New research, published in Biological Reviews and conducted by researchers from the University of Liverpool and Escola Superior de Ciências da Saúde (Brasília, Brazil) has found some type of cancers unique to humans may be a result of evolutionary accidents.
Cancer is a major cause of death worldwide. But humans are not the only species affected by cancer; in fact, only a few primitive animals are thought to escape the disease. Furthermore, incidence rates and cancer types differ widely among species. However, how cancer patterns in humans compare to those of other species remains largely unknown.
Researchers, led by Dr Joao Pedro De Magalhaes from the University of Liverpool's Institute of Ageing and Chronic Disease, aimed to identify further clues about cancer and its evolutionary underpinnings in humans and across a wide range of animals by conducting the largest survey of animal cancer data to date.
The researchers began examining data relating to primates then continued onto other mammals before examining cancer in birds, amphibians, reptiles, fish and finally invertebrates and plants. They then reviewed the cancer incidence and types for humans and animal types.
They found that some types of cancer are widespread across nearly all species, like blood cancers (lymphomas and leukemia), and there are some types of cancer that seem to be unique of humans, like lung cancer, prostate and testicular cancers. These could be evolutionary accidents, a product of random events in the evolution of our species.
Dr De Magalhaes, said: "Perhaps unique mutations during the evolution of the human lineage contribute to the disproportionately high incidence of some cancers in our species when compared to all other studied species."
Another hypothesis is that the increasing life expectancy of humans is allowing the appearance of cancers that would not have affected our ancestors.
First author Thales Albuquerque, said: "Cancer rates among humans are high, and they are bound to keep increasing. We still do not know all mechanisms that lead to such a high incidence of cancer in our species, but one hypothesis is that cultural changes and technological advances have produced the greatest of evolutionary mismatches -- a situation where the environment changes into something different from that which a species is adapted to, and that provokes stress and may increase susceptibility to cancer.
Dr De Magalhaes: "Our work highlights the different evolutionary pressures acting on cancer early in life (with a high prevalence of blood cancers presumably driven by the need to fight pathogens) and cancer late in life that escapes natural selection, including human-specific cancers that may be evolutionary accidents or related to a mismatch with the modern environment and lifestyle."
From Science Daily
Apr 17, 2018
Scientists decipher the magma bodies under Yellowstone
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| Graphic by University of Oregon scientists provides new structural information, based on supercomputer modeling, about the location of a mid-crustal sill that separates magma under Yellowstone. |
Yellowstone, a supervolcano famous for explosive eruptions, large calderas and extensive lava flows, has for years attracted the attention of scientists trying to understand the location and size of magma chambers below it. The last caldera forming eruption occurred 630,000 years ago; the last large volume of lava surfaced 70,000 years ago.
Crust below the park is heated and softened by continuous infusions of magma that rise from an anomaly called a mantle plume, similar to the source of the magma at Hawaii's Kilauea volcano. Huge amounts of water that fuel the dramatic geysers and hot springs at Yellowstone cool the crust and prevent it from becoming too hot.
With computer modeling, a team led by UO doctoral student Dylan P. Colón has shed light on what's going on below. At depths of 5-10 kilometers (3-6 miles) opposing forces counter each other, forming a transition zone where cold and rigid rocks of the upper crust give way to hot, ductile and even partially molten rock below, the team reports in a paper in Geophysical Research Letters.
This transition traps rising magmas and causes them to accumulate and solidify in a large horizontal body called a sill, which can be up to 15 kilometers (9 miles) thick, according to the team's computer modeling.
"The results of the modeling matches observations done by sending seismic waves through the area," said co-author Ilya Bindeman, a professor in the UO's Department of Earth Sciences. "This work appears to validate initial assumptions and gives us more information about Yellowstone's magma locations."
This mid-crustal sill is comprised of mostly solidified gabbro, a rock formed from cooled magma. Above and below lay separate magma bodies. The upper one contains the sticky and gas-rich rhyolitic magma that occasionally erupts in explosions that dwarf the 1980 eruption of Mount St. Helens in Washington state.
Similar structures may exist under super volcanoes around the world, Colón said. The geometry of the sill also may explain differing chemical signatures in eruptive materials, he said.
Colón's project to model what's below the nation's first national park, which was sculpted 2 million years ago by volcanic activity, began soon after a 2014 paper in Geophysical Research Letters by a University of Utah-led team revealed evidence from seismic waves of a large magma body in the upper crust.
Scientists had suspected, however, that huge amounts of carbon dioxide and helium escaping from the ground indicated that more magma is located farther down. That mystery was solved in May 2015, when a second University of Utah-led study, published in the journal Science, identified by way of seismic waves a second, larger body of magma at depths of 20 to 45 kilometers (12-27 miles).
However, Colón said, the seismic-imaging studies could not identify the composition, state and amount of magma in these magma bodies, or how and why they formed there.
To understand the two structures, UO researchers wrote new codes for supercomputer modeling to understand where magma is likely to accumulate in the crust. The work was done in collaboration with researchers at the Swiss Federal Institute of Technology, also known as ETH Zurich.
The researchers repeatedly got results indicating a large layer of cooled magma with a high melting point forms at the mid-crustal sill, separating two magma bodies with magma at a lower melting point, much of which is derived from melting of the crust.
"We think that this structure is what causes the rhyolite-basalt volcanism throughout the Yellowstone hotspot, including supervolcanic eruptions," Bindeman said. "This is the nursery, a geological and petrological match with eruptive products. Our modeling helps to identify the geologic structure of where the rhyolitic material is located."
The new research, for now, does not help to predict the timing of future eruptions. Instead, it provides a never-before-seen look that helps explain the structure of the magmatic plumbing system that fuels these eruptions, Colón said. It shows where the eruptible magma originates and accumulates, which could help with prediction efforts further down the line.
"This research also helps to explain some of the chemical signatures that are seen in eruptive materials," Colón said. "We can also use it to explore how hot the mantle plume is by comparing models of different plumes to the actual situation at Yellowstone that we understand from the geologic record."
Colón is now exploring what influences the chemical composition of magmas that erupt at volcanoes like Yellowstone.
Read more at Science Daily
Can we tell black holes apart?
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| Can we tell black holes apart? Astrophysicists at Goethe University Frankfurt answer this question by computing images of feeding non-Einsteinian black holes: at present it is hard to tell them apart from standard black holes. |
Not all of the light rays (or photons) produced by matter falling into a black hole are trapped by the event horizon, a region of spacetime from which nothing can escape. Some of these photons will reach distant observers, so that when a black hole is observed directly a "shadow" is expected against the background sky. The size and shape of this shadow will depend on the black-hole's properties but also on the theory of gravity.
Because the largest deviations from Einstein's theory of relativity are expected very close to the event horizon and since alternative theories of gravity make different predictions on the properties of the shadow, direct observations of Sgr A* represent a very promising approach for testing gravity in the strongest regime. Making such images of the black-hole shadow is the primary goal of the international Event Horizon Telescope Collaboration (EHTC), which combines radio data from telescopes around the world.
Scientists from the BlackHoleCam team in Europe, who are part of the EHTC, have now gone a step further and investigated whether it is possible to distinguish between a "Kerr" black hole from Einstein's gravity and a "dilaton" black hole, which is a possible solution of an alternative theory of gravity.
The researchers studied the evolution of matter falling into the two very different types of black holes and calculated the radiation emitted to construct the images. Furthermore, real-life physical conditions in the telescopes and interstellar medium were used to create physically realistic images. "To capture the effects of different black holes we used realistic simulations of accretion disks with near-identical initial setups. These expensive numerical simulations used state-of-the-art codes and took several months on the Institute's supercomputer LOEWE," says Dr. Yosuke Mizuno, lead author of the study.
Moreover, expected radio images obviously have a limited resolution and image fidelity. When using realistic image resolutions, the scientists found, to their surprise, that even highly non-Einsteinian black holes could disguise themselves as normal black holes.
"Our results show that there are theories of gravity in which black holes can masquerade as Einsteinian, so new techniques of analyzing EHT data may be needed to tell them apart," remarks Luciano Rezzolla, professor at Goethe University and leader of the Frankfurt team. "While we believe general relativity is correct, as scientists we need to be open-minded. Luckily, future observations and more advanced techniques will eventually settle these doubts," concludes Rezzolla.
Read more at Science Daily
First an alga, then a squid, enigmatic fossil is actually a fish
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| A photo of the Platylithophycus cretaceus specimen. The scale bar is 5 centimeters. |
"There are many examples of temporarily misplaced taxa in paleontological history, including ferns that were once thought to be sponges and lungfish teeth thought to be fungi," said the lead author, Allison Bronson, a comparative biology Ph.D.-degree student in the Museum's Richard Gilder Graduate School. "In this case, the misidentification didn't happen because of a lack of technology at the time -- scientists familiar with cartilage structure could easily see this was a chondrichthyan fish. The researchers used reasonable arguments for their interpretations, but didn't look outside of their own fields."
The enigmatic specimen, Platylithophycus cretaceum, is roughly 1.5-feet long by 10-inches wide and from the Niobrara Formation in Kansas. The Niobrara Formation is one of the most diverse fish-fossil sites in North America, preserving late Cretaceous animals that lived in and around the Western Interior Seaway, a broad expanse of water that split North America into two land masses.
In 1948, two paleobotanists from the Colorado School of Mines and Princeton University compared the texture of the fossil slab with that of green algae. They described two parts of a plant: surfaces covered with hexagonal plates, which they called "fronds," and supposedly calcium carbonate-covered thread-like filaments. In 1968, two researchers from Fort Hays Kansas State College studying cephalopods from the Niobrara Formation compared the specimen with a cuttlefish, based primarily on its textural similarities to a cuttlebone -- the unique internal shell of cuttlefish. The reclassification made Platylithophycus the oldest sepiid squid then on record.
In both of these earlier studies, the hard tissue was assumed to be composed of calcium carbonate, but no tests were performed. For the new study, Bronson and co-author John Maisey, a curator in the Museum's Division of Paleontology, applied a small amount of dilute organic acid to the specimen -- a method that has been widely used in paleontology since the time of the initial description of Platylithophycus. If there is a reaction, the fossilized material is likely made from calcium carbonate. But if there is no reaction, which was the case when Bronson and Maisey performed the test, it is likely made from calcium phosphate, as are the fossilized skeletons of cartilaginous fish like sharks and rays.
The most obvious clue that Platylithophycus was a cartilaginous fish are the hexagonal plates on the surface of the specimen. After taking a closer look with a scanning electron microscope, Bronson and Maisey reinterpreted that feature as tessellated calcified cartilage, found on both extinct and living sharks and rays. The new study suggests that the "filaments" earlier described are actually part of the gill arches, made up of tessellated cartilage. Gill arches are cartilaginous curved bars along the pharynx, or throat, that support the gills of fish. The "fronds" are reinterpreted as gill rakers, finger-like projections that extend from the gill arches and help with feeding.
"We think this was a rather large cartilaginous fish, possibly related to living filter-feeding rays such as Manta and Mobula," Maisey said. "This potentially expands the range of diversity in the Niobrara fauna."
Read more at Science Daily
Apr 16, 2018
Education, not income, the best predictor of a long life
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| This is a curve showing the relationship between income and life expectancy in 1970, 1990 and 2010. |
In 1975, Samuel Preston developed the Preston Curve, which plotted the GDP per person on the horizontal axis against life expectancy on the vertical axis. The curve shows a clear but flattening upward trend in life expectancy with increasing GDP. The curves also shift upwards over time which has been explained by better healthcare.
In 1985, John Caldwell and Pat Caldwell suggested instead that lowered mortality resulted from better female education. In their new paper, Lutz and Kebede used global data from 174 countries from 1970-2015 to test the two hypotheses. Whether income or education is more important for improving health and life expectancy is an important question for policymakers deciding where to direct funding.
Lutz and Kebede also plotted life expectancy against the mean years of schooling of the adult population. The curve created is much more linear, suggesting that education is a much better predictor. There is no upward shift of the curve requiring explanation by other factors. Data was subject to multivariate analyses to validate the findings. The same link was found when the curves were adjusted for child mortality.
The researchers point out that better education leads to improved cognition and in turn to better choices for health-related behaviours. Recent decades have seen a shift in the disease burden from infectious to chronic diseases, the latter of which are largely lifestyle-related. As time goes on, the link between education and better health choices, and therefore life expectancy, will become even more apparent.
"This paper is more radical than previous analyses in terms of challenging the ubiquitous view that income and medical interventions are the main drivers of health. It even shows that the empirical association between income and health is largely spurious," says Lutz.
Previous lines of research at the Wittgenstein Centre, a collaboration between IIASA, WU and the Vienna Institute of Demography, have emphasised the importance of improving education for poverty eradication and economic growth, as well as the ability to adapt to climate change. These findings further back up the call for improved access to education.
The apparent link between health and income found by Preston can be explained by the fact that better education results in both better health and higher incomes.
Read more at Science Daily
Dinosaurs ended -- and originated -- with a bang!
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| Dinosaur fossil |
But their origins have been less understood. In a new study, scientists from MUSE -- Museum of Science, Trento, Italy, Universities of Ferrara and Padova, Italy and the University of Bristol show that the key expansion of dinosaurs was also triggered by a crisis -- a mass extinction that happened 232 million years ago.
In the new paper, published today in Nature Communications, evidence is provided to match the two events -- the mass extinction, called the Carnian Pluvial Episode, and the initial diversification of dinosaurs.
Dinosaurs had originated much earlier, at the beginning of the Triassic Period, some 245 million years ago, but they remained very rare until the shock events in the Carnian 13 million years later.
The new study shows just when dinosaurs took over by using detailed evidence from rock sequences in the Dolomites, in north Italy -- here the dinosaurs are detected from their footprints.
First there were no dinosaur tracks, and then there were many. This marks the moment of their explosion, and the rock successions in the Dolomites are well dated. Comparison with rock successions in Argentina and Brazil, here the first extensive skeletons of dinosaurs occur, show the explosion happened at the same time there as well.
Lead author Dr Massimo Bernardi, Curator at MUSE and Research associate at Bristol's School of Earth Sciences, said: "We were excited to see that the footprints and skeletons told the same story. We had been studying the footprints in the Dolomites for some time, and it's amazing how clear cut the change from 'no dinosaurs' to 'all dinosaurs' was."
The point of explosion of dinosaurs matches the end of the Carnian Pluvial Episode, a time when climates shuttled from dry to humid and back to dry again.
It was long suspected that this event had caused upheavals among life on land and in the sea, but the details were not clear. Then, in 2015, dating of rock sections and measurement of oxygen and carbon values showed just what had happened.
There were massive eruptions in western Canada, represented today by the great Wrangellia basalts -- these drove bursts of global warming, acid rain, and killing on land and in the oceans.
Co-author Piero Gianolla, from the University of Ferrara, added: "We had detected evidence for the climate change in the Dolomites. There were four pulses of warming and climate perturbation, all within a million years or so. This must have led to repeated extinctions."
Professor Mike Benton, also a co-author, from the University of Bristol, said: "The discovery of the existence of a link between the first diversification of dinosaurs and a global mass extinction is important.
Read more at Science Daily
Study identifies more than a hundred new genes that determine hair color
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| Scientists have discovered 124 genes that play a major role in determining human hair color variation. |
The discovery sheds new light on our understanding of the genetic complexity underpinning variations in human pigmentation, and could advance our knowledge of conditions linked to pigmentation, such as skin, testicular, prostate and ovarian cancers. The new findings are also relevant for forensic sciences.
Although previous studies have found that a large percentage of hair colour variation is explained by heritable factors, previous genetic studies only identified a dozen or so hair colour genes. The new study, published today in Nature Genetics, largely explains the genetic knowledge gap.
In order to identify the previously unknown hair colour genes, researchers analysed DNA data from almost 300,000 people of European descent, together with their self-reported hair colour information. The data was supplied by UK Biobank, 23andMe Inc., the International Visible Trait Genetics Consortium and their study partners.
By comparing the hair colour of the group with their genetic information, stored at several million locations across the human genome, the team identified 124 genes involved in the development of hair colour, of which more than 100 were not previously known to influence pigmentation.
The scientists also demonstrated that predicting hair colour with this new genetic information is more accurate than with previously known genes.
Joint lead author Professor Tim Spector from King's College London said: "This work will impact several fields of biology and medicine. As the largest ever genetic study on pigmentation, it will improve our understanding of diseases like melanoma, an aggressive form of skin cancer.
The genes that affect hair colour also affect other cancer types, while other pigment genes affect the chances of having Crohn's and other forms of bowel disease.
"Our work helps us to understand what causes human diversity in appearance by showing how genes involved in pigmentation subtly adapted to external environments and even social interactions during our evolution. We found that women have significantly fairer hair than men, which reflects how important cultural practices and sexual preferences are in shaping our genes and biology."
Joint lead author Professor Manfred Kayser from Erasmus MC said: "Besides substantially increasing our understanding of human pigmentation genetics in general, finding these new hair colour genes is also important for further increasing the accuracy of hair colour prediction from DNA traces in future forensic applications, which can help to find unknown perpetrators of crime."
Read more at Science Daily
'Mono' virus linked to 7 serious diseases
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| Blood sample for Epstein-Barr virus (EBV) test. |
Those diseases are: systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes. Combined, these seven diseases affect nearly 8 million people in the U.S.
Study results published April 12 in the journal Nature Genetics. The project was led by three scientists: John Harley, MD, PhD, Director of the Center for Autoimmune Genomics and Etiology (CAGE) at Cincinnati Children's and a faculty member of the Cincinnati VA Medical Center; Leah Kottyan, PhD, an immunobiology expert with CAGE; and Matthew Weirauch, PhD, a computational biologist with the center. Critical contributions were provided by Xiaoting Chen, PhD, and Mario Pujato, PhD, both also in CAGE.
The study shows that a protein produced by the Epstein-Barr virus, called EBNA2, binds to multiple locations along the human genome that are associated with these seven diseases.
Overall, the study sheds new light on how environmental factors, such as viral or bacterial infections, poor diet, pollution or other hazardous exposures, can interact with the human genetic blueprint and have disease-influencing consequences.
"Now, using genomic methods that were not available 10 years ago, it appears that components made by the virus interact with human DNA in the places where the genetic risk of disease is increased," Harley says. "And not just for lupus, but all these other diseases, too."
The full impact of this study could take years to explore. Here are some of the initial implications:
New concern about the 'kissing disease'
EBV is a strikingly common virus. In the US and other developed nations, more than 90 percent of the population becomes infected by age 20. In less-developed nations, 90 percent of people become infected by age 2. Once infected, the virus remains in people for their entire lives.
Mononucleosis, which causes weeks of extreme fatigue, is the most common illness caused by EBV. Mono was nicknamed the "kissing disease" years ago because the virus spreads primarily via contact with saliva.
Over the years, scientists have linked EBV to a few other rare conditions, including certain cancers of the lymphatic system. Harley, who has devoted much of his career to studying lupus, found possible connections between lupus and EBV years ago. That work includes proposing mechanisms that the immune system uses in response to the virus that lead to lupus, and showing that children with lupus almost always are infected with EBV.
Today's study adds weight to those lupus findings and adds six more well-known diseases to the list.
"This discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders," Harley says. "As a consequence, and assuming that others can replicate our findings, that could lead to therapies, ways of prevention, and ways of anticipating disease that don't now exist." So far, no vaccine exists that will prevent EBV infection.
"I think we've come up with a really strong rationale for encouraging people to come up with more of an effort," Kottyan says. "Some EBV vaccines are under development. I think this study might well encourage them to push forward faster and with rededicated effort."
How EBV hijacks our immune system
When viral and bacterial infections strike, our bodies respond by commanding B cells within our immune systems to crank out antibodies to battle the invaders. However, when EBV infections occur, something unusual happens.
The EBV virus invades the B cells themselves, re-programs them, and takes over control of their functions. The Cincinnati Children's research team has discovered a new clue about how the virus does this, a process that involves tiny proteins called transcription factors.
Our bodies have about 1,600 known transcription factors at work within our genome. Each cell uses a subset of these to become what they are and to respond to their environment. These proteins constantly move along the strands of our DNA, turning specific genes on and off to make sure cells function as expected.
However, when the transcription factors change what they do, the normal functions of the cell can also change, and that can lead to disease. The Cincinnati Children's team suspects that the EBNA2 transcription factor from EBV is helping change how infected B cells operate, and how the body responds to those infected cells.
The new paper shows that seven seemingly unrelated disease states actually share a common set of abnormal transcription factors, each affected by the EBNA2 protein from the Epstein-Barr virus. When these EBNA2-related clusters of transcription factors attach themselves to one portion of the genetic code, the risk of lupus appears to rise. When those same transcription factors land on another part of the code, the risk of multiple sclerosis appears to rise. And so on.
"Normally, we think of the transcription factors that regulate human gene expression as being human," Kottyan says. "But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease."
New leads emerge for improving treatment
It remains unclear how many cases of the seven diseases listed in the study can be traced to prior EBV infection. More genomic analyses involving many more patients with these diseases will be required to make reliable estimates.
"The impact of the virus is likely to vary across the diseases," Harley says. "In lupus and MS, for example, the virus could account for a large percentage of those cases. We do not have a sense of the proportion in which the virus could be important in the other EBNA2-associated diseases."
However, the breakthrough identification of specific transcription factors connected to EBV infections opens new lines of study that could accelerate efforts to find cures.
"This same cast of characters is a villain in multiple immune-related diseases," Weirauch says. "They're playing that role through different ways, and doing it at different places in your genome, but it's the same sinister characters. So if we could develop therapies to stop them from doing this, then it would help multiple diseases."
A number of compounds -- some experimental, some approved as medications for other conditions -- already are known to be capable of blocking some of the high-risk transcription factors listed in the paper, Weirauch says. Teams at Cincinnati Children's have begun deeper studies of some of these compounds.
Findings go far, far beyond EBV
While the EBV-related findings involved more than 60 human proteins linked to seven diseases, the Cincinnati Children's research team already has taken a huge next step. They applied the same analytic techniques to tease out connections between all 1,600 known transcription factors and the known gene variants associated with more than 200 diseases.
The results of that massive cross-analysis also appear in today's study. Intriguing associations were documented involving 94 conditions.
"Our study has uncovered potential leads for many other diseases, including breast cancer," Harley says. "We cannot possibly follow up on all of these, but we are hoping that other scientists will."
After devoting decades of research to hunting down the causes of lupus, Harley says this study represents the most important discovery of his career. "I've been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research," he says.
Software behind discoveries to be made public
Detecting and tracking the activities of these transcription factors took years of work involving dozens of laboratory and computational experts.
The project required gathering massive sets of genetic data, then analyzing every genetic change affecting the activity of the virus. Doing this required creating two new algorithms, called RELI and MARIO, which were developed at Cincinnati Children's by Weirauch and colleagues.
Both software tools and a related website will be made publicly available.
"We are going to great lengths to not only make the computer code available, but all of the data and all of the results," Weirauch says. "We think it's an interesting approach that could have implications for many diseases, so we're contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow up on them."
GLOSSARY OF TERMS
What is the Epstein-Barr virus?
The Epstein-Barr virus (EBV) is an extremely common virus usually spread by saliva. EBV causes mononucleosis, and has been associated with a growing number of other diseases. A study led by Cincinnati Children's, published today in Nature Genetics, adds seven diseases to that list.
What is mononucleosis?
Also known as "mono," and nicknamed the "kissing disease," the symptoms of this condition include extreme fatigue, fever, sore throat, head and body aches, swollen lymph nodes in the neck and armpits, swollen liver or spleen or both, and rash, according to the Centers for Disease Control and Prevention. Most people get better in two to four weeks. However, some people may feel fatigued for several more weeks.
What is a B cell?
B cells are a type of white blood cell found in the immune system. These cells produce antibodies in reaction to infections by bacteria, viruses and other invaders. Epstein-Barr virus infects a small proportion of these cells.
What is a transcription factor?
Transcription factors are proteins that "turn on and turn off" genes. These proteins help direct cell growth, division, and death. They also control cell migration and organization. There are about 1,600 known human transcription factors that do their work along the human genome. These proteins change the expression of genes to make RNA, which in many cases results in forming other proteins that change how cells form and function.
What is a DNA variant?
The DNA genome of every person contains over 3 billion DNA bases. Most of the bases are exactly the same for every person. However, about 1 percent of the bases can be different and these create diversity between people. The variants can change the way proteins are made or change the regulatory processes that lead to protein production.
Read more at Science Daily
Apr 15, 2018
Circumbinary castaways: Short-period binary systems can eject orbiting worlds
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| This artist’s concept illustrates Kepler-16b, the first planet known to orbit two stars – what’s called a circumbinary planet. The planet, which can be seen in the foreground, was discovered by NASA’s Kepler mission. New research from the University of Washington indicates that certain shot-period binary star systems eject circumbinary planets as a consequence of the host stars’ evolution. |
The findings help explain why astronomers have detected few circumbinary planets -- which orbit stars that in turn orbit each other -- despite observing thousands of short-term binary stars, or ones with orbital periods of 10 days or less.
It also means that such binary star systems are a poor place to aim coming ground- and space-based telescopes to look for habitable planets and life beyond Earth.
There are several different types of binary stars, such as visual and spectroscopic binaries, named for the ways astronomers are able to observe them. In a paper accepted for publication in Astrophysical Journal, lead author David Fleming, a UW astronomy doctoral student, studies eclipsing binaries, or those where the orbital plane is so near the line of sight, both stars are seen to cross in front of each other. Fleming will present the paper at the Division on Dynamical Astronomy conference April 15-19.
When eclipsing binaries orbit each other closely, within about 10 days or less, Fleming and co-authors wondered, do tides -- the gravitational forces each exerts on the other -- have "dynamical consequences" to the star system?
"That's actually what we found" using computer simulations, Fleming said. "Tidal forces transport angular momentum from the stellar rotations to the orbits. They slow down the stellar rotations, expanding the orbital period."
This transfer of angular momentum causes the orbits not only to enlarge but also to circularize, morphing from being eccentric, or football-shaped, to perfect circles. And over very long time scales, the spins of the two stars also become synchronized, as the moon is with the Earth, with each forever showing the same face to the other.
The expanding stellar orbit "engulfs planets that were originally safe, and then they are no longer safe -- and they get thrown out of the system," said Rory Barnes, UW assistant professor of astronomy and a co-author on the paper. And the ejection of one planet in this way can perturb the orbits of other orbiting worlds in a sort of cascading effect, ultimately sending them out of the system as well.
Making things even more difficult for circumbinary planets is what astronomers call a "region of instability" created by the competing gravitational pulls of the two stars. "There's a region that you just can't cross -- if you go in there, you get ejected from the system," Fleming said. "We've confirmed this in simulations, and many others have studied the region as well."
This is called the "dynamical stability limit." It moves outward as the stellar orbit increases, enveloping planets and making their orbits unstable, and ultimately tossing them from the system.
Another intriguing characteristic of such binary systems, detected by others over the years, Fleming said, is that planets tend to orbit just outside this stability limit, to "pile up" there. How planets get to the region is not fully known; they may form there, or they may migrate inward from further out in the system.
Applying their model to known short-period binary star systems, Fleming and co-authors found that this stellar-tidal evolution of binary stars removes at least one planet in 87 percent of multiplanet circumbinary systems, and often more. And even this is likely a conservative estimate; Barnes said the number may be as high as 99 percent.
The researchers have dubbed the process the Stellar Tidal Evolution Ejection of Planets, or STEEP. Future detections -- "or non-detections" -- of circumbinary around short-period binary stars, the authors write, will "will provide the best indirect observational test of the STEEP process.
Read more at Science Daily
NASA’s Newest Satellite Will Scan the Universe for Undiscovered Exoplanets
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| NASA's Transiting Exoplanet Survey Satellite |
TESS is scheduled to launch from Vandenberg Air Force Base April 16 and will make its way to an Earth orbit with lowest and highest altitudes of 67,000 miles and 232,000 miles. It will study different parts of the sky in observing campaigns of almost one month each, ferrying data back to Earth about what it sees.
Like Kepler, TESS will examine stars and look for the telltale dimming, or “transit,” that takes place when a planet goes across the star's face. The observatory's information will be beamed back to the ground where other telescopes can look for small tugs or wobbles in the star's position, which would confirm a planet has been discovered.
"TESS was designed so the targets would be optimally based for ground-based follow up," principal investigator George Ricker, a senior scientist at the Massachusetts Institute of Technology, told Seeker. "We want to make sure we can communicate to ground-based observers the information that we get in terms of candidate transit events, or planets."
With 200,000 high-priority targets, TESS investigators expect the first possible planets will come back to Earth within just a few weeks or months. The mission is currently funded for two years. In that time, it will locate hundreds of possible exoplanets, including a few dozen that are close to the size of Earth. Kepler has already located well over 2,000 planets, but the TESS stars will be brighter, closer, and easier to examine.
Kepler investigators, however, will get the second chance to look at planets discovered by the telescope during the second year of TESS’s operations. At first, TESS will spend a year moving its view around the southern hemisphere. Kepler's original field of view was the constellation Cygnus, in the north. Sometime during its second year of operations, TESS will spend a month staring at the same spot that Kepler examined for four years, between 2009 and 2013.
Engineers constructed TESS to last well beyond its original mission lifetime, as long as funding persists. The telescope will act as a finder telescope, searching for objects that are interesting, which other telescopes might zoom in on. A prominent follow-up telescope will be the James Webb Space Telescope, which is now expected to launch in 2020. Ideally, TESS and James Webb observations will overlap.
"The longer the mission will operate, the more precisely we can determine the properties of the [planetary] transits," Ricker said. Once they pinpoint the time it takes for a planet to go around a star, Webb can peer at the planet to learn more about its atmosphere. Other instruments, such as HARPS (High Accuracy Radial velocity Planet Searcher) at the La Silla Observatory, could measure a planet’s wobbles in order to estimate its mass.
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