cells to certain cancer antigens, many of which are self-antigens. One of the central challenges in tumor immunology is to somehow short-circuit T cell tolerance to tumor/self-antigens, without provoking autoimmunity.

Dr. Blattman and his group sought to illuminate the underlying molecular mechanisms of self-tolerance and the regulatory programs that maintain or break it. Contrary to prevailing theory, the group demonstrated in a mouse model that T cells return to the tolerant state even in the absence of self-antigen. Further, such cells could be induced to proliferate and become functional if the lymphocyte cell numbers fell to appropriately low levels -- a condition known as lymphopenia -- and that this effect is observed even when self-antigen is present.

Because T cells are known to proliferate in lymphopenic environments, such as after chemotherapy and/or irradiation in cancer patients, the researchers used this to 'trick' T cells into proliferating in order to reset their function. This strategy did restore their function temporarily, but within a month afterwards, the T cells once again became tolerant even if they did not continue to encounter the tumor antigen.

The current research overturns a central paradigm regarding T-cell tolerance to self-antigens and may provoke a fundamental rethinking of the underlying mechanisms that govern the immune response. The results will help identify the molecular events that lead to T cell tolerance to tumor antigens, which should aid in development of strategies to permanently restore the function of T cells. This, in turn, should suggest new approaches for the treatment of cancer and chronic viral infections that employ adoptive transfer of modified cancer-specific T cells that make these cells resistant to becoming tolerant.

"Adoptive immunotherapy with T cells is an exciting strategy for combating cancer because the transferred T cells don't kill all dividing cells, but instead only target the cells expressing the cancer antigen. The problem has been that the transferred T cells usually become tolerant to the cancer" said Dr. Blattman. "By knowing the rules governing T cell tolerance, we will be able to identify what regulates this process and design ways of overcoming it in order to provide more effective cancer therapies."

The rescue of CT8 T cell functionality was indeed transient, in the mouse studies undertaken. When lymphocyte numbers in mice rebounded (having been reduced through irradiation), CD8 T cell tolerance snapped back into place, and the genetic master plan for these cells was reestablished. This fact implies that while a genetic blueprint oversees T cell tolerance, this characteristic is not entirely fixed, but may be subject to epigenetic regulation, that is, non-genetically encoded regulation that is transferred to each dividing cell.

Using techniques of genome-wide mRNA and microRNA profiling, Dr. Blattman and his colleagues uncovered a tolerance-specific gene profile for CD8 T cells, further demonstrating that this gene-based regulatory system could be overridden under lymphopenic conditions.

The rescue of CD8 T cells through this method has been dubbed homeostasis-driven proliferation. The mechanism operates even in the absence of a cognate antigen, but apparently shuts down once T cell homeostasis has been reestablished. Rescued T cells showed a reduction or down-regulation of tolerance-specific genes as well as an up-regulation of some 475 "rescue-associated" genes.

Evidentially, T cells are able to recall the tolerance program initially established after their first encounter with self-antigen, returning to it as a default, following repletion of lymphocyte numbers. While the precise mechanisms that account for this tolerant memory remain unclear, various forms of epigenetic gene regulation, not reliant on DNA sequence, are implied.

Future research will attempt to identify the signaling pathways associated with the interruption and reacquisition of T cell tolerance, which appears to operate independently of surface T cell receptors. Further, use of lymphopenia-mediated rescue of CD8 T cells for cancer therapy will require that tolerance-specific epigenetic memory somehow be erased.

Finally, lymphopenia-based T cell proliferation and activation also provides a model to describe heightened autoimmunity following organ transplantation, particularly cases of graft-host rejection. Such autoimmunity is often of a transient nature, again suggesting that T cell tolerance is reset once lymphocyte populations rebound following surgery.

"These results clearly suggest that epigenetic mechanisms are in place to maintain tolerance in T cells specific for self antigens. Uncovering precisely which key molecules and genes are important in this process should help us to improve T cell based approaches to the treatment of cancer, as well as to induce tolerance in T cells causing autoimmunity," said Dr. Blattman.

The new work, led by Dr Diederik Kruijssen of the Max Planck Institute for Astrophysics in Garching, Germany, appears in a paper in the journal Monthly Notices of the Royal Astronomical Society.

Globular star clusters have a remarkable characteristic: the typical number of stars they contain appears to be about the same throughout the Universe. This is in contrast to much younger stellar clusters, which can contain almost any number of stars, from fewer than 100 to many thousands. The team of scientists proposes that this difference can be explained by the conditions under which globular clusters formed early on in the evolution of their host galaxies.

The researchers ran simulations of isolated and colliding galaxies, in which they included a model for the formation and destruction of stellar clusters. When galaxies collide, they often generate spectacular bursts of star formation (“starbursts”) and a wealth of bright, young stellar clusters of many different sizes. As a result it was always thought that the total number of star clusters increases during starbursts. But the Dutch-German team found the opposite result in their simulations.

While the very brightest and largest clusters were indeed capable of surviving the galaxy collision due to their own gravitational attraction, the numerous smaller clusters were effectively destroyed by the rapidly changing gravitational forces that typically occur during starbursts due to the movement of gas, dust and stars. The wave of starbursts came to an end after about 2 billion years and the researchers were surprised to see that only clusters with high numbers of stars had survived. These clusters had all the characteristics that should be expected for a young population of globular clusters as they would have looked about 11 billion years ago.

Dr Kruijssen comments: “It is ironic to see that starbursts may produce many young stellar clusters, but at the same time also destroy the majority of them. This occurs not only in galaxy collisions, but should be expected in any starburst environment. In the early Universe, starbursts were commonplace – it therefore makes perfect sense that all globular clusters have approximately the same large number of stars. Their smaller brothers and sisters that didn’t contain as many stars were doomed to be destroyed.”

According to the simulations, most of the star clusters were destroyed shortly after their formation, when the galactic environment was still very hostile to the young clusters. After this episode ended, the surviving globular clusters have lived quietly until the present day.

The researchers have further suggestions to test their ideas. Dr Kruijssen continues: “In the nearby Universe, there are several examples of galaxies that have recently undergone large bursts of star formation. It should therefore be possible to see the rapid destruction of small stellar clusters in action. If this is indeed found by new observations, it will confirm our theory for the origin of globular clusters.”

The simulations suggest that most of a globular cluster’s traits were established when it formed. The fact that globular clusters are comparable everywhere then indicates that the environments in which they formed were very similar, regardless of the galaxy they currently reside in. In that case, Dr Kruijssen believes, they can be used as fossils to shed more light on the conditions in which the first stars and galaxies were born.

The results are now published inSolid Earth, an open-access journal of the European Geosciences Union (EGU).

The research suggests authorities should strengthen the security of the Fukushima Daiichi nuclear power plant to withstand large earthquakes that are likely to directly disturb the region. The power plant witnessed one of the worst nuclear disasters in history after it was damaged by the 11 March 2011 magnitude 9 earthquake and tsunami. But this tremor occurred about 160 km from the site, and a much closer one could occur in the future at Fukushima.

"There are a few active faults in the nuclear power plant area, and our results show the existence of similar structural anomalies under both the Iwaki and the Fukushima Daiichi areas. Given that a large earthquake occurred in Iwaki not long ago, we think it is possible for a similarly strong earthquake to happen in Fukushima," says team-leader Dapeng Zhao, geophysics professor at Japan's Tohoku University.

The 11 April 2011 magnitude 7 Iwaki earthquake was the strongest aftershock of the 11 March earthquake with an inland epicentre. It occurred 60 km southwest of the Fukushima nuclear power plant, or 200 km from the 11 March epicentre.

The research now published in EGU's Solid Earth shows that the Iwaki earthquake was triggered by fluids moving upwards from the subducting Pacific plate to the crust. The Pacific plate is moving beneath northeast Japan, which increases the temperature and pressure of the minerals in it. This leads to the removal of water from minerals, generating fluids that are less dense than the surrounding rock. These fluids move up to the upper crust and may alter seismic faults.

"Ascending fluids can reduce the friction of part of an active fault and so trigger it to cause a large earthquake. This, together with the stress variations caused by the 11 March event, is what set off the Iwaki tremor," says Ping Tong, lead author of the paper.

The number of earthquakes in Iwaki increased greatly after the March earthquake. The movements in Earth's crust induced by the event caused variations in the seismic pressure or stress of nearby faults. Around Iwaki, Japan's seismic network recorded over 24,000 tremors from 11 March 2011 to 27 October 2011, up from under 1,300 detected quakes in the nine years before, the scientists report.

The 6,000 of these earthquakes selected for the study were recorded by 132 seismographic stations in Japan from June 2002 to October 2011. The researchers analysed these data to take pictures of Earth's interior, using a technique called seismic tomography.

"The method is a powerful tool to map out structural anomalies, such as ascending fluids, in the Earth's crust and upper mantle using seismic waves. It can be compared to a CT or CAT scan, which relies on X-rays to detect tumours or fractures inside the human body," explains Zhao.

While the scientists can't predict when an earthquake in Fukushima Daiichi will occur, they state that the ascending fluids observed in the area indicate that such an event is likely to occur in the near future. They warn that more attention should be paid to the site's ability to withstand strong earthquakes, and reduce the risk of another nuclear disaster.....