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2013年8月29日星期四

Space laser to prove increased broadband possible

Aug. 28, 2013 — When NASA's Lunar Laser Communication Demonstration (LLCD) begins operation aboard the Lunar Atmosphere and Dust Environment Explorer (LADEE) mission managed by NASA's Ames Research Center in Moffett Field, Calif., it will attempt to show two-way laser communication beyond Earth is possible, expanding the possibility of transmitting huge amounts of data. This new ability could one day allow for 3-D High Definition video transmissions in deep space to become routine.

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"The goal of the LLCD experiment is to validate and build confidence in this technology so that future missions will consider using it," said Don Cornwell, LLCD manager. "This unique ability developed by MIT (Massachusetts Institute of Technology Lincoln Laboratory), has incredible application possibilities and we are very excited to get this instrument off the ground."

Since NASA first ventured into space, through the moon landings, shuttle program, and unmanned exploration missions, radio frequency communication also known as RF, has been the communications platform used. But RF is reaching its limit just as demand for more data capacity continues to increase. The development of laser communications will give NASA the ability to extend communication applications such as increased image resolution and even 3-D video transmission into deep space.

LLCD is NASA's first dedicated system for two-way communication using laser instead of radio waves. "LLCD is designed to send six times more data from the moon using a smaller transmitter with 25 percent less power as compared to the equivalent state-of-the-art radio (RF) system," said Cornwell. "Lasers are also more secure and less susceptible to interference and jamming."

The LLCD experiment is hosted aboard NASA's LADEE: a 100-day robotic mission designed, built, integrated, tested and will be operated by Ames. LADEE will attempt to confirm whether dust caused a mysterious glow on the lunar horizon astronauts observed during several Apollo missions and explore the moon's tenuous, exotic atmosphere. Launch of the LADEE spacecraft is set for September aboard a U.S. Air Force Minotaur V rocket, an excess ballistic missile converted into a space launch vehicle and operated by Orbital Sciences Corp. of Dulles, Va., from NASA's Wallops Flight Facility on Wallops Island, Va.

The LADEE spacecraft will take 30 days to reach the moon because of its flight path. LLCD will begin operations shortly after arrival into lunar orbit and continue for 30 days afterward.

LLCD's main mission objective is to transmit hundreds of millions of bits of data per second from the moon to Earth. This is equivalent to transmitting more than 100 HD television channels simultaneously. LLCD receiving capability will also be tested as tens of millions of bits per second are sent from Earth to the spacecraft. These demonstrations will prove the technology for increased bandwidth for future missions is possible.

There is a primary ground terminal at NASA's White Sands Complex in New Mexico, to receive and transmit LLCD signals. The team at MIT designed, built, and tested the terminal. They also will be responsible for LLCD's operation at that site.

There are two alternate sites, one located at NASA's Jet Propulsion Laboratory in California, which is for receiving only. The other is being provided by the European Space Agency on the Spanish island of Tenerife, off the coast of Africa. It will have two-way communication capability with LLCD. "Having several sites gives us alternatives which greatly reduces the possibility of interference from clouds," said Cornwell.

LLCD is a short duration experiment and the precursor to NASA's long duration demonstration, the Laser Communications Relay Demonstration (LCRD). It also is a part of the agency's Technology Demonstration Missions Program, which is working to develop crosscutting technology capable of operating in the rigors of space. LCRD is scheduled to launch in 2017.

NASA engineers believe this technology becomes even more advantageous for communications beyond Earth's orbit. In the past, NASA has experimented with sending low amounts of individual pulses to cameras on far-away space probes near Jupiter, Mars, and Mercury.

Recently, an image of Leonardo da Vinci's painting, the Mona Lisa, was transmitted to NASA's Lunar Reconnaissance Orbiter (LRO) spacecraft orbiting the moon. "But this was done at only hundreds of data bits per second," said Cornwell. "LLCD will be the first dedicated optical communication system and will send data millions of times faster."

The European Space Agency already has successfully demonstrated laser communication between satellites in Earth orbit. Recently they launched Alphasat to demonstrate laser transmission between a low-earth orbit satellite and a satellite in geostationary Earth orbit. LLCD's laser link from the moon will be ten times farther away.

NASA is looking upon laser communication as the next paradigm shift in future space communication, especially deep space. "We can even envision such a laser-based system enabling a robotic mission to an asteroid," said Cornwell. "It could have 3-D, high-definition video signals transmitted to Earth providing essentially 'telepresence' to a human controller on the ground."

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Migraine may permanently change brain structure

"Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain," said study author Messoud Ashina, MD, PhD, with the University of Copenhagen in Denmark. "Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways."

The study found that migraine raised the risk of brain lesions, white matter abnormalities and altered brain volume compared to people without the disorder. The association was even stronger in those with migraine with aura.

For the meta-analysis, researchers reviewed six population-based studies and 13 clinic-based studies to see whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans compared to those without the conditions.

The results showed that migraine with aura increased the risk of white matter brain lesions by 68 percent and migraine with no aura increased the risk by 34 percent, compared to those without migraine. The risk for infarct-like abnormalities increased by 44 percent for those with migraine with aura compared to those without aura. Brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.

"Migraine affects about 10 to 15 percent of the general population and can cause a substantial personal, occupational and social burden," said Ashina. "We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease. We also want to find out how these lesions may influence brain function."

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Intestinal flora determines health of obese people

The international consortium MetaHIT, which includes the research group of Jeroen Raes (VIB/Vrije Universiteit Brussel) were involved with the research. Jeroen Raes (VIB/VUB) said, "This is an amazing result with possibly enormous implications for the treatment and even prevention of the greatest public health issue of our time. But we are not there yet, now we need studies in which we can monitor people for a longer period. We want to perform these types of long-term studies together with the "Vlaams Darmflora Project" (Flemish Gut Flora Project), which is only possible thanks to the selfless efforts of thousands of Flemish residents."

Obesity, a health problem

Metabolic conditions have become an epidemic partly due to the modern lifestyle without a lot of exercise and easy access to (a lot of) energy-dense food. It is expected that obesity will increase tremendously all over the world; from 400 million obese people in 2005, to more than 700 million in 2015. A trend that will persist at least until 2030. Some people appear to be more sensitive to obesity than others. Many studies over the years have examined the possible cause of this.

Bacterial richness in your intestines is associated with susceptibility to obesity

Over the last years it has become very clear that there is a link between the bacterial population in our intestines and our health. As a result, scientists also started studying the link between obesity and intestinal flora. An international consortium, including the VIB scientists Falk Hildebrand, Gwen Falony and Jeroen Raes in Brussels, examined the intestinal flora of 169 obese Danes and 123 non-obese Danes.

Jeroen Raes: "We were able to distinguish between two groups based on their intestinal flora: people with a large richness of bacterial species in their intestines and people with a few less bacterial species. A species-rich bacterial flora appeared to function differently compared to the poorer variety. It was surprising to see that obese and non-obese people were found in both groups."

The scientists did see that the group with lower species richness in the intestinal flora was more susceptible to developing obesity-related conditions and chronic inflammation. The obese people in this group are more at risk of cardiovascular conditions than the obese people in the other group. These are important results that suggest that it is not only weight gain and dietary habits that play a role in the development of medical complications in obese people.

The Flemish Gut Flora Project

The question that remains is whether these results also translate to other countries and populations. Therefore, Jeroen Raes has established the Flemish Intestinal Flora Project to follow up on these types of studies on a larger scale. Such efforts are crucial to confirm the insights acquired in smaller studies and to make an effective step towards improved treatments and medicines.

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A major cause of age-related memory loss identified: Potentially reversible

Aug. 28, 2013 — A team of Columbia University Medical Center (CUMC) researchers, led by Nobel laureate Eric R. Kandel, MD, has found that deficiency of a protein called RbAp48 in the hippocampus is a significant contributor to age-related memory loss and that this form of memory loss is reversible. The study, conducted in postmortem human brain cells and in mice, also offers the strongest causal evidence that age-related memory loss and Alzheimer's disease are distinct conditions.

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The findings were published today in the online edition of Science Translational Medicine.

"Our study provides compelling evidence that age-related memory loss is a syndrome in its own right, apart from Alzheimer's. In addition to the implications for the study, diagnosis, and treatment of memory disorders, these results have public health consequences," said Dr. Kandel, who is University Professor & Kavli Professor of Brain Science, co-director of Columbia's Mortimer B. Zuckerman Mind Brain Behavior Institute, director of the Kavli Institute for Brain Science, and senior investigator, Howard Hughes Medical Institute, at CUMC. Dr. Kandel received a share of the 2000 Nobel Prize in Physiology or Medicine for his discoveries related to the molecular basis of memory.

The hippocampus, a brain region that consists of several interconnected subregions, each with a distinct neuron population, plays a vital role in memory. Studies have shown that Alzheimer's disease hampers memory by first acting on the entorhinal cortex (EC), a brain region that provides the major input pathways to the hippocampus. It was initially thought that age-related memory loss is an early manifestation of Alzheimer's, but mounting evidence suggests that it is a distinct process that affects the dentate gyrus (DG), a subregion of the hippocampus that receives direct input from the EC.

"Until now, however, no one has been able to identify specific molecular defects involved in age-related memory loss in humans," said co-senior author Scott A. Small, MD, the Boris and Rose Katz Professor of Neurology and director of the Alzheimer's Research Center at CUMC.

The current study was designed to look for more direct evidence that age-related memory loss differs from Alzheimer's disease. The researchers began by performing microarray (gene expression) analyses of postmortem brain cells from the DG of eight people, ages 33 to 88, all of whom were free of brain disease. The team also analyzed cells from their EC, which served as controls since that brain structure is unaffected by aging. The analyses identified 17 candidate genes that might be related to aging in the DG. The most significant changes occurred in a gene called RbAp48, whoseexpressiondeclined steadily with aging across the study subjects.

To determine whether RbAp48plays an active role in age-related memory loss, the researchers turned to mouse studies. "The first question was whether RbAp48is downregulated in aged mice," said lead author Elias Pavlopoulos, PhD, associate research scientist in neuroscience at CUMC. "And indeed, that turned out to be the case -- there was a reduction of RbAp48 protein in the DG."

When the researchers genetically inhibited RbAp48inthe brains ofhealthy young mice, they found the same memory loss as in aged mice, as measured by novel object recognition and water maze memory tests. When RbAp48inhibition was turned off, the mice's memory returned to normal.

The researchers also did functional MRI (fMRI) studies of the mice with inhibited RbAp48 and found a selective effect in the DG, similar to that seen in fMRI studies of aged mice, monkeys, and humans. This effect of RbAp48 inhibition on the DG was accompanied by defects in molecular mechanisms similar to those found in aged mice. The fMRI profile and mechanistic defects of the mice with inhibited RbAp48 returned to normal when the inhibition was turned off.

In another experiment, the researchers used viral gene transfer and increased RbAp48expression inthe DG of aged mice. "We were astonished that not only did this improve the mice's performance on the memory tests, but their performance was comparable to that of young mice," said Dr. Pavlopoulos.

"The fact that we were able to reverse age-related memory loss in mice is very encouraging," said Dr. Kandel. "Of course, it's possible that other changes in the DG contribute to this form of memory loss. But at the very least, it shows that this protein is a major factor, and it speaks to the fact that age-related memory loss is due to a functional change in neurons of some sort. Unlike with Alzheimer's, there is no significant loss of neurons."

Finally, the study data suggest that RbAp48 protein mediates its effects, at least in part, through the PKA-CREB1-CBP pathway, which the team had found in earlier studies to be important for age-related memory loss in the mouse. According to the researchers, RbAp48 and the PKA-CREB1-CBP pathway are valid targets for therapeutic intervention. Agents that enhance this pathway have already been shown to improve age-related hippocampal dysfunction in rodents.

"Whether these compounds will work in humans is not known," said Dr. Small. "But the broader point is that to develop effective interventions, you first have to find the right target. Now we have a good target, and with the mouse we've developed, we have a way to screen therapies that might be effective, be they pharmaceuticals, nutraceuticals, or physical and cognitive exercises."

"There's been a lot of handwringing over the failures of drug trials based on findings from mouse models of Alzheimer's," Dr. Small said. "But this is different. Alzheimer's does not occur naturally in the mouse. Here, we've caused age-related memory loss in the mouse, and we've shown it to be relevant to human aging."

The paper is titled, "A Molecular Mechanism for Age-Related Memory Loss: The Histone Binding Protein RbAp48." The other contributors are Sidonie Jones, Stylianos Kosmidis, Maggie Close, Carla Kim, and Olga Kovalerchik, all at CUMC.

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Blocking molecular pathway reverses pulmonary hypertension in rats

Pulmonary hypertension, a deadly form of high blood pressure that develops in the lungs, may be caused by an inflammation-producing molecular pathway that damages the inner lining of blood vessels, according to a new study by researchers at the Stanford University School of Medicine.

The results, published Aug. 28 in Science Translational Medicine, suggest that using medications to block this pathway could lead to the first-known cure for the disease, apart from lung transplantation. The new research could also lead to a better understanding of other diseases involving inflammation of blood vessels, such as coronary artery disease, said Mark Nicolls, MD, senior author of the study and division chief of pulmonary and critical care medicine at Stanford, as well as a staff physician at the Veterans Affairs Palo Alto Health Care System.

"We believe that targeting inflammation is an exciting approach to augment current treatments for pulmonary hypertension because it may reverse the underlying cause of the disease," said Nicolls, who is also director of the Lung Immunology Program and an associate professor of medicine. "We believe this is going to be an approach that helps a large number of patients."

The lead author of the study is Wen Tian, PhD, a research associate in Nicolls' lab.

Pulmonary hypertension, while rare, usually strikes young and middle-aged women, leaving them short of breath and often unable to complete simple daily tasks. The condition can be fatal. The risk is higher for people with certain autoimmune diseases (such as scleroderma or lupus), HIV, congenital heart disease or liver disease. The risk also is higher for those who have used street drugs, such as amphetamines or cocaine, or the diet drug fenphen.

About 100,000 people in the United States and Europe have been diagnosed with pulmonary hypertension, but many others are believed to go undiagnosed because the main symptom, shortness of breath, is nonspecific. Until the 1990s, there were no treatments except lung transplantation, which has varying degrees of success.

What is known about the disease is that the narrowing of blood vessels in the lungs is caused by a mysterious proliferation of the smooth muscle cells that ring those vessels. As the vessel walls thicken, they become increasingly occluded, choking off blood flow.

Blood vessels are elastic tubes that have an outer layer of smooth muscle and an inner layer of endothelial cells. The current treatment for patients with pulmonary hypertension is vasodilators, drugs that cause smooth muscle cells to relax, permitting more blood to flow through the diseased vessels. These drugs help to extend survival and relieve some symptoms, but they don't provide a cure.

"Current approved therapies for pulmonary hypertension have focused on dilating blood vessels without special attention being paid to the inflammation that is frequently seen around blood vessels," Nicolls said. "We were interested in finding out how inflammation contributes to the disease."

In laboratory experiments, researchers removed inflammation-producing cells called macrophages from the lung tissue of rats dying of pulmonary hypertension and put the cells in cultures with healthy rat endothelial cells.

"We were shocked to find that half of the endothelial cells were dead within 24 hours," Nicolls said. "That totally surprised us."

In subsequent lab experiments, researchers found that if they blocked the molecular pathway triggered by the macrophages, the endothelial cells didn't die. Researchers conducted similar experiments in human tissue taken from the diseased lungs of patients. The results were similar. "The same pathways were at play in the human lungs," Nicolls said.

In experiments in live rats with induced pulmonary hypertension, the disease was reversed when researchers blocked the inflammation-producing pathway.

"It was dramatic," Nicolls said. "We could start the drug as late as three weeks when animals were breathing hard and walking slowly, and the disease reversed."

Other Stanford authors were research associates Xinguo Jiang, MD, PhD, and Rasa Tamosiuniene, MD, PhD; postdoctoral scholars Yon Sung, MD, and Jin Qian, MD, PhD; Gundeep Dhillon, MD, assistant professor of pulmonary and critical care medicine; Marlene Rabinovitch, MD, professor of pediatric cardiology; Roham Zamanian, MD, assistant professor of pulmonary and critical care medicine; Mohammed Inayathullah, PhD, senior research associate; consulting scientist Marina Fridlib; and Jayakumar Rajadas, director of the Biomaterials and Advanced Drug Delivery and Service Center.

The study was funded by the National Institutes of Health (grants NHLBI-HV-10-05 and HL082662) and the National Heart, Lung and Blood Institute Proteomics Center at Stanford. Additional support came from Stanford's Vera Mouton Wall Center for Pulmonary Vascular Disease and SPARK, a Stanford program that helps researchers translate innovations from bench to bedside.

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A potential cause of autism? Key enzymes are found to have a 'profound effect' across dozens of genes linked to autism

"Our study shows the magnitude of what can happen if topoisomerases are impaired," said senior study author Mark Zylka, PhD, associate professor in the Neuroscience Center and the Department of Cell Biology and Physiology at UNC. "Inhibiting these enzymes has the potential to profoundly affect neurodevelopment -- perhaps even more so than having a mutation in any one of the genes that have been linked to autism."

The study could have important implications for ASD detection and prevention.

"This could point to an environmental component to autism," said Zylka. "A temporary exposure to a topoisomerase inhibitor in utero has the potential to have a long-lasting effect on the brain, by affecting critical periods of brain development. "

This study could also explain why some people with mutations in topoisomerases develop autism and other neurodevelopmental disorders.

Topiosomerases are enzymes found in all human cells. Their main function is to untangle DNA when it becomes overwound, a common occurrence that can interfere with key biological processes.

Most of the known topoisomerase-inhibiting chemicals are used as chemotherapy drugs. Zylka said his team is searching for other compounds that have similar effects in nerve cells. "If there are additional compounds like this in the environment, then it becomes important to identify them," said Zylka. "That's really motivating us to move quickly to identify other drugs or environmental compounds that have similar effects -- so that pregnant women can avoid being exposed to these compounds."

Zylka and his colleagues stumbled upon the discovery quite by accident while studying topotecan, a topoisomerase-inhibiting drug that is used in chemotherapy. Investigating the drug's effects in mouse and human-derived nerve cells, they noticed that the drug tended to interfere with the proper functioning of genes that were exceptionally long -- composed of many DNA base pairs. The group then made the serendipitous connection that many autism-linked genes are extremely long.

"That's when we had the 'Eureka moment,'" said Zylka. "We realized that a lot of the genes that were suppressed were incredibly long autism genes."

Of the more than 300 genes that are linked to autism, nearly 50 were suppressed by topotecan. Suppressing that many genes across the board -- even to a small extent -- means a person who is exposed to a topoisomerase inhibitor during brain development could experience neurological effects equivalent to those seen in a person who gets ASD because of a single faulty gene.

The study's findings could also help lead to a unified theory of how autism-linked genes work. About 20 percent of such genes are connected to synapses -- the connections between brain cells. Another 20 percent are related to gene transcription -- the process of translating genetic information into biological functions. Zylka said this study bridges those two groups, because it shows that having problems transcribing long synapse genes could impair a person's ability to construct synapses.

"Our discovery has the potential to unite these two classes of genes -- synaptic genes and transcriptional regulators," said Zylka. "It could ultimately explain the biological mechanisms behind a large number of autism cases."

The study's coauthors include Benjamin Philpot (co-senior author), Terry Magnuson, Ian King, Chandri Yandava, Angela Mabb, Hsien-Sung Huang, Brandon Pearson, J. Mauro Calabrese, Joshua Starmer and Joel Parker from UNC and Jack S. Hsiao and Stormy Chamberlain of the University of Connecticut Health Center.

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Obesity and diabetes risk: One in four has alarmingly few intestinal bacteria, Danish study finds

All people have trillions of bacteria living in their intestines. If you place them on a scale, they weigh around 1.5 kg. Previously, a major part of these 'blind passengers' were unknown, as they are difficult or impossible to grow in laboratories. But over the past five years, an EU-funded research team, MetaHIT, coordinated by Professor S. Dusko Ehrlich at the INRA Research Centre of Jouy-en-Josas, France and with experts from Europe and China have used advanced DNA analysis and bioinformatics methods to map human intestinal bacteria.

"The genetic analysis of intestinal bacteria from 292 Danes shows that about a quarter of us have up to 40% less gut bacteria genes and correspondingly fewer bacteria than average. Not only has this quarter fewer intestinal bacteria, but they also have reduced bacterial diversity and they harbour more bacteria causing a low-grade inflammation of the body. This is a representative study sample, and the study results can therefore be generalised to people in the Western world," says Oluf Pedersen, Professor and Scientific Director at the Faculty of Health and Medical Sciences, University of Copenhagen.

Oluf Pedersen and Professor Torben Hansen have headed the Danish part of the MetaHIT project, and the findings are reported in scientific journal Nature.

The gut is like a rainforest

Oluf Pedersen compares the human gut and its bacteria with a tropical rainforest. He explains that we need as much diversity as possible, and -- as is the case with the natural tropical rainforests -- decreasing diversity is a cause for concern. It appears that the richer and more diverse the composition of our intestinal bacteria, the stronger our health. The bacteria produce vital vitamins, mature and strengthen our immune system and communicate with the many nerve cells and hormone-producing cells in the intestinal system. And, not least, the bacteria produce a wealth of bioactive substances which penetrate into the bloodstream and affect our biology in countless ways.

"Our study shows that people having few and less diverse intestinal bacteria are more obese than the rest. They have a preponderance of bacteria which exhibit the potential to cause mild inflammation in the digestive tract and in the entire body, which is reflected in blood samples that reveal a state of chronic inflammation, which we know from other studies to affect metabolism and increase the risk of type 2 diabetes and cardiovascular diseases," says Oluf Pedersen.

"And we also see that if you belong to the group with less intestinal bacteria and have already developed obesity, you will also gain more weight over a number of years. We don't know what came first, the chicken or the egg, but one thing is certain: it is a vicious circle that poses a health threat," says the researcher.

Take care of your intestinal bacteria

The researchers thus still cannot explain why some people have fewer intestinal bacteria, but the researchers are focusing their attention at dietary components, genetic variation in the human host, exposure to antimicrobial agents during early childhood and the chemistry we encounter daily in the form of preservatives and disinfectants.

A French research team reports a study in the same issue of Nature showing that by maintaining a low-fat diet for just six weeks, a group of overweight individuals with fewer and less diverse intestinal bacteria may, to some extent, increase the growth of intestinal bacteria, both in terms of actual numbers and diversity.

"This indicates that you can repair some of the damage to your gut bacteria simply by changing your dietary habits. Our intestinal bacteria are actually to be considered an organ just like our heart and brain, and the presence of health-promoting bacteria must therefore be cared for in the best way possible. Over the next years, we will be gathering more knowledge of how best to do this," says Oluf Pedersen, whose research team is studying, among other things, the impact of dietary gluten on gut bacteria composition and gut function.

Towards innovative early diagnostics and treatment options

Obesity and type 2 diabetes are not just a result of unfortunate combinations of intestinal bacteria or lack of health-promoting intestinal bacteria, Oluf Pedersen emphasises. There are likely many causal factors at play. But the MetaHit researchers' contribution opens a new universe in which we begin to understand how gut bacteria in direct contact with the surrounding environment have a decisive impact on our health and risk of disease.

"At present we cannot do anything about our own DNA, individual variation in which also plays a crucial role in susceptibility for lifestyle diseases. But thanks to the new gut microbiota research, we now can start exploring interactions between host genetics and the gut bacteria- related environment which we may be able to change. That is why it is so exciting for us scientist within this research field- the possibilities are huge," says Oluf Pedersen.

"The long-term dream is to map and characterize any naturally occurring gut bacteria that produce appetite-inhibiting bioactive substances and in this way learn to exploit the body's own medicine to prevent the obesity epidemic and type 2 diabetes," says Oluf Pedersen.

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New Cassini data from Saturn's largest moon Titan indicate a rigid, weathered ice shell

Aug. 28, 2013 — An analysis of gravity and topography data from Saturn's largest moon, Titan, has revealed unexpected features of the moon's outer ice shell. The best explanation for the findings, the authors said, is that Titan's ice shell is rigid and that relatively small topographic features on the surface are associated with large roots extending into the underlying ocean. The study is published in the August 29 issue of the journal Nature.

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Led by planetary scientists Douglas Hemingway and Francis Nimmo at the University of California, Santa Cruz, the study used new data from NASA's Cassini spacecraft. The researchers were surprised to find a negative correlation between the gravity and topography signals on Titan.

"Normally, if you fly over a mountain, you expect to see an increase in gravity due to the extra mass of the mountain. On Titan, when you fly over a mountain the gravity gets lower. That's a very odd observation," said Nimmo, a professor of Earth and planetary sciences at UC Santa Cruz.

To explain that observation, the researchers developed a model in which each bump in the topography on the surface of Titan is offset by a deeper "root" big enough to overwhelm the gravitational effect of the bump on the surface. The root is like an iceberg extending below the ice shell into the ocean underneath it. "Because ice is lower density than water, you get less gravity when you have a big chunk of ice there than when you have water," Nimmo explained.

An iceberg floating in water is in equilibrium, its buoyancy balancing out its weight. In this model of Titan, however, the roots extending below the ice sheet are so much bigger than the bumps on the surface that their buoyancy is pushing them up against the ice sheet. "It's like a big beach ball under the ice sheet pushing up on it, and the only way to keep it submerged is if the ice sheet is strong," said Hemingway, a doctoral candidate in planetary geophysics at UCSC and lead author of the paper. "If large roots are the reason for the negative correlation, it means that Titan's ice shell must have a very thick rigid layer."

The researchers calculated that, in this model, Titan's ice shell would have to have a rigid layer at least 40 kilometers thick. They also found that hundreds of meters of surface erosion and deposition are needed to account for the observed imbalance between the large roots and small surface topography. The results from their model are similar to estimates obtained by geomorphologists studying the erosion of impact craters and other features on Titan.

These findings have several implications. For example, a thick rigid ice shell makes it very difficult to produce ice volcanoes, which some have proposed to explain certain features seen on the surface.

Unlike Earth's geologically active crust, Titan's ice shell isn't getting recycled by convection or plate tectonics. "It's just sitting there, and weather and erosion are acting on it, moving stuff around and redepositing sediments," Nimmo said. "It may be like the surface of Earth would be if you turned plate tectonics off."

The researchers are not sure what could have given rise to Titan's topographical features with their deep roots. Titan's eccentric orbit around Saturn generates tides that flex the moon's surface and create tidal heating, which could cause variations to develop in the thickness of the ice shell, Hemingway said.

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Using a form of 'ice that burns' to make potable water from oil and gas production

The study on the method, which removes more than 90 percent of the salt, appears in the journal ACS Sustainable Chemistry & Engineering.

Yongkoo Seol and Jong-Ho Cha explain that salty wastewater is a byproduct of oil and gas production, including hydraulic fracturing, or fracking. These methods use water and produce as a byproduct almost 10 barrels of salty water for every barrel of oil. That water could help people in water-stressed regions. But it can't be desalinated economically with traditional methods. Seol and Cha knew that an alternative called "gas hydrate desalination" showed promise.

A gas hydrate consists of only water and a gas such as methane, the stuff of natural gas. Thus, when hydrates form, salts and other impurities are left behind. When the hydrate breaks down, the gas and pure water are released. However, forming the gas hydrate used in desalination required costly chilling of the water to 28 degrees Fahrenheit. Seol and Cha sought to develop a less costly version of the method, which involves a variation on methane hydrates, chunks of ice retrieved from deep below the sea that burst into flame when brought to the surface.

They describe development and laboratory testing of a new type of gas hydrate desalination technique. They formed the hydrates from water and carbon dioxide with the gases cyclopentane and cyclohexane, which made the method work more efficiently. It removed more than 90 percent of the salt compared to 70 percent with the previous gas hydrate technique. And the process works at near-room temperature, reducing the need for chilling.

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Modified law of gravity predicts dwarf galaxy feature prior to observations

Aug. 28, 2013 — A modified law of gravity correctly predicted, in advance of the observations, the velocity dispersion -- the average speed of stars within a galaxy relative to each other -- in 10 dwarf satellite galaxies of the Milky Way's giant neighbor Andromeda.

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The relatively large velocity dispersions observed in these types of dwarf galaxies is usually attributed to dark matter. Yet predictions made using the alternative hypothesis Modified Newtonian Dynamics (MOND) succeeded in anticipating the observations.

Stacy McGaugh, professor of astronomy at Case Western Reserve, and Mordehai Milgrom, the father of MOND and professor of physics at Weizmann Institute in Israel, report their findings, which have been accepted for publication by the Astrophysical Journal.

The researchers tested MOND on quasi-spherical, very low-surface brightness galaxies that are satellites of Andromeda. In the cosmic scale, they are among the smallest galaxies, containing only a few hundred thousand stars. But with conventional gravity, they are inferred to contain huge amounts of dark matter.

"Most scientists are more comfortable with the dark matter interpretation," McGaugh said. "But we need to understand why MOND succeeds with these predictions. We don't even know how to make this prediction with dark matter."

While this study is very specific, it's part of a broader effort to understand how the universe, the Milky Way and Earth formed and what it's all made of. This informs human understanding of our place in the universe, McGaugh said. Such issues have been of such importance that they've changed religion and philosophy over the centuries, sometimes sending people to be burnt at the stake.

"At stake now is whether the universe is predominantly made of an invisible substance that persistently eludes detection in the laboratory, or whether we are obliged to modify one of our most fundamental theories, the law of gravity," McGaugh continued.

The MOND hypothesis says that Newton's force law must be tweaked at low acceleration -- 11 orders of magnitude lower than what we feel on the surface of Earth. Acceleration above that threshold is linearly proportional to the force of gravity -- as Newton's law says -- but below the threshold, no. At these tiny accelerations, the modified force law resolves the mass discrepancy.

The paper's calculations using MOND also reveal subtle differences in the gravity fields of dwarfs near and far from the host galaxy Andromeda. The gravity fields of dwarfs far from the host appear to be dominated by stars within the dwarf, while the gravity fields of dwarfs close to the host appear to be dominated by the host. No such distinction is expected with dark matter.

"The influence of the host galaxy may provide a test to distinguish between dark matter and MOND," McGaugh says. "Dark matter provides a cocoon for the dwarfs, protecting the stars from tidal influence by the host galaxy. With MOND, the influence of the host is more pronounced."

In a comparison of the predictions calculated using MOND with observations of pairs of similar dwarfs, "the data appears to show MOND's prediction for the influence of the host, but it's fairly subtle," McGaugh said. MOND's predictions of the velocity dispersion were less subtle. These predictions were "really bang on," McGaugh said.

The finding bolsters the case McGaugh and Milgrom made for MOND's effectiveness in predicting properties in dwarf galaxies in a paper published earlier this year. In that paper, they successfully predicted the velocity dispersion in 17 of the galaxies.

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