domingo, 6 de julho de 2014
Biological signal processing: Body cells -- instrumentalists in a symphony orchestra
Like an isolated note in a symphony orchestra, an isolated signal in the cell is of subordinate importance.
Every organism has one aim: to survive. Its body cells all work in concert to keep it alive. They do so through finely tuned means of communication. Together with cooperation partners from Berlin and Cambridge, scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have now successfully revealed for the first time the laws by which cells translate signals from their surroundings into internal signals. Like an isolated note in a symphony orchestra, an isolated signal in the cell is of subordinate importance. "What is important is the relative variation of intensity and frequency at which the signals are transmitted from the cell membrane into the cell," says Dr. Alexander Skupin, who led the studies at LCSB. The research group published their results now in the scientific journal Science Signaling.
The instruments in an orchestra produce signals -- musical notes -- by causing the air to vibrate. Inside a cell, calcium ions carry signals. When a piece of information from the environment -- say a biological messenger -- meets the outer envelope of the cell, calcium ions are released inside the cell. There, they control various adaptation processes. "At first sight, there is no simple pattern to the ion impulses," Skupin explains; "yet they still culminate in a meaningful response inside the cell, like the activation of a specific gene, for instance."
In order to determine the laws underlying this phenomenon, the researchers studied human kidney cells and rat liver cells using a combination of imaging technologies and mathematical methods. They discovered that the intensity and frequency of calcium impulses undergo extreme variation -- both cell-internally and cell-to-cell. Accordingly, the information they convey cannot be interpreted by analyzing isolated signals alone. "It's like in an orchestra, where studying an isolated note on its own allows no inference of the melody," Skupin continues the musical analogy. "You have to hear how the frequency and volume of all instruments vary and produce the melody. Then you gain an impression of the musical piece."
Now, for the first time, the researchers have managed to gain such an impression of the whole by listening in on the cells' communications. They discovered that the plethora of calcium impulses vary relatively to one another in a specific relationship: A stimulus from outside does not lead to an absolute increase in calcium impulses, but instead to a change in the frequency at which they occur -- in the concert hall, the notes of the instruments rise and fall in symphony. "This pattern is the actual signal that leads to a response in the cells," Skupin says. "With our analyses, we have rendered it interpretable."
"The results are of great importance for analyzing diseases," says Director of LCSB Prof. Dr. Rudi Balling. "We know that, in Parkinson's disease, the calcium balance in the nerve cells is disrupted, and suspect that errant communications between the cells could play a role in the onset of neurodegenerative diseases. With the discovery of the fundamental laws of these communications, as Alexander Skupin, his team and our cooperation partners have now achieved, we are set to take a major step forward in the analysis of Parkinson's disease."
Story Source:
The above story is based on materials provided by University of Luxembourg. Note: Materials may be edited for content and length.
Journal Reference:
- K. Thurley, S. C. Tovey, G. Moenke, V. L. Prince, A. Meena, A. P. Thomas, A. Skupin, C. W. Taylor, M. Falcke. Reliable Encoding of Stimulus Intensities Within Random Sequences of Intracellular Ca2 Spikes. Science Signaling, 2014; 7 (331): ra59 DOI: 10.1126/scisignal.2005237
Explaining 'healthy' obesity
July 3, 2014
Cell Press
Up to one-quarter of individuals currently labeled as obese are actually metabolically healthy. Though obesity is a major risk factor for diabetes, the two conditions aren't always linked. A new study sheds light on a possible explanation, revealing that high levels of a molecule HO-1 are linked to poor metabolic health and an increased risk of type 2 diabetes in obese humans. HO-1 blockers could represent a promising new strategy for the treatment of metabolic disease.
Up to one-quarter of individuals currently labeled as obese are actually metabolically healthy and do not have a high risk of developing type 2 diabetes. Though obesity is a major risk factor for diabetes, the two conditions aren't always linked. A study published by Cell Press July 3rd in the journal Cell sheds light on a possible explanation, revealing that high levels of a molecule called heme oxygenase-1 (HO-1) are linked to poor metabolic health and an increased risk of type 2 diabetes in obese humans. Moreover, HO-1 inhibition improves metabolic health in obese mice, suggesting that HO-1 blockers could represent a promising new strategy for the treatment of metabolic disease.
"The results indicate that HO-1 is in fact necessary for the development of metabolic disease and call for a re-evaluation of numerous findings in the field," says senior study author Harald Esterbauer of the Medical University of Vienna. "The study also reveals HO-1 as a candidate biomarker for the stratification of metabolically healthy and unhealthy obesity and provides a framework for selective, personalized therapy."
The factors that determine whether obesity leads to poor metabolic health have been unclear, but the evidence suggests that a maladaptive immune response called metabolic inflammation plays an important role. However, studies examining the relationship between a supposedly anti-inflammatory molecule called HO-1 and metabolic disease have produced conflicting results.
To address this question, Esterbauer teamed up with senior study author J. Andrew Pospisilik of the Max Planck Institute of Immunobiology and Epigenetics. In contrast to past findings, they found higher levels of HO-1 in liver and fat biopsies from obese, insulin-resistant humans compared with obese, metabolically healthy individuals. When the researchers deleted the HO-1 gene in immune cells called macrophages, molecular signs of inflammation decreased in mice, suggesting that HO-1 actually promotes inflammation, contrary to widespread belief. Moreover, deletion of the HO-1 gene specifically in the liver or macrophages of mice fed a high-fat diet led to better liver function and an increase in insulin sensitivity -- a clear sign of improved metabolic health.
"Our findings show that HO-1 is among the strongest predictors of metabolically unhealthy obesity in humans, and it could have a high prognostic value for detecting disease onset," Pospisilik says. "This could allow clinicians to use targeted interventions to prevent disease progression specifically in obese individuals who show early signs of type 2 diabetes."
New strategy could uncover genes at the root of psychiatric illnesses
July 3, 2014
Cell Press
Understanding the basis of psychiatric disorders has been extremely challenging because there are many genetic variants that may increase risk but are insufficient to cause disease. Now investigators describe a strategy that may help reveal how such 'subthreshold' genetic risks interact with other risk factors or environmental exposures to affect the development of the nervous system. Their research pinpoints a genetic variant that may predispose individuals to schizophrenia.
Yoon et al. use modeling in iPSCs and mice to examine the functional effects of 15q11.2 CNVs, a known risk factor for several neuropsychiatric disorders including schizophrenia. Their analysis highlights defects in adherens junctions and polarity in neural stem cells associated with haploinsufficiency of the cytoskeletal regulator CYFIP1. The cover image was created using images of neural rosettes derived from human iPSCs with and without a 15q11.2 microdeletion (round circles) and images of radial glial cells in the developing mouse cortex (thin filaments), and it is inspired by July 4th fireworks.
Understanding the basis of psychiatric disorders has been extremely challenging because there are many genetic variants that may increase risk but are insufficient to cause disease. Now investigators reporting in the July 3rd issue of the Cell Press journal Cell Stem Cell describe a strategy that may help reveal how such "subthreshold" genetic risks interact with other risk factors or environmental exposures to affect the development of the nervous system. Their research pinpoints a genetic variant that may predispose individuals to schizophrenia.
The work takes advantage of a recently developed technology that allows skin cells from patients to be reprogrammed into induced pluripotent stem cells (iPSCs) that can then generate any cell type in the body. Through this technology, scientists obtained stem cells from individuals with a genetic abnormality that confers increased susceptibility to schizophrenia, and they observed deficits during nerve development that could be traced to a specific gene called CYFIP1, which helps maintain a nerve cell's structure. The team then blocked the expression of this gene in developing mouse embryos and noticed defects in the formation of the cerebral cortex, a brain region that plays an important role in consciousness.
Next, the scientists turned to human genetic studies to see how CYFIP might interact with other factors. They found that mutations in two genes within a cellular pathway linked to CYFIP1 led to a significantly increased risk of schizophrenia. The findings support the theory that multiple factors within the same pathway may interact to affect one's risk for psychiatric disorders.
"We were able to use a set of cutting-edge tools to gain insight into a critical cellular process for normal brain development, the dysregulation of which may be a manifestation of a genetic predisposition for schizophrenia," says senior author Dr. Guo-li Ming, of Johns Hopkins University School of Medicine. The researchers' strategy -- generating disease-specific nerve cells, identifying a causative gene for developmental defects, validating the gene-specific defect in animal models, and then investigating interactions with other genes both in animal models and in humans -- represents a promising new approach for understanding the mechanisms underlying some of the most intractable psychiatric illnesses.
The work also highlights the promise of iPSC technology as a discovery tool in understanding and treating human disorders. "Despite an enormous amount of time and resources devoted to producing solid, reproducible results in animal models, far too often, results from preclinical trials deviate from our expectations," says co-author Dr. Hongjun Song. "The lack of access to disease-relevant human cell types has been a missing link in our current drug discovery process, which has now been resolved through advances in cellular reprogramming."
Story Source:
The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.
Journal Reference:
- Ki-Jun Yoon, Ha Nam Nguyen, Gianluca Ursini, Fengyu Zhang, Nam-Shik Kim, Zhexing Wen, Georgia Makri, David Nauen, Joo Heon Shin, Youngbin Park, Raeeun Chung, Eva Pekle, Ce Zhang, Maxwell Towe, Syed Mohammed Qasim Hussaini, Yohan Lee, Dan Rujescu, David St. Clair, Joel E. Kleinman, Thomas M. Hyde, Gregory Krauss, Kimberly M. Christian, Judith L. Rapoport, Daniel R. Weinberger, Hongjun Song, Guo-li Ming. Modeling a Genetic Risk for Schizophrenia in iPSCs and Mice Reveals Neural Stem Cell Deficits Associated with Adherens Junctions and Polarity. Cell Stem Cell, 2014; 15 (1): 79 DOI: 10.1016/j.stem.2014.05.003
Genetic link to autism found, known as CHD8 mutation
July 3, 2014
University of Washington - Health Sciences/UW News, Community Relations & Marketing
In a collaboration involving 13 institutions around the world, researchers have broken new ground in understanding what causes autism. This is the first time researchers have shown a definitive cause of autism to a genetic mutation. Previously identified genetic events like Fragile X, which account for a greater number of autism cases, are associated with other impairments, such as intellectual disability, more than autism.
To confirm the findings, researchers worked with scientists at Duke University who do zebra fish modeling.
In a collaboration involving 13 institutions around the world, researchers have broken new ground in understanding what causes autism. The results are being published in Cell magazine July 3, 2014: "Disruptive CHD8 Mutations Define a Subtype of Autism in Early Development."
"We finally got a clear cut case of an autism specific gene," said Raphael Bernier, the lead author, and UW associate professor in the Department of Psychiatry and Behavioral Sciences and the clinical director of the Autism Center at Seattle Children's.
Bernier said people with a mutation in the CHD8 gene have a very "strong likelihood" that they will have autism marked by gastrointestinal disorders, a larger head and wide set eyes.
In their study of 6,176 children with autism spectrum disorder, researchers found 15 had a CHD8 mutation and all these cases had similar characteristics in appearance and issues with sleep disturbance and gastrointestinal problems.
Bernier and his team interviewed all 15 cases with CHD8 mutations.
To confirm the findings, researchers worked with scientists at Duke University who do zebra fish modeling. The researchers disrupted the CHD8 gene in the fish and the fish developed large heads and wide set eyes. They then fed the fish fluorescent pellets and found that the fish had problems discarding food waste and were constipated.
Bernier said this is the first time researchers have shown a definitive cause of autism to a genetic mutation. Previously identified genetic events like Fragile X, which account for a greater number of autism cases, are associated with other impairments, such as intellectual disability, more than autism. Although less than half a percent of all kids will have this kind of autism related to the CHD8 mutation, Bernier said there are lots of implications from this study.
"This will be a game changer in the way scientists are researching autism," he said.
The results could lead the way to a "genetics-first approach" that could uncover hundreds more genetic mutations and lead to genetic testing. Genetic testing could be offered to families as a way of guiding them on what to expect and how to care for their child. Currently, autism is diagnosed based on behavior, said Bernier.
In the short term, Bernier said, clinicians can pay attention to the small population with this CHD8 mutation and provide targeted treatment.
Researchers say autism has currently been linked to different types of genetic events. The most commonly researched genetic events associated with autism are chromosomal re-arrangements, called "copy number variations," in which a chunk of chromosome is copied or deleted. But no one rearrangement affects more than 1 percent of all autism cases. While these copy number events are associated with autism, they do not have a definitive link, or as they say among researchers, a "strong penetrance."
Then there are genetic mutations in which a gene has been disrupted and is not creating the kind of protein it should create. The CHD8 gene mutation is the first gene mutation to show a very strong penetrance linked to a certain subtype of autism.
Story Source:
The above story is based on materials provided by University of Washington - Health Sciences/UW News, Community Relations & Marketing. Note: Materials may be edited for content and length.
Journal Reference:
- Raphael Bernier, Christelle Golzio, Bo Xiong, Holly A. Stessman, Bradley P. Coe, Osnat Penn, Kali Witherspoon, Jennifer Gerdts, Carl Baker, Anneke T. Vulto-van Silfhout, Janneke H. Schuurs-Hoeijmakers, Marco Fichera, Paolo Bosco, Serafino Buono, Antonino Alberti, Pinella Failla, Hilde Peeters, Jean Steyaert, Lisenka E.L.M. Vissers, Ludmila Francescatto, Heather C. Mefford, Jill A. Rosenfeld, Trygve Bakken, Brian J. O’Roak, Matthew Pawlus, Randall Moon, Jay Shendure, David G. Amaral, Ed Lein, Julia Rankin, Corrado Romano, Bert B.A. de Vries, Nicholas Katsanis, Evan E. Eichler. Disruptive CHD8 Mutations Define a Subtype of Autism Early in Development. Cell, 2014; DOI: 10.1016/j.cell.2014.06.017
Host genetics can contribute to lung damage in severe tuberculosis
Schematic illustration of a hypothetical model to explain the high and low involvement of the P2X7R during severe and mild TB.
A third of the global population is infected with the bacterial pathogen, a mycobacterium, that causes tuberculosis (TB). Most carriers control the infection and are asymptomatic, but severe forms of the disease (more common in children and immune-compromised adults, and often caused by particularly aggressive -- or hypervirulent -- mycobacterial strains) kill over a million people every year. An article published on July 3rd in PLOS Pathogens now identifies a factor made by the host that exacerbates lung damage in severe TB. The results also suggest why gene mutations that render the factor inactive are common.
To understand the mechanisms underlying aggressive TB, Elena Lasunskaia from the Universidade Estadual do Norte Fluminense, Rio de Janeiro, Maria Regina D'Império-Lima from the Universidade de São Paulo, Brazil, and colleagues studied mouse models which recapitulate the symptoms of severe pulmonary TB in humans. Like human patients, mice infected with two different hypervirulent mycobacterial strains develop necrotic lesions in the lung, that is, areas of dead cells that break open and release their contents. The necrotic debris contains molecules that promote an influx of immune cells from the host, and the resulting local inflammation causes further damage to the lung tissue.
One of the contents of necrotic debris is the energy-storage molecule ATP, and when it is found outside cells, it is known to stimulate immune cells through the binding to the P2X7 receptor (P2X7R). The researchers asked whether this molecular pathway plays a role in the severe forms of TB that are associated with lung necrosis. They studied mice that were lacking P2X7R and found that those mice survived otherwise deadly infections with either of the two hypervirulent mycobacterial strains.
A more detailed analysis suggested that P2X7R has a dual role in the development of aggressive TB. First, it appears to facilitate the dissemination of hypervirulent mycobacteria by killing infected immune cells but releasing their content, namely viable mycobacteria that have survived the process. Second, P2X7R also seems to contribute to lung inflammation and damage by promoting widespread tissue destruction.
The better outcomes in mice without P2X7R were only seen after infection with hypervirulent mycobacteria. When the researchers infected mice with a less aggressive TB strain, they found that P2X7R actually helped to control this infection. In this case, P2X7R-mediated stimulation of infected immune cells did not result in the cell death and release of viable mycobacteria, and so actually contained the infection rather than spreading it.
The observed opposite effects of P2X7R on lung infection with hypervirulent and less aggressive mycobacterial strains, respectively, could explain an epidemiological puzzle: P2X7R loss-of-function alleles (that is defective variants of the P2X7R gene) are common in humans despite the fact that they are linked to a higher risk of developing pulmonary TB. Based on their results, the researchers suggest that such variants might increase the risk of mild TB but reduce the risk of severe TB. This, they say "could explain why evolutionary pressure has maintained these gene polymorphisms at high rates in the human population."
They also state that their study "provides a perspective for the development of new therapeutic approaches in which drugs designed to inhibit P2X7R are used to ameliorate the outcomes of aggressive forms of TB."
Story Source:
The above story is based on materials provided by PLOS. Note: Materials may be edited for content and length.
Journal Reference:
- Eduardo P. Amaral, Simone C. M. Ribeiro, Verônica R. Lanes, Fabrício M. Almeida, Marcelle R. M. de Andrade, Caio Cesar Barbosa Bomfim, Érika M. Salles, Karina R. Bortoluci, Robson Coutinho-Silva, Mario H. Hirata, José M. Alvarez, Elena B. Lasunskaia, Maria Regina D'Império-Lima. Pulmonary Infection with Hypervirulent Mycobacteria Reveals a Crucial Role for the P2X7 Receptor in Aggressive Forms of Tuberculosis. PLoS Pathogens, 2014; 10 (7): e1004188 DOI: 10.1371/journal.ppat.1004188
sábado, 5 de julho de 2014
Carnegie Mellon researchers demonstrate one of the most advanced autonomous vehicles ever designed
Carnegie Mellon researchers demonstrate one of the most advanced autonomous vehicles ever designed This week in Washington, D.C., researchers from Carnegie Mellon University (CMU) marked a significant milestone, demonstrating one of the most advanced autonomous vehicles ever designed, capable of navigating on urban roads and highways without human intervention. Developed with support from the National Science Foundation (NSF), the U.S. Department of Transportation, DARPA and General Motors, the car is the result of more than a decade of research and development by scientists and engineers at CMU and elsewhere. Credit: NSF
Amtrak Looking To Boost Acela Express Capacity, Speeds
Amtrak’s Acela Express service may not be true high-speed rail, but as ridership hits new records and trains consistently packed, Amtrak is looking to prepare for the future by replacing its current rolling stock.
On Wednesday afternoon, Amtrak said it has issued a request for proposal to “acquire new trainsets to supplement and eventually replace its aging Acela Express.” Acela Express, which runs exclusively along the Northeast Corridor (NEC), is currently operating near capacity and frequently sells out before and after major holidays.
The RFP seeks up to 28 next-generation high-speed trainsets capable of meeting or exceeding current Acela trip-times on the existing NEC infrastructure. Aside from faster trains, Amtrak is also looking to boost the passenger capacity of each trainset by 40 percent, or 120 passengers. Just how Amtrak plans to do this is unknown, however.
I wonder how much of the 40% increase in pax on new Acela train sets will come from 10 car sets vs current 8 car, or denser config? @Amtrak
— Edward Russell (@e_russell) July 2, 2014
“The Northeast Corridor needs more high-speed rail capacity to help move the American economy forward,” said President and CEO Joseph Boardman. “More and more people are choosing Amtrak for travel between Washington, New York and Boston. New equipment means more seats and more frequent departures to help meet that growing demand.”
If Amtrak is taking cues from the commercial aviation industry, a denser configuration could very well be in the cards. Acela currently offers a seat pitch (the distance from one point on a seat to the same point in the forward seat) of 42 inches. In the airline industry, seat pitch has generally been reduced to around 30″-31″ over the past decade, with 34″ being considered roomy. Amtrak could shave a few inches off the seat pitch and still maintain a comfortable ride, while boosting the capacity of each car.
Dimensions of the Amtrak Acela Business Class seat. (Courtesy: Amtrak)
Alternatively, Amtrak could be looking to squeeze another seat into every row. Seat width is currently 21″ in Business Class (the lowest level of service offered on Acela), which is wider than just about any airline economy seat. Adding an additional seat to each row would mirror the actions of many airlines operating the Boeing 777 and Airbus A330, but puts serious dent in passenger comfort. Given Amtrak’s marketing of Acela as being a more comfortable ride than regular NEC trains and airlines, this option seems unlikely.
English: Acela Express business class interior with some overhead bins open at the end of a Boston-to-Washington run. (Photo credit: Wikipedia)
Of course, the simplest option may just be the most likely. Acela is configured in 8 car setup- two engines, four Business Class cars, one First Class car, and a cafe car. Amtrak could simply extend the trainsets to 10 cars and leave the passenger seating configuration as is. Adding two additional Business Class cars would boost the total passenger load of each trainset by 130, more than the 40 percent required. Also possible is the elimination of the First Class car, which only seats 44 passengers as opposed to 65 in Business Class, or the elimination the Cafe car.
An Amtrak spokesman tells Railway Age that responses to the RFP are due by October 1, 2014. Once the proposals are in, we should have a better idea of what the next generation of Acela will look like.
Concept rendering of a next generation Acela trainset (Source: Amtrak)
Forbes Tech
Doing something is better than doing nothing for most people, study shows
Most people are just not comfortable in their own heads, according to a new psychological investigation. (stock image)
The investigation found that most would rather be doing something -- possibly even hurting themselves -- than doing nothing or sitting alone with their thoughts, said the researchers, whose findings will be published July 4 in the journal Science.
In a series of 11 studies, U.Va. psychologist Timothy Wilson and colleagues at U.Va. and Harvard University found that study participants from a range of ages generally did not enjoy spending even brief periods of time alone in a room with nothing to do but think, ponder or daydream. The participants, by and large, enjoyed much more doing external activities such as listening to music or using a smartphone. Some even preferred to give themselves mild electric shocks than to think.
"Those of us who enjoy some down time to just think likely find the results of this study surprising -- I certainly do -- but our study participants consistently demonstrated that they would rather have something to do than to have nothing other than their thoughts for even a fairly brief period of time," Wilson said.
The period of time that Wilson and his colleagues asked participants to be alone with their thoughts ranged from six to 15 minutes. Many of the first studies involved college student participants, most of whom reported that this "thinking period" wasn't very enjoyable and that it was hard to concentrate. So Wilson conducted another study with participants from a broad selection of backgrounds, ranging in age from 18 to 77, and found essentially the same results.
"That was surprising -- that even older people did not show any particular fondness for being alone thinking," Wilson said.
He does not necessarily attribute this to the fast pace of modern society, or the prevalence of readily available electronic devices, such as smartphones. Instead, he thinks the devices might be a response to people's desire to always have something to do. In his paper, Wilson notes that broad surveys have shown that people generally prefer not to disengage from the world, and, when they do, they do not particularly enjoy it. Based on these surveys, Americans spent their time watching television, socializing or reading, and actually spent little or no time "relaxing or thinking."
During several of Wilson's experiments, participants were asked to sit alone in an unadorned room at a laboratory with no cell phone, reading materials or writing implements, and to spend six to 15 minutes -- depending on the study -- entertaining themselves with their thoughts. Afterward, they answered questions about how much they enjoyed the experience and if they had difficulty concentrating, among other questions. Most reported they found it difficult to concentrate and that their minds wandered, though nothing was competing for their attention. On average the participants did not enjoy the experience. A similar result was found in further studies when the participants were allowed to spend time alone with their thoughts in their homes.
"We found that about a third admitted that they had 'cheated' at home by engaging in some activity, such as listening to music or using a cell phone, or leaving their chair," Wilson said. "And they didn't enjoy this experience any more at home than at the lab."
An additional experiment randomly assigned participants to spend time with their thoughts or the same amount of time doing an external activity, such as reading or listening to music, but not to communicate with others. Those who did the external activities reported that they enjoyed themselves much more than those asked to just think, that they found it easier to concentrate and that their minds wandered less. The researchers took their studies further. Because most people prefer having something to do rather than just thinking, they then asked, "Would they rather do an unpleasant activity than no activity at all?"
The results show that many would. Participants were given the same circumstances as most of the previous studies, with the added option of also administering a mild electric shock to themselves by pressing a button.
Twelve of 18 men in the study gave themselves at least one electric shock during the study's 15-minute "thinking" period. By comparison, six of 24 females shocked themselves. All of these participants had received a sample of the shock and reported that they would pay to avoid being shocked again.
"What is striking," the investigators write, "is that simply being alone with their own thoughts for 15 minutes was apparently so aversive that it drove many participants to self-administer an electric shock that they had earlier said they would pay to avoid." Wilson and his team note that men tend to seek "sensations" more than women, which may explain why 67 percent of men self-administered shocks to the 25 percent of women who did.
Wilson said that he and his colleagues are still working on the exact reasons why people find it difficult to be alone with their own thoughts. Everyone enjoys daydreaming or fantasizing at times, he said, but these kinds of thinking may be most enjoyable when they happen spontaneously, and are more difficult to do on command.
"The mind is designed to engage with the world," he said. "Even when we are by ourselves, our focus usually is on the outside world. And without training in meditation or thought-control techniques, which still are difficult, most people would prefer to engage in external activities."
Discovery expands search for Earth-like planets: Newly spotted frozen world orbits in a binary star system
At twice the mass of Earth, the planet orbits one of the stars in the binary system at almost exactly the same distance from which Earth orbits the sun. However, because the planet's host star is much dimmer than the sun, the planet is much colder thanEarth -- a little colder, in fact, than Jupiter's icy moon Europa.
Four international research teams, led by professor Andrew Gould of The Ohio State University, published their discovery in the July 4 issue of the journal Science.
The study provides the first evidence that terrestrial planets can form in orbits similar to Earth's, even in a binary star system where the stars are not very far apart. Although this planet itself is too cold to be habitable, the same planet orbiting a sun-like star in such a binary system would be in the so-called "habitable zone" -- the region where conditions might be right for life.
"This greatly expands the potential locations to discover habitable planets in the future," said Scott Gaudi, professor of astronomy at Ohio State. "Half the stars in the galaxy are in binary systems. We had no idea if Earth-like planets in Earth-like orbits could even form in these systems. "
Very rarely, the gravity of a star focuses the light from a more distant star and magnifies it like a lens. Even more rarely, the signature of a planet appears within that magnified light signal. The technique astronomers use to find such planets is called gravitational microlensing, and computer modeling of these events is complicated enough when only one star and its planet are acting as the lens, much less two stars.
Searching for planets within binary systems is tricky for most techniques, because the light from the second star complicates the interpretation of the data. "But in gravitational microlensing," Gould explained, "we don't even look at the light from the star-planet system. We just observe how its gravity affects light from a more distant, unrelated, star. This gives us a new tool to search for planets in binary star systems."
When the astronomers succeeded in detecting this new planet, they were able to document that it produced two separate signatures -- the primary one, which they typically use to detect planets, and a secondary one that had previously been only hypothesized to exist.
The first was a brief dimming of light, as the planet's gravity disrupted one of the magnified images of the source star. But the second effect was an overall distortion of the light signal.
"Even if we hadn't seen the initial signature of the planet, we could still have detected it from the distortion alone," Gould said, pointing to a graph of the light signal. "The effect is not obvious. You can't see it by eye, but the signal is unmistakable in the computer modeling."
Gaudi explained the implications.
"Now we know that with gravitational microlensing, it's actually possible to infer the existence of a planet -- and to know its mass, and its distance from a star -- without directly detecting the dimming due to the planet," he said. "We thought we could do that in principle, but now that we have empirical evidence, we can use this method to find planets in the future."
The nature of these distortions is still somewhat of a mystery, he admitted.
"We don't have an intuitive understanding of why it works. We have some idea, but at this point, I think it would be fair to say that it's at the frontier of our theoretical work."
The planet, called OGLE-2013-BLG-0341LBb, first appeared as a "dip" in the line tracing the brightness data taken by the OGLE (Optical Gravitational Lensing Experiment) telescope on April 11, 2013. The planet briefly disrupted one of the images formed by the star it orbits as the system crossed in front of a much more distant star 20,000 light-years away in the constellation Sagittarius.
"Before the dip, this was just another microlensing event," Gould said. It was one of approximately 2,000 discovered every year by OGLE, with its new large-format camera that monitors 100 million stars many times per night searching for such events.
"It's really the new OGLE-IV survey that made this discovery possible," he added. "They got a half dozen measurements of that dip and really nailed it." From the form of the dip, whose "wings" were traced out in MOA (Microlensing Observations in Astrophysics) data, they could see that the source was headed directly toward the central star.
Then, for two weeks, astronomers watched the magnified light continue to brighten from telescopes in Chile, New Zealand, Israel and Australia. The teams included OGLE, MOA, MicroFUN (the Microlensing Follow Up Network), and the Wise Observatory.
Even then, they still didn't know that the planet's host star had another companion -- a second star locked into orbit with it. But because they were already paying close attention to the signal, the astronomers noticed when the binary companion unexpectedly caused a huge eruption of light called a caustic crossing.
By the time they realized that the lens was not one star, but two, they had captured a considerable amount of data -- and made a surprising discovery: the distortion.
Weeks after all signs of the planet had faded, the light from the binary-lens caustic crossing became distorted, as if there were a kind of echo of the original planet signal.
Intensive computer analysis by professor Cheongho Han at Chungbuk National University in Korea revealed that the distortion contained information about the planet -- its mass, separation from its star, and orientation -- and that information matched perfectly with what astronomers saw during their direct observation of the dip due to the planet. So the same information can be captured from the distortion alone.
This detailed analysis showed that the planet is twice the mass of Earth, and orbits its star from an Earth-like distance, around 90 million miles. But its star is 400 times dimmer than our sun, so the planet is very cold -- around 60 Kelvin (-352 degrees Fahrenheit or -213 Celsius), which makes it a little colder than Jupiter's moon Europa. The second star in the star system is only as far from the first star as Saturn is from our sun. But this binary companion, too, is very dim.
Still, binary star systems composed of dim stars like these are the most common type of star system in our galaxy, the astronomers said. So this discovery suggests that there may be many more terrestrial planets out there -- some possibly warmer, and possibly harboring life.
Three other planets have been discovered in binary systems that have similar separations, but using a different technique. This is the first one close to Earth-like size that follows an Earth-like orbit, and its discovery within a binary system by gravitational microlensing was by chance.
"Normally, once we see that we have a binary, we stop observing. The only reason we took such intensive observations of this binary is that we already knew there was a planet," Gould said. "In the future we'll change our strategy."
In particular, Gould singled out the work of amateur astronomer and frequent collaborator Ian Porritt of Palmerston North, New Zealand, who watched for gaps in the clouds on the night of April 24 to get the first few critical measurements of the jump in the light signal that revealed that the planet was in a binary system. Six other amateurs from New Zealand and Australia contributed as well.
Other project collaborators hailed from Ohio State, Warsaw University Observatory, Chungbuk National University, Harvard-Smithsonian Center for Astrophysics, University of Cambridge, Universidad de Concepción, Auckland Observatory, Auckland University of Technology, University of Canterbury, Texas A&M University, Korea Astronomy and Space Science Institute, Solar-Terrestrial Environment Laboratory, University of Notre Dame, Massey University, University of Auckland, National Astronomical Observatory of Japan, Osaka University, Nagano National College of Technology, Tokyo Metropolitan College of Aeronautics, Victoria University, Mt. John University Observatory, Kyoto Sangyo University, Tel-Aviv University and the University of British Columbia.
Funding came from the National Science Foundation, NASA (including a NASA Sagan Fellowship), European Research Council, Polish Ministry of Science and Higher Education, National Research Foundation of Korea, U.S.-Israel Binational Science Foundation, Japan Society for the Promotion of Science, Marsden Fund from the Royal Society of New Zealand and the Israeli Centers of Research Excellence.
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