American Political Science Association : Why Do People Vote? Genetic Variation in Political Participation

Washington, DC—A groundbreaking study finds that genes significantly affect variation in voter turnout, shedding new light on the reasons why people vote and participate in the political system.

The research, conducted by political scientists James H. Fowler, Christopher T. Dawes (of UC San Diego) and psychologist Laura A. Baker (of University of Southern California), appears in the May issue of the American Political Science Review, a journal of the American Political Science Association (APSA). The article is available online at: www.apsanet.org/imgtest/APSRMay08Fowler_etal.pdf.

“Although we are not the first to suggest a link between genes and political participation,” note the authors, “this study is the first attempt to test the idea empirically.” They do so by conducting three tests of the claim that part of the variation in political participation can be attributed to genetic factors. The results suggest that individual genetic differences make up a large and significant portion of the variation in political participation, even after taking socialization and other environmental factors into account. They also suggest that, contrary to decades of conventional wisdom, family upbringing may have little or no effect on children’s future participatory behavior.

In conducting their study, the authors examine the turnout patterns of identical and non-identical twins—including 396 twins in Los Angeles County and 806 twins in the National Longitudinal Study of Adolescent Health. Their findings suggest that 53% of the variation in turnout can be accounted for by genetic effects in the former, with similar outcomes in the latter. Moreover, genetic-based differences extend to a broad class of acts of political participation, including donating to a campaign, contacting an official, running for office, and attending a rally. According to Fowler, “we expected to find that genes played some role in political behavior, but we were quite surprised by the size of the effect and how widely it applies to all kinds of participation.” “The fact that we have found genetic variation in voting, and political participation in general, should not be surprising given the large numbers of behaviors that have already been found to be heritable,” observe the authors. They conclude by noting that “the next step in this line of research must move beyond estimates…and attempt to identify why genes matter so much.” Some potential avenues include examining the interaction of genes and the environment on political participation, tracing the connections between participation in small groups and large-scale participation, and identifying the genes or groups of genes implicated in political behavior.

# # #

The American Political Science Association (est. 1903) is the leading professional organization for the study of politics and has over 14,000 members in 80 countries. For more news and information about political science research visit the APSA media website, www.politicalsciencenews.org.

University of Arkansas, Fayetteville : Canine Tooth Strength Provides Clues To Behavior Of Early Human Ancestors

Measuring and testing the teeth of living primates could provide a window into the behavior of the earliest human ancestors, based on their fossilized remains. Research funded by the National Science Foundation and led by University of Arkansas anthropologist Michael Plavcan takes us one step closer to understanding the relationship between canine teeth, body size and the lives of primates.
Skull and canine teeth of a patas monkey, Erythrocebus patas.

In an article published in American Journal of Physical Anthropology, Plavcan and colleague Christopher B. Ruff of Johns Hopkins School of Medicine report on an initial examination of the function of the shape of canine teeth in primates. This is the first published comparative analysis of canine strength for primates.

Understanding more about the function of canine teeth can lead to new models for understanding human evolution. Plavcan has been studying primate teeth and skulls for 24 years and spent four years collecting dental data for this analysis.

The researchers compared the size, shape and strength of canine teeth from 144 primates with similar measurements taken from 45 carnivores. They examined the relationship of the size of primates’ canines to body size and the relative strength of the teeth. This comparison could help answer the speculation about the function of male primates’ canine teeth in the competition for females. Are the canines used as weapons or simply for display?

“The reason we wanted to use the carnivores is that we know carnivores use their canines for killing,” Plavcan said. “If primates’ canines are too weak to function as weapons, then they’re all just for show.”

Among anthropoid primates, it is well known that the canine teeth of males are up to four times as long as those of females. The researchers compared the canine teeth of male and female primates.

“If the male’s canines are stronger than the female’s canines that would imply there is sexual selection for strength and that the tooth is actually used as a weapon,” Plavcan said. “Female’s canines are short, and shorter, stubbier objects are harder to break. So, if the long, thin male canines are as strong or stronger than those of the female, that would also suggest they are capable of being used for fighting.”

The results were mixed in an interesting way.

“We found that the primate canines are generally as strong as or stronger than carnivore canines," Plavcan said. “But they are not associated with any sort of estimate of sexual selection.”

Generally the canines of males and females were equally strong. Given that primates have such strong teeth in general, the researchers suggested a couple of possible explanations. It could be that all primate males have strong teeth because of a significant risk to reproductive success for any male who breaks a canine tooth. Or it could be that the strong teeth are due to basic inherited design.

Hominids – the primate family that produced humans – retain body mass sexual dimorphism; that is, males typically have a greater body mass size than females. At the same time, the difference in size in canine teeth between males and females is lost.

“This goes back to the earliest hominids,” Plavcan said. “In fact, one of the few diagnostic characteristics of hominid evolution is reduction in canine size dimorphism while maintaining strong body mass dimorphism.”

For example, gorillas have chunky teeth set in massive bodies. To have canines proportionately as long as other primates, a male gorilla’s canines would have to be 25 centimeters long, and the teeth at the base would then be too wide for his jaw.

“This suggests that there may be an upper limit on canine size in primates simply due to spatial constraints on fitting such teeth in the jaws,” the researchers wrote.

The difference in body size between male and female hominids has been the subject of study because it is an obvious and important trait. Yet there are drawbacks to using body size to understand sexual selection. A change in body size can impact many other aspects of life, including metabolism, feeding patterns and vulnerability to predators. Canine teeth, on the other hand, are a far simpler system.

“With canines, we can go in and effectively construct an experiment that allows us to control for all these other variables and look at only one thing,” Plavcan said. “The same phenomenon that works on the canines, we can translate into the body mass and then into behavioral models for the fossil record.”

Plavcan is an associate professor of anthropology in the J. William Fulbright College of Arts and Sciences at the University of Arkansas. He and Ruff are authors of “Canine Size, Shape, and Bending Strength in Primates and Carnivores” in the May issue of American Journal of Physical Anthropology.

University of Michigan Health System : Stillbirths, infant deaths lead to anxiety, guilt and stress among obstetricians

Nearly 1 in 10 say they considered giving up obstetrics due to perinatal death

ANN ARBOR, Mich. — Nearly one in 10 obstetricians in a new study has considered giving up obstetric practice because of the emotional toll of stillbirths and infant deaths.

Three-quarters of the 804 obstetricians who responded to a survey by researchers at the University of Michigan Health System reported that the experience took a large emotional toll on them personally.

"Our survey reveals that perinatal death has a profound effect on obstetricians, and 8 percent had considered giving up obstetrics because of the emotional difficulty of caring for patients with perinatal death," says lead author Katherine Gold, M.D., MSW, of U-M's Department of Family Medicine and Department of Obstetrics and Gynecology.

"We know that stillbirth and infant death are traumatic events for families; this study suggests that they are also traumatic for the physician."

The study appears in the July issue of the journal Obstetrics & Gynecology.

Approximately 15 percent of pregnancies end in early losses (before 20 weeks gestation). In the United States, 1.3 percent of pregnancies end in either stillbirth (losses after 20 weeks but before delivery) or infant death (deaths in the first year of life, most of which occur in the first week). On average, the typical obstetrician performing 140 deliveries a year could encounter nearly two dozen women with a miscarriage and one to two with stillbirth or infant death, the study says.

"Obstetricians want to see a healthy baby. When a fetus or baby dies, the loss can be devastating for the physician," Gold notes. "Half of the time, the medical cause of a stillbirth is unknown, but physicians still may struggle with feelings of guilt or self-blame.

"When a fetus or baby dies, we focus on the family's needs, but obstetricians are often struggling with their own emotions too."

The threat of lawsuits also weighs heavily on physicians. Stillbirths are the number two reason for lawsuits against obstetricians in the United States, preceded only by allegations involving births with adverse neurologic outcomes. In the study, 43 percent of obstetricians who responded said they had worried about disciplinary or legal action due to a perinatal death with no identified cause.

Improved physician training would help obstetricians, according to a majority of the study's respondents. Physicians who said they'd had adequate bereavement training were less likely to report that they had considered giving up obstetric practice because of the emotional difficulty of perinatal death, the study notes. Physicians who perceived their own training as adequate were less likely to worry about disciplinary or legal action when cause of death was unknown.

"As physicians, we get a lot of training in medicine but little in death and bereavement. Sudden and unexpected losses can be terribly difficult both for families and for the physicians involved in caring for the family," Gold says. "This study shows that stillbirths and infant deaths can have profound and persistent effects on obstetricians. We need to find ways to help both families and physicians cope with these devastating events."

Two-thirds of physicians supported training by formal presentations or seminars, and nearly half recommended informal gatherings for physicians to discuss difficult experiences. Many respondents suggested that a meeting with bereaved parents could serve as a useful training strategy as well as a way of helping physicians cope with their own feelings about the loss.

###

Methodology: A total of 1,500 randomly selected U.S. obstetricians were mailed a self-administered survey with 51 questions about their experiences and attitudes in dealing with perinatal death. Eight hundred four physicians (54 percent) completed the entire survey.

Authors: In addition to Gold, authors were Rodney Hayward, M.D., of the Department of Internal Medicine and the School of Public Health, and Angela L. Kuznia, MPH, of the Department of Obstetrics and Gynecology and School of Public Health.

Funding: The research was supported by the Robert Wood Johnson Clinical Scholars Program and the U-M Department of Obstetrics and Gynecology.

Reference: Obstetrics & Gynecology, "How physicians cope when a baby dies: a national survey of obstetricians," Vol. 112, issue 1, pages 29-34.

For more information:

Pregnancy complications www.womenshealth.gov/pregnancy/complications/complicationssp.cfm

Information about stillbirth from the March of Dimes www.marchofdimes.com/professionals/14332_1198.asp

Dr. Katherine Gold www2.med.umich.edu/pcdv2/provider/dsp_provprofile.cfm?individual_id=93928&um_department=Family%20Medicine

Hospital for Special Surgery study Find Heavy birthweight increases risk of developing rheumatoid arthritis

New York, June 30, 2008– People who have a birthweight over 10 pounds are twice as likely to develop rheumatoid arthritis when they are adults compared to individuals born with an average birthweight, according to a study published by researchers from Hospital for Special Surgery online in advance of print in the Annals of the Rheumatic Diseases. While the mechanism for this association is unclear, the study identifies a potentially modifiable risk factor and highlights a potential way to decrease the incidence of the disease.

"There may be a relationship between being born over 10 pounds and getting rheumatoid arthritis later in life," said Lisa Mandl, M.D., MPH, who led the study and is an attending rheumatologist at Hospital for Special Surgery (HSS) in New York City. "If there was some way that you could prevent someone from getting rheumatoid arthritis by making sure their birth weight wasn't over 10 pounds, this is a risk factor that could be modifiable. You can't change someone's age. You can't change someone's gender, but potentially you could change someone's birth weight. This is however only speculative at this point."

Previously, investigators have demonstrated that an increased risk of adult onset chronic disease can be a function of the fetal environment. Strong associations between low birth weight and an increased risk of type 2 diabetes mellitus, coronary heart disease and hypertension have been documented in a number of different populations. Published in 2003, a case-control study of roughly 400 individuals in Sweden identified an association between high birthweight and rheumatoid arthritis.

To see if this association played out in a larger population, Dr. Mandl and colleagues turned to a study of 87,077 women in the Nurses' Health Study. In 1976, nurses were invited to participate in this study that involved a baseline survey and then a biennial questionnaire regarding health status, lifestyle, family medical history and health practices. The investigators excluded women who had cancer or any type of connective tissue disease at baseline or follow-up because these can cause joint swelling, symptoms that can be confused with rheumatoid arthritis. Also excluded were women who reported having rheumatoid arthritis or connective tissue disease during follow-up, but in whom the diagnosis could not be confirmed by review of their medical record. The study population included only women who answered a 1992 survey that collected information about birthweight. After these exclusions, 87,077 individuals were included in the study and 619 of them developed rheumatoid arthritis.

Through statistical analysis, the investigators discovered that a birthweight of greater than 4.54 kg doubled the risk that a person would develop rheumatoid arthritis as an adult compared with individuals who had an average birthweight.

"In utero, the fetus will react appropriately to different stressors. However, this may preprogram the fetus so that when it gets out into the world, this preprogramming is not helpful out in the 'real world'," said Dr. Mandl. In other words, the fetal environment may be preprogramming people's brains or endocrine systems to be maladapted in later life.

"There have now been two different groups, in different countries with different patients born at different times, that both suggest a similar relationship between birthweight and rheumatoid arthritis," said Dr. Mandl. "I hope that other people will think about looking for this association in other populations."

Dr. Mandl says that patients with rheumatoid arthritis are known to have a dysregulated hypothalamic-pituitary-adrenal (HPA) axis, and this axis may be affected in utero. The HPA axis is the body's neuroendocrine system that involves the hypothalamus, pituitary and adrenal glands; this system is responsible for handling stress by regulating the production of cortisol, neurotransmitters and key hormones.

"If you look at this as a theoretic biologic underpinning for why this might be true, it might give basic scientists interesting ideas to think about regarding what causes rheumatoid arthritis, and provide support for a new hypothesis," Dr. Mandl said.

According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, about 2.1 million people, or between 0.5 and 1 percent of the U.S. adult population, have rheumatoid arthritis, an autoimmune disease that causes chronic inflammation of the joints. The disease is more common in women and has no cure, but can be managed in a way that allows individuals to live productive lives.

###

In addition to researchers from Hospital for Special Surgery and Weill Cornell Medical College, investigators from the Brigham and Women's Hospital, Harvard Medical School contributed to the study. This research was supported by grants from the National Institutes of Health.

About Hospital for Special Surgery

Founded in 1863, Hospital for Special Surgery (HSS) is a world leader in orthopedics, rheumatology and rehabilitation. HSS is nationally ranked No. 1 in orthopedics and No. 3 in rheumatology by U.S. News & World Report (2007), and has received Magnet Recognition for Excellence in Nursing Service from the American Nurses Credentialing Center. In 2008 and 2007, HSS was a recipient of the HealthGrades Joint Replacement Excellence Award. A member of the NewYork-Presbyterian Healthcare System and an affiliate of Weill Cornell Medical College, HSS provides orthopedic and rheumatologic patient care at NewYork-Presbyterian Hospital at New York Weill Cornell Medical Center. All Hospital for Special Surgery medical staff are on the faculty of Weill Cornell Medical College. The hospital's research division is internationally recognized as a leader in the investigation of musculoskeletal and autoimmune diseases. Hospital for Special Surgery is located in New York City and online at www.hss.edu.

UT Southwestern Medical Center Researcher Find More severe bone infections, health complications in children linked to MRSA,

Drs. Octavio Ramilo (top) and Asunción Mejías have shown that the emergence of methicillin-resistant Staphylococcus aureus has led to more complications and longer hospital stays for children with acute bone...

DALLAS – June 30, 2008 – The emergence of methicillin-resistant Staphylococcus aureus (MRSA) as a major pathogen has led to more complications and longer hospital stays for children with acute bone infections, UT Southwestern Medical Center researchers report.

Acute osteomyelitis, a bone infection that predominantly occurs in children, is usually caused by the staph bacteria. Treatment has traditionally been straightforward because most S. aureus bacteria can be killed with existing antibiotics.

Recently, however, more children with osteomyelitis have been developing the more severe, antibiotic-resistant, community-associated MRSA, resulting in more complications and prolonged antibiotic therapy and hospital stays.

"This study shows the transition from the normal S. aureus to the methicillin-resistant one that everybody calls the superbug," said Dr. Octavio Ramilo, professor of pediatrics at UT Southwestern and senior author of a study available online and in the July/August issue of the Journal of Pediatric Orthopaedics. "What's important about this is not only that MRSA infections are harder to treat because they are more resistant to the traditional antibiotics, but they are also more aggressive and cause more severe disease manifestations. This is reflected very clearly in this study."

Dr. Asunción Mejías, assistant professor of pediatrics and co-lead author, said MRSA isn't a new problem among children.

"But the MRSA that we used to see was acquired in the hospital," she said. "This is a different strain that patients acquire in the community. Now, we see kids with osteomyelitis who have bone abscesses in the legs and who get blood clots that lead to pulmonary embolisms.

"We don't want to alarm parents, but kids who limp or have backaches and fever after an otherwise minor trauma need to be evaluated by a physician," Dr. Mejías said.

Dr. Ramilo said osteomyelitis might be more common in children because kids tend to be more accident-prone. Most commonly, the bones get infected when bacteria reach the bone through the blood supply. It is thought that minor trauma to the bone facilitates the start of the infection.

For the study, researchers culled the medical records of 290 children admitted to Children's Medical Center Dallas between January 1999 and December 2003 with acute osteomyelitis. The median age of those surveyed was 6 years and most children were white or Hispanic. Sixty percent were male. Symptoms such as localized pain, fever, tenderness, swelling and limping were observed in more than half the patients.

The researchers divided the patient population into two groups (January 1999 to June 2001 and July 2001 to December 2003) to verify whether MRSA infections were becoming more common and more severe.

They then compared patients with MRSA osteomyelitis to children with non-MRSA osteomyelitis, which included those with methicillin-sensitive S. aureus (MSSA) infections. They also reviewed outcomes, including duration of fever, the type and length of antibiotic therapy, and the frequency of complications, such as muscle inflammation, bone abscesses, disseminated disease and the need to drain the bone surgically.

Though the clinical characteristics of the participants didn't change significantly between the first and second study periods, children who were treated in the latter period for osteomyelitis fared far worse, possibly because MRSA infections were more common, Dr. Ramilo said.

For example, in the second study period, bone abscesses were observed in 69 percent of the patients with MRSA osteomyelitis versus 26 percent among those with MSSA infections. Children admitted with MRSA osteomyelitis during the second study period also spent an average of 42 days on antibiotics, almost two weeks longer than those diagnosed with MSSA.

Dr. Ramilo said the number of children who needed surgery was also striking. Seventy-eight percent of the patients with MRSA required surgery, compared with 49 percent of those with MSSA.

He said the findings underscore the need for multicenter studies to identify the best antibiotic regimens as well as the best surgical approaches for complications.

"For now, the key is to treat the infection as early as possible with appropriate antibiotics and if needed, surgical drainage of the bone," Dr. Ramilo said.

###

Other UT Southwestern researchers involved in the study were Dr. Monica Ardura, postdoctoral trainee clinician in pediatrics; Dr. Dominick Cavuoti, assistant professor of pathology; Dr. Naveed Ahmad, biostatistician in clinical research; Drs. Estrella Peromingo and Sara Guillen, international research fellows; Dr. Ali Syed, former medical student; and co-lead author Dr. Jesús Saavedra-Lozano, a former fellow in infectious diseases.

Visit http://www.utsouthwestern.org/pediatrics for additional information about UT Southwestern's clinical services in pediatrics.

This news release is available on our World Wide Web home page at http://www.utsouthwestern.edu/home/news/index.html

To automatically receive news releases from UT Southwestern via e-mail, subscribe at http://www.utsouthwestern.edu/receivenews

Dr. Octavio Ramilo -- http://www.utsouthwestern.edu/findfac/professional/0,2356,15916,00.html

Dr. Asunción Mejías -- http://www.utsouthwestern.edu/findfac/professional/0,2356,52881,00.html

Georgia Institute of Technology Research News : Tongue Drive system lets persons with disabilities operate powered wheelchairs, computers

A new assistive technology developed by engineers at the Georgia Institute of Technology could help individuals with severe disabilities lead more independent lives.

The novel system allows individuals with disabilities to operate a computer, control a powered wheelchair and interact with their environments simply by moving their tongues.

"This device could revolutionize the field of assistive technologies by helping individuals with severe disabilities, such as those with high-level spinal cord injuries, return to rich, active, independent and productive lives," said Maysam Ghovanloo, an assistant professor in the Georgia Tech School of Electrical and Computer Engineering. Ghovanloo developed the system with graduate student Xueliang Huo.

The tongue-operated assistive technology, called the Tongue Drive system, was described on June 29 at the 2008 Rehabilitation Engineering and Assistive Technology Society of North America (RESNA) Annual Conference in Washington, D.C. An article about this system is also scheduled to appear in an upcoming issue of the Journal of Rehabilitation Research and Development. This research was funded by the National Science Foundation and the Christopher and Dana Reeve Foundation.

Georgia Tech Electrical and Computer Engineering graduate student Xueliang Huo moves his tongue to direct the Tongue Drive system to move the powered wheelchair in a different direction.

o operate the Tongue Drive system, potential users only need to be able to move their tongues. Attaching a small magnet, the size of a grain of rice, to an individual's tongue by implantation, piercing or tissue adhesive allows tongue motion to direct the movement of a cursor across a computer screen or a powered wheelchair around a room.

"We chose the tongue to operate the system because unlike hands and feet, which are controlled by the brain through the spinal cord, the tongue is directly connected to the brain by a cranial nerve that generally escapes damage in severe spinal cord injuries or neuromuscular diseases," said Ghovanloo, who started working on this project about three years ago at North Carolina State University. "Tongue movements are also fast, accurate and do not require much thinking, concentration or effort."

Movement of the magnetic tracer attached to the tongue is detected by an array of magnetic field sensors mounted on a headset outside the mouth or on an orthodontic brace inside the mouth. The sensor output signals are wirelessly transmitted to a portable computer, which can be carried on the user's clothing or wheelchair.

The sensor output signals are processed to determine the relative motion of the magnet with respect to the array of sensors in real-time. This information is then used to control the movements of a cursor on the computer screen or to substitute for the joystick function in a powered wheelchair.

The system can potentially capture a large number of tongue movements, each of which can represent a different user command. A unique set of specific tongue movements can be tailored for each individual based on the user's abilities, oral anatomy, personal preferences and lifestyle.

"An individual could potentially train our system to recognize touching each tooth as a different command," explained Ghovanloo. "The ability to train our system with as many commands as an individual can comfortably remember is a significant advantage over the common sip-n-puff device that acts as a simple switch controlled by sucking or blowing through a straw."

The Tongue Drive system is also non-invasive and does not require brain surgery like some of the brain-computer interface technologies.

Georgia Tech Electrical and Computer Engineering graduate student Xueliang Huo moves his tongue to direct the Tongue Drive system to move the powered wheelchair in a different direction.

Ghovanloo's group recently completed trials in which six able-bodied individuals tested the Tongue Drive system. Each participant defined six tongue commands that would substitute for computer mouse tasks – left, right, up and down pointer movements and single- and double-click. For each trial, the individual began by training the system. During the five-minute training session, the individual repeated each of the six designated tongue movements 10 times.

During the testing session, the user moved his or her tongue to one of the predefined command positions and the mouse pointer started moving in the selected direction. To move the cursor faster, users could hold their tongue in the position of the issued command to gradually accelerate the pointer until it reached a maximum velocity.

Results of the computer access test by novice users with the current Tongue Drive prototype showed a response time of less than one second with almost 100 percent accuracy for the six individual commands. This is equivalent to an information transfer rate of approximately 150 bits per minute, which is much faster than the bandwidth of most brain-computer interfaces, according to Ghovanloo.

The researchers have also tested the ability of twelve able-bodied individuals to operate an electric-powered wheelchair with the Tongue Drive system. The next step is to test and assess the usability and acceptability of the system by people with severe disabilities, said Ghovanloo. He is teaming with the Shepherd Center, an Atlanta-based catastrophic care hospital, and the Georgia Tech Center for Assistive Technology and Environmental Access, to conduct those trials.

The research team has also begun to develop software to connect the Tongue Drive system to a wide variety of readily available communication tools such as text generators, speech synthesizers and readers. In addition, the researchers plan to add control commands, such as switching the system into standby mode to permit the user to eat, sleep or engage in a conversation while extending battery life.

"We hope this technology will reduce the need of individuals with severe disabilities to receive continuous assistance from family members or caregivers, thus significantly reducing healthcare and assistance costs," noted Ghovanloo. "This system may also make it easier for them to work and communicate with others, such as friends and family."

###

[Video available: http://gtresearchnews.gatech.edu/movies/tongue-drive.mov (Maysam Ghovanloo describing the Tongue Drive system) and http://www.gtresearchnews.gatech.edu/movies/wheelchair.mov (Xueliang Huo demonstrating the use of the system to operate a powered wheelchair)]

Canadian Medical Association Journal : Limit sucrose as painkiller for newborns

Randomized controlled trial

Using sucrose to reduce pain in newborns undergoing painful procedures should be limited to babies having blood taken (venipuncture) for the newborn screening test but not for intramuscular injections, write Dr. Anna Taddio and co-authors.

In this double-blind, randomized controlled trial of 240 newborns at Toronto's Mount Sinai Hospital, researchers found that "sucrose reduced overall pain in newborns when administered before painful medical procedures during the first 2 days after birth." However, "unexpectedly, we did not observe analgesic effects during either intramuscular injection of vitamin K in either group [newborns of diabetic and nondiabetic mothers] or during repeated heel-lancing for blood glucose monitoring in newborns of diabetic mothers."

As all newborns experience pain from medical procedures in the first days of life, the results of this study will be helpful in reducing pain responses. The authors recommend updating pain management guidelines to reflect these findings.

University of California - San Diego : A single mechanism for hypertension, insulin resistance and immune suppression

Researchers identify the underlying molecular mechanism for hypertension, insulin resistance and other metabolic complications

These fluorescent microscopic images of tissue taken from spontaneously hypertensive rats reveal activity of proteases MMP-1 and MMP-9 as bright spots. The lower image shows tissue from an SHR animal...

Many of the 75 million Americans with essential hypertension also develop diabetes and other complications in addition to their high blood pressure, and researchers have discovered a common molecular mechanism in a strain of rat that explains why such metabolic disorders arise together in mammals.

The bioengineering researchers at UC San Diego’s Jacobs School of Engineering also showed that a drug developed for unrelated purposes in humans was effective in counteracting the underlying molecular mechanism in the spontaneously hypertensive rat (SHR), a strain predisposed to develop high blood pressure.

In a paper published June 30 in the online version of Hypertension, Frank DeLano, a research scientist at UC San Diego, and Geert Schmid-Schönbein, a professor of bioengineering, describe how they successfully reversed the SHR animals’ symptoms of high blood pressure, a pre-diabetes condition called insulin resistance, and immune suppression.

H. Glenn Bohlen, a professor in the Department of Cellular and Integrative Physiology at Indiana University Medical School, wrote in an accompanying editorial in Hypertension that the new study will likely be important to people suffering from obesity as well as hypertension. “With the national and international emphasis on obesity and its attendant cardiovascular problems, there is a tendency to forget that essential hypertension affects about the same percentage of humans as does serious obesity and an even higher percentage of the population than does type 2 diabetes mellitus,” wrote Bohlen. “The elegant study by Delano and Schmid-Schönbein points to a potentially very important overlap of an insulin resistance mechanism with hypertension in the spontaneously hypertensive rat (SHR).”

The SHR strain is a model for essential hypertension in humans because both the rodent and many humans with hypertension also develop a variety of other metabolic complications when high blood pressure strikes.

In the circulation of SHR rodents, Schmid-Schönbein and DeLano found significant levels of proteases, which are enzymes that break down proteins. Natural enzyme inhibitors found in normal healthy rats did not lower the level of protease activity in the SHR strain to normal levels.

“We were looking for a common cause of diverse but concurrent metabolic problems and we were testing our theory that enhanced proteolytic activity in the circulation may be the root cause,” said Schmid-Schönbein. “In the hypertensive rat we studied, enzymes cleave extracellular portions of several protein receptors, such as the insulin receptor, so that insulin can no longer bind and facilitate normal metabolism of glucose.”

Under normal conditions, the pancreas releases insulin in the bloodstream. The molecule then binds to insulin receptors on the cell-surface membrane, which signals the cells to absorb glucose, a main source of cellular energy. However, when a cell loses the binding site for insulin on the insulin receptors, it becomes “resistant,” or unresponsive to insulin and no longer absorbs glucose in healthy amounts on cue, which is the problem in type 2 diabetes.

The researchers showed that the SHR animals have protease activity in their circulation that cleaves more than just insulin receptors. In these animals, proteases also cleave significant numbers of CD18, an important binding receptor on the surface of infection-fighting leukocytes. CD18 gives these cells the ability to adhere to the walls of blood vessels as a way to home in on infections. With the loss of CD18 receptors, leukocytes of the SHR animals are unable to bind to the wall of blood vessels, resulting in a compromised immune system.

“These results point to a single mechanism that explains multiple and diverse cell dysfunctions encountered in hypertensive rats, and they also suggest that a similar mechanism may be operating in humans suffering simultaneously from hypertension, diabetes, and other metabolic conditions,” said Schmid-Schönbein.

The team went on to test whether administration of a protease-blocking drug could reverse the multiple metabolic complications in the rat strain. They administered doxycycline, a seemingly unlikely candidate to have such a beneficial effect. Infectious disease specialists often prescribe doxycycline, an antibiotic, to counter bacterial infections. However, in laboratory tests doxycycline also blocks the activity of certain proteases in the SHR strain of rat.

The researchers found that protein receptors on the surface of SHR cells become clipped off as the animals develop hypertension. They used a novel visualization technique to show that after several weeks of ingesting doxycycline in their drinking water, the SHR rats developed cells that again bristled with normal CD18 and insulin receptors. The animals’ metabolic conditions simultaneously improved; blood pressure normalized and symptoms of immune suppression disappeared.

“These studies indicate the first time that hypertension and cell dysfunctions associated with the metabolic syndrome may be part of an enzymatic auto-digestion process in which proteases in our body become uncontrolled and break down proteins,” Schmid-Schönbein said. “Our observations provide a conceptual framework in which we can start to understand how diverse complications in the metabolic syndrome arise.”

Schmid-Schönbein said his findings will likely spark follow-up studies of this mechanism in humans.

“Even if future studies only support the clear linkage of hypertension to insulin receptor cleavage in the current study of SHRs, this observation should lead to many studies of how these two problems perhaps interact,” wrote Bohlen in the Hypertension editorial. “To what extent this interaction is part of the cause or consequences of mechanisms associated with hypertension will remain controversial for some time to come. However, it is tempting to speculate that treatment of hypertension may be inadvertently improving insulin sensitivity and likely many other abnormalities associated with cell surface receptors that have been unknowingly damaged by protease activation associated with elevated blood pressure.”

###

The research by DeLano and Schmid-Schönbein was supported by the National Institutes of Health. With support from the NIH and Leading Ventures, a San Diego-based venture capital firm, the team led by Schmid-Schönbein is exploring the cleavage of other cell-receptors involved in other important physiological processes.

Rockefeller University Press : Cellular self-eating promotes pancreatitis

To survive tough times, cells sometimes resort to a form of self-cannibalism called autophagy. But as Hashimoto et al. reveal, autophagy can have a down side, destroying the pancreas by prematurely activating a digestive enzyme.

In autophagy, a vesicle swallows a portion of cytoplasm and ferries it to the lysosome for digestion. The process is often beneficial, allowing hungry cells to recycle molecules, for example. However, the researchers previously discovered that in mice with pancreatitis the level of autophagy in pancreatic cells surges. Pancreatitis occurs when the enzyme trypsin dissolves cells from within. Normally, pancreatic cells fashion and discharge an inactive form of trypsin called trypsinogen, which remains inert until it reaches the small intestine. But if trypsinogen converts to trypsin before its release, it can damage or kill a pancreatic cell. Hashimoto et al. tested whether autophagy promotes this early activation by delivering trypsinogen to the lysosome, where enzymes turn it on.

The researchers gave mice injections of the compound cerulein, which spurs pancreatitis. Control animals suffered severe damage to the organ, which harbored numerous deteriorating cells. But rodents that lack a gene necessary for autophagy displayed almost no symptoms. To determine whether autophagy promotes trypsinogen activation, the team dosed pancreatic cells from both types of mice with cerulein. Cells from the autophagy-impaired animals carried much less activated trypsinogen than did cells from controls.

In rodents capable of autophagy, cerulein injections triggered much higher levels of trypsin activity in pancreatic tissue than did shots of saline, confirming that autophagy switches on the enzyme. The study is the first to reveal that autophagy can initiate a disease. The next step, the researchers say, is determining what triggers pancreatic cells to start eating themselves.

###

Hashimoto, D., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200712156.

Nasa Mission on Mars : NASA Images Suggest Water Still Flows in Brief Spurts on Mars

Image Left: A new gully deposit in a crater in the Centauri Montes Region. Image credit: NASA/JPL/Malin Space Science Systems


NASA photographs have revealed bright new deposits seen in two gullies on Mars that suggest water carried sediment through them sometime during the past seven years.

"These observations give the strongest evidence to date that water still flows occasionally on the surface of Mars," said Michael Meyer, lead scientist for NASA's Mars Exploration Program, Washington.
Liquid water, as opposed to the water ice and water vapor known to exist at Mars, is considered necessary for life. The new findings heighten intrigue about the potential for microbial life on Mars. The Mars Orbiter Camera on NASA's Mars Global Surveyor provided the new evidence of the deposits in images taken in 2004 and 2005.

"The shapes of these deposits are what you would expect to see if the material were carried by flowing water," said Michael Malin of Malin Space Science Systems, San Diego. "They have finger-like branches at the downhill end and easily diverted around small obstacles." Malin is principal investigator for the camera and lead author of a report about the findings published in the journal Science.

The atmosphere of Mars is so thin and the temperature so cold that liquid water cannot persist at the surface. It would rapidly evaporate or freeze. Researchers propose that water could remain liquid long enough, after breaking out from an underground source, to carry debris downslope before totally freezing. The two fresh deposits are each several hundred meters or yards long.
Image left: A new gully deposit in a crater in Terra Sirenum. Image credit: NASA/JPL/Malin Space Science Systems

The light tone of the deposits could be from surface frost continuously replenished by ice within the body of the deposit. Another possibility is a salty crust, which would be a sign of water's effects in concentrating the salts. If the deposits had resulted from dry dust slipping down the slope, they would likely be dark, based on the dark tones of dust freshly disturbed by rover tracks, dust devils and fresh craters on Mars.

Mars Global Surveyor has discovered tens of thousands of gullies on slopes inside craters and other depressions on Mars. Most gullies are at latitudes of 30 degrees or higher. Malin and his team first reported the discovery of the gullies in 2000. To look for changes that might indicate present-day flow of water, his camera team repeatedly imaged hundreds of the sites. One pair of images showed a gully that appeared after mid-2002. That site was on a sand dune, and the gully-cutting process was interpreted as a dry flow of sand.

Image Left: A colorized view of a new crater on the upper north flank of the Martian volcano Ulysses Patera. Image credit: NASA/JPL/Malin Space Science Systems

Today's announcement is the first to reveal newly deposited material apparently carried by fluids after earlier imaging of the same gullies. The two sites are inside craters in the Terra Sirenum and the Centauri Montes regions of southern Mars.

"These fresh deposits suggest that at some places and times on present-day Mars, liquid water is emerging from beneath the ground and briefly flowing down the slopes. This possibility raises questions about how the water would stay melted below ground, how widespread it might be, and whether there's a below-ground wet habitat conducive to life. Future missions may provide the answers," said Malin.

Besides looking for changes in gullies, the orbiter's camera team assessed the rate at which new impact craters appear. The camera photographed approximately 98 percent of Mars in 1999 and approximately 30 percent of the planet was photographed again in 2006. The newer images show 20 fresh impact craters, ranging in diameter from 7 feet (2 meters) to 486 feet (148 meters) that were not present approximately seven years earlier. These results have important implications for determining the ages of features on the surface of Mars. These results also approximately match predictions and imply that Martian terrain with few craters is truly young.

Mars Global Surveyor began orbiting Mars in 1997. The spacecraft is responsible for many important discoveries. NASA has not heard from the spacecraft since early November. Attempts to contact it continue. Its unprecedented longevity has allowed monitoring Mars for over several years past its projected lifetime.

NASA's Jet Propulsion Laboratory, Pasadena, manages the Mars Global Surveyor mission for the NASA Science Mission Directorate, Washington. For more information about NASA and agency programs, visit:

http://www.nasa.gov

Media contacts: Guy Webster 818-354-6278
Jet Propulsion Laboratory, Pasadena, Calif.

Erica Hupp/Dwayne Brown 202-358-1237/1726
NASA Headquarters, Washington

California Institute of Technology research news : Caltech Scientists Decipher the Neurological Basis of Timely Movement

PASADENA, Calif--Contrary to what one might imagine, the way in which each of us interacts with the world is not a simple matter of seeing (or touching, or smelling) and then reacting. Even the best baseball hitter eyeing a fastball does not swing at what he sees. The neurons and neural connections that make up our sensory systems are far too slow for this to work. "Everything we sense is a little bit in the past," says Richard A. Andersen of the California Institute of Technology, who has now uncovered the trick the brain uses to get around this puzzling problem.

Work by Andersen, the James G. Boswell Professor of Neuroscience at Caltech, and his colleagues Grant Mulliken of MIT and Sam Musallam of McGill University, offers the first neural evidence that voluntary limb movements are guided by our brain's prediction of what will happen an instant into the future. "The brain is generating its own version of the world, a 'forward model,' which allows you to know where you actually are in real time. It takes the delays out of the system," Andersen says.

The research in Andersen's laboratory is focused on understanding the neurobiological underpinnings of brain processes, including the senses of sight, hearing, balance, and touch, and the neural mechanisms of action. The lab is working toward the development of implanted neural prosthetic devices that would serve as an interface between severely paralyzed individuals' brain signals and their artificial limbs--allowing thoughts to control movement.

Research along these lines conducted at the University of Pittsburgh and Carnegie Mellon University recently allowed monkeys to feed themselves using a robotic limb that they controlled only with their thoughts. Their thoughts were picked up via an array of electrodes sitting on top of the primary motor cortex, a lower level brain region responsible for carrying out motor functions.

Andersen's group focuses on a more high-level area of cortex called the posterior parietal cortex (PPC), which is where sensory stimuli are actually transformed into movement plans.

In their experiments, Andersen and his colleagues trained two monkeys to use a joystick to move a cursor on a computer screen from a small red circle into a green circle, while keeping their gaze fixed on the red circle. The monkeys typically generated curved trajectories, but to increase the curvature one monkey was trained to move the cursor around an obstacle. The obstacle (a large blue circle) was placed between the initial location of the cursor and the target circle, and the monkey had to guide the cursor around the obstacle, without touching it, and over to the green circle. As the monkeys conducted the tasks, electrodes measured the activity of neurons in the PPC. This allowed Andersen and his colleagues to monitor signals--commands for movement--in real time.

The studies showed that neurons in the PPC produce signals that represent the brain's estimation of the current and upcoming movement of the cursor. "An internal estimate of the current state of the cursor can be used immediately by the brain to rapidly correct a movement, avoiding having to rely entirely on late-arriving sensory information, which can result in slow and unstable control," Mulliken says.

"The idea is that you feed back the command you make for movement into those areas of the brain that plan the movement (i.e., the PPC)," Andersen says. "The signal about the movement taking place is adjusted to be perfectly aligned in time with the actual movement--what you're moving in your head matches with what you're moving in the real world." The effect is akin to an athlete visualizing his performance in his mind. Studies have previously shown that these simulations of movement trajectories run through the posterior parietal cortex, and run at actual speed, taking the same amount of time as the activity would in real life.

In the Pittsburgh robotic arm study, the neural signal driving the robotic limb was what is known as a "trajectory signal," which represents the path that must be taken to move from one point to another, like using a computer mouse to drag an object across a screen. Previously Andersen's lab had shown that a different signal in the posterior parietal cortex, called the "goal signal," can also be used to directly jump an object from one point to another.

"This goal signal is much faster for reaching a goal than a trajectory signal," Andersen says. "Fast goal decoding is very advantageous for rapid sequences such as typing. Our new study shows that the posterior parietal cortex codes the trajectory as well as the goal, which makes this brain area an attractive target for neural prosthesis. Not only does this increase the versatility and the number of prosthetic applications, but it also makes the decoding easier since the trajectories can be better estimated if the goal is known."

The paper, "Forward Estimation of Movement State in Posterior Parietal Cortex," will be published in a future print issue the Proceedings of the National Academy of Sciences but is now available online. First author, Grant Mulliken, was a graduate student at Caltech and is now a postdoctoral fellow at the Massachusetts Institute of Technology; coauthor Sam Musallam was a postdoctoral fellow at Caltech and is currently an assistant professor at McGill University in Montreal, Canada.

###

Contact: Kathy Svitil (626) 395-8022 ksvitil@caltech.edu

Visit the Caltech Media Relations website at: http://pr.caltech.edu/media.

California Institute of Technology research news :Caltech Helps Open the Universe in "WorldWide Telescope"

Caltech Helps Open the Universe in "WorldWide Telescope"

PASADENA, Calif.-- Panoramic images of the sky obtained at Palomar Observatory and by the Two Micron All Sky Survey (2MASS), plus pointed observations from the Spitzer Space Telescope, form a significant part of the "World Wide Telescope" (WWT), a new product released today by Microsoft aimed at bringing exploration of the Universe and its many wonders to the general public.

WorldWide Telescope is a rich Web application that combines imagery from the best ground- and space-based observatories across the world, stitching together terabytes of high-resolution images of celestial bodies and displaying them in a way that relates to their actual relative position in the sky. Using their own computers, people from all walks of life can freely browse through the solar system, galaxy, and beyond. They can choose which telescope they want to look through, including NASA's Hubble, Chandra, and Spitzer Telescopes, to view the locations of planets in the night sky--in the past, present or future--and the universe through different wavelengths of light to reveal hidden structures in other parts of the galaxy. Taken as a whole, the application provides a top-to-bottom view of the science of astronomy.

"The progression from William and Caroline Herschel's visual catalogs in the late 1700s to digital pictures available to anyone with a home computer shows the amazing advances in astronomy over two centuries, and also the continuity of our subject," says Wallace Sargent, Ira S. Bowen Professor of Astronomy at the California Institute of Technology. Scientists at Caltech provided many of the images displayed in WWT and are working with the Microsoft team to enrich and expand the content and the educational possibilities offered by the application.

The WWT combines cosmic imagery and educational content from many sources, including major ground-based sky surveys. One of those was the survey conducted at Palomar Observatory in visible light; another was the 2MASS survey in the infrared. Both projects are managed and distributed at Caltech's Infrared Processing and Analysis Center (IPAC).

Palomar Observatory, which is operated by Caltech, has conducted a number of major sky surveys since the 1950s, initially with photographic plates, and now with modern digital detectors. The surveys are conducted using the 48-inch Samuel Oschin Telescope.

Images of the northern sky used in the WWT are based on the second major photographic Palomar Sky Survey (POSS-II), conducted in the late 1980s and early 1990s. A digital version of this survey was produced in collaboration with the Space Telescope Science Institute in Baltimore, Maryland, and processed and calibrated at Caltech under the leadership of Caltech Professor of Astronomy S. George Djorgovski. This survey has detected over 50 million galaxies and about a billion stars, as well as many other interesting objects. Additional images for the WWT were provided by the currently ongoing Palomar-Quest digital sky survey. All of the images were processed at Caltech's Center for Advanced Computing Research (CACR). "Astronomy is now a computationally intensive field. We hope to use the WWT as a gateway to learning, not just about astronomy, but also about information technology and computational thinking, which are so important for all aspects of modern scholarship and society," says Roy Williams of CACR.

Using data collected from twin 1.3-meter telescopes in Arizona and Chile over a 3.5-year period, 2MASS produced the first high-resolution digital survey of the complete infrared sky, providing the international astronomical community with an unprecedented global view of the Milky Way and nearby galaxies. 2MASS was the most thorough census ever made of the Milky Way galaxy and the nearby universe. It detected infrared wavelengths, which are longer than the red light in the rainbow of visible colors. Infrared light penetrates dust more effectively than visible light, so it is particularly useful for detecting objects obscured within the Milky Way, as well as the faint heat of very cool objects that give off very little visible light of their own.

"Humans have always been fascinated by the universe, by the starry sky," says Djorgovski. "We are hoping to help reignite that sense of wonder and exploration among students and curious people everywhere."

More information is available at the following:

The Digital Palomar Observatory Sky Survey website: http://www.astro.caltech.edu/~george/dposs/

The Palomar-Quest sky survey website: http://palquest.org/

The "Big Picture" outreach website: http://bigpicture.caltech.edu/

Palomar Observatory website: http://www.astro.caltech.edu/palomar/

The Samuel Oschin Telescope: http://www.astro.caltech.edu/palomar/sot.html

The Center for Advanced Computing Research website: http://www.cacr.caltech.edu/

Caltech's Infrared Processing and Analysis Center: http://ipac.caltech.edu.

WorldWide Telescope can be accessed at http://www.worldwidetelescope.org/

Wallace Sargent's description of the POSS-II survey: http://www.astro.caltech.edu/~wws/poss2.html

###

Contact: S. George Djorgovski Caltech Astronomy george@astro.caltech.edu (626) 395-4415

Roy Williams Caltech Center for Advanced Computing Research roy@cacr.caltech.edu (626) 395-3670

Kathy Svitil (626) 395-8022 ksvitil@caltech.edu

Visit the Caltech Media Relations website at: http://pr.caltech.edu/media.

California Institute of Technology research news : Getting Better with a Little Help from Our "Micro" Friends

PASADENA, Calif.-- A naturally occurring molecule made by symbiotic gut bacteria may offer a new type of treatment for inflammatory bowel disease, according to scientists at the California Institute of Technology.

"Most people tend to think of bacteria as insidious organisms that only make us sick," says Sarkis K. Mazmanian, an assistant professor of biology at Caltech, whose laboratory examines the symbiotic relationship between "good" bacteria and their mammalian hosts. Instead, he says, "bacteria can be beneficial and actively promote health."

For example, the 100 trillion bacteria occupying the human gut have evolved along with the human digestive and immune systems for millions of years. Some harmful microbes are responsible for infection and acute disease, while "other bacteria, the more intelligent ones, have taken the evolutionary route of shaping their environment by positively interacting with the host immune system to promote health, which gives them an improved place to live; it's like creating bacterial nirvana," says Mazmanian.

If bacteria are actively modifying the gut, their work would have to be mediated by molecules. In their recent work, Mazmanian and his colleagues have identified one such molecule, a sugar called polysaccharide A, or PSA, which is produced by the symbiotic gut bacterium Bacteroides fragilis. They have termed this molecule a "symbiosis factor," and predict that many other bacterial compounds with diverse beneficial activities await discovery.

To identify the molecule and its action, the collaborative team, which included Dennis L. Kasper, Professor of Microbiology and Molecular Genetics at Harvard Medical School, used experimental mice and induced changes to their intestinal bacteria by exposing them to a pathogenic bacterium called Helicobacter hepaticus. This microbe causes a disease in the mice that is similar to Crohn's disease and ulcerative colitis. However, when the animals were co-colonized with B. fragilis, they were protected from the disease--as were animals that were given oral doses of just the PSA molecule.

In particular, Mazmanian and his colleagues found that PSA induced particular immune-system cells called CD4+ T cells to produce interleukin-10 (IL-10), a molecule that has previously been shown to suppress inflammation--and offer protection from inflammatory bowel disease. "Thus, bacteria help reprogram our own immune system to promote health," he says.

"The most immediate and obvious implication is that PSA may potentially be developed as a natural therapeutic for inflammatory bowel disease," says Mazmanian.

Inflammatory bowel disease, a constellation of illnesses that cause inflammation in the intestines, including ulcerative colitis and Crohn's disease, is estimated to affect one million Americans. The rates of inflammatory bowel diseases have skyrocketed in recent years; for example, the incidence of Crohn's disease, a condition that causes debilitating pain, diarrhea, and other gastrointestinal symptoms, has increased by 400 percent over the past 20 years.

The current research, along with other work by Mazmanian and June L. Round, a Caltech postdoctoral researcher, suggests that the interplay between various groups of bacteria living in the intestines has profound effects on human health.

This notion gels with the so-called "hygiene hypothesis." The hypothesis, first proposed two decades ago, links modern practices like sanitation, vaccination, a Western diet, and antibiotic use, which reduce bacterial infections, to the increased prevalence of a variety of illnesses in the developed world, including inflammatory bowel disease, asthma, multiple sclerosis, and Type 1 diabetes. However, it is now clear that increased living standards and antibacterial drugs affect not only infectious microbes, but all of the beneficial ones that we may depend on for our well-being.

"Through societal measures we have changed our association with the microbial world in a very short time span. We don't have the same contact with microbes as we have for millions of years--we just live too clean now," Mazmanian says. So while it is useful to eliminate disease-causing organisms, "perhaps disease results from the absence of beneficial bacteria and their good effects," he suggests. "This study is the first demonstration of that. What it hopefully will do is allow people to re-evaluate our opinions of bacteria. Not all are bad and some, maybe many, are beneficial."

The article, "A microbial symbiosis factor prevents intestinal inflammatory disease," will be featured on the cover of the May 29 issue of the journal Nature. Mazmanian's coauthors are June L. Round of Caltech and Dennis L. Kasper of Harvard Medical School. ###

Contact: Kathy Svitil (626) 395-8022 ksvitil@caltech.edu

Visit the Caltech Media Relations website at: http://pr.caltech.edu/media

Ecole Polytechnique Fédérale de Lausanne New efficiency benchmark for dye-sensitized solar cells

In a paper published online June 29 in the journal Nature Materials, EPFL professor Michael Graetzel, Shaik Zakeeruddin and colleagues from the Changchun Institute of Applied Chemistry at the Chinese Academy of Sciences have achieved a record light conversion efficiency of 8.2% in solvent-free dye-sensitized solar cells. This breakthrough in efficiency without the use of volatile organic solvents will make it possible to pursue large scale, outdoor practical application of lightweight, inexpensive, flexible dye-sensitized solar films that are stable over long periods of light and heat exposure.

Dye-sensitized solar cell technology, invented by Michael Grätzel at EPFL in the 1990s, shows great promise as a cheap alternative to expensive silicon solar cells. Dye-sensitized cells imitate the way that plants and certain algae convert sunlight into energy. The cells are made up of a porous film of tiny (nanometer sized) white pigment particles made out of titanium dioxide. The latter are covered with a layer of dye which is in contact with an electrolyte solution. When solar radiation hits the dye it injects a negative charge in the pigment nanoparticle and a positive charge into the electrolyte resulting in the conversion of sunlight into electrical energy. The cells are inexpensive, easy to produce and can withstand long exposure to light and heat compared with traditional silicon-based solar cells. Currently, state-of-the-art dye-sensitized cells have an overall light conversion efficiency greater than 11%, still about two times lower than silicon cell technology. A major drawback to the dye-sensitized cell technology is the electrolyte solution, which is made up of volatile organic solvents and must be carefully sealed. This, along with the fact that the solvents permeate plastics, has precluded large-scale outdoor application and integration into flexible structures.

To overcome these limitations, Grätzel and his colleagues developed a new concept -- a mixture of three solid salts as an alternative to using organic solvents as an electrolyte solution. When the three solid components are mixed together in the right proportion they turn into a melt showing excellent stability and efficiency. Grätzel is confident that further development of these types of electrolyte mixtures will lead to large-scale practical application of dye-sensitized solar cell technology, reinforcing solar energy's role as a cornerstone of alternative energy production.

Massachusetts General Hospital International team identifies 21 new genetic risk factors for Crohn's disease

Study combines efforts of 3 research groups, brings total risk sites to 32

An international consortium of Crohn's disease researchers has combined data from three independent studies to identify 21 new genetic variants associated with the inflammatory bowel disorder, bringing the total number of risk factors to 32. Several of these are involved with the immune system's inital response to pathogens, supporting earlier evidence that disruptions in a process called autophagy may lead to the disorder's characteristic immune system overactivity. The report will appear in the journal Nature Genetics and is receiving early online release.

"This greatly increases our knowledge of the genetic architecture of Crohn's and gives us more detailed insight into the biological underpinnings of the disease," says Mark Daly, PhD, of the Massachusetts General Hospital (MGH) Center for Human Genetic Research and the Broad Institute of MIT and Harvard, the report's senior author. "Better understanding of the precise functions of these genes and the molecular effects of Crohn's-associated variants should lead us to novel strategies for therapies and, someday, prevention."

In 2007 three separate research teams – a North American-based team, involving Daly and colleagues at six other institutions and clinical sites; a U.K. team supported by the Wellcome Trust; and a group of French and Belgian investigators – each published genome-wide association studies (GWAS) of Crohn's disease that, combined with earlier studies, brought the total number of Crohn's-associated gene sites to 11. Those explained only a small proportion of the heritability of Crohn's, which affects nearly half a million people in the U.S.

Since the power of any GWAS is limited by the number of samples available for screening, the three teams combined their data through a process called meta-analysis, allowing the comparison of data from more than 3,200 Crohn's patients with more than 4,800 controls. That was supplemented by an analysis of new data from an additional 3,700 patients and matching controls.

Both of those analyses strongly confirmed the 11 previously-identified sites and found an additional 21 areas associated with susceptibility to Crohn's. While the newly identified sites are not as strong as those found in earlier studies, they continue to build a picture of factors leading to the inappropriate immune-system activation that characterizes the disorder.

"It's amazing that all of the genes indentified in GWAS studies of Crohn's so far align with the pathways that we know are disrupted, systems that sense the presence of microbes and effectively clear them from the body." says Ramnik Xavier, MD, of the Center for the Study of Inflammatory Bowel Disease in the MGH Gastroenterology Unit and the MGH Center for Computational and Integrative Biology, a co-author of the Nature Genetics study. "Mapping the internal circuitry of these systems and identifying the molecular switches that control those circuits should lead to better targeted drugs for Crohn's and other inflammatory bowel diseases." Daly is an assistant professor of Medicine at Harvard Medical School and Xavier is an associate professor.

###

Lead author Jeffrey Barrett of the University of Oxford led the extensive meta-analysis in conjuntion with Daly and investigators at the University of Liege, Belgium, and the University of Chicago. In total, the effort constituted a collaboration between clinical genetic researchers from 25 institutions across North America – including Yale University, University of Pittsburgh, University of Montreal, University of Toronto, Johns Hopkins University, and Cedars-Sinai Medical Center in Los Angeles – the United Kingdom, Belgium and France. The team is committed to further advancing these results in collaboration with investigators from additional countries. Support for the study came from several organizations, including the National Institute of Diabetes and Digestive and Kidney Diseases, through the Inflammatory Bowel Disease Genetic Consortium.

Massachusetts General Hospital (www.massgeneral.org), established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, systems biology, transplantation biology and photomedicine.

University of Illinois at Chicago researchers make promising finding in severe lung disease

Researchers at the University of Illinois at Chicago have identified a novel function for an enzyme that plays a role in the tissue injury in acute respiratory distress syndrome, also known as ARDS.

The finding offers a new therapeutic target for the prevention and treatment of lung inflammation and injury. The research will be published in the journal Nature Immunology later this year and online June 29.

ARDS is an often fatal complication of bacterial infections, blood transfusions, overdoses of some medications, or traumatic injury. According to the National Heart, Lung, and Blood Institute, it affects nearly 150,000 people each year in the United States.

In ARDS, the lungs become swollen with water and protein, and breathing becomes impossible, leading to death in 30 percent to 40 percent of cases. There is no effective treatment.

It has previously been shown that the enzyme, called nonmuscle myosin light-chain kinase, or MYLK, plays a pivotal role in the disruption of the endothelial barrier -- a single thin layer of cells that line blood vessels -- which prevents water and protein from accumulating in tissues.

In addition to the disruption of the endothelial barrier and build-up of water in lungs in ARDS, a circulating blood cell, the neutrophil, "migrates into lung tissue and, when activated, can cause profound injury," said Jingsong Xu, assistant professor in pharmacology and dermatology and lead author of the paper.

Neutrophils are the most common type of white blood cells and are critical to what is called the innate immune response. They normally engulf and destroy invading bacteria and fungi and act as the first line of immune system defense.

In acute respiratory distress syndrome, they misfire and attack healthy tissue.

"Although there have been many studies into how MYLK disrupts the endothelial barrier, no one has investigated how MYLK functions to regulate the neutrophil transmigration into tissues," said Xu. "We decided to look at this."

The researchers found that MYLK was essential to the movement of neutrophils through the endothelial barrier. It unleashes a cascade of molecular events inside the neutrophil that changes the cell's shape, which is necessary for adhesion and migration.

"To our surprise, the pathway was a completely novel one that did not involve the well-studied and expected target of (the enzyme)," Xu said.

The unexpected finding of a novel pathway "opens up a completely new set of possible therapeutic targets for the prevention and treatment of this deadly disease," said Dr. Asrar Malik, distinguished professor, head of pharmacology and co-author on the paper.

###

The study was supported by grants from National Institutes of Health. Xiao-Pei Gao, Ram Ramchandran, You-Yang Zhao and Stephen Vogel of UIC's department of pharmacology also contributed to the study.

For more information about UIC, visit http://www.uic.edu.

Wellcome Trust research team find Complexity of Crohn's disease revealed as 'gene' count tops 30

New research has trebled the number of genetic regions known to be implicated in Crohn's disease, a form of inflammatory bowel disease, to over thirty. The research, published today in the journal Nature Genetics, has identified a number of potential new targets for drug development as well as providing surprising new links between the condition and other common diseases including asthma.

Crohn's disease affects between 1 in 500 and 1 in 1000 people within the UK, causing inflammation of gastrointestinal tract and leading to pain, ulcers and diarrhoea. The disease can strike at any age, but onset is typically between 15 and 40 years old. As many as 80% of people suffering from the disease will require surgery at some point.

Previous studies have already identified 11 genes and loci (regions of the genome typically including one or more genes) that increase susceptibility to the disease. Now an international collaboration of researchers has identified a further 21 new genes and loci. The team of scientists and clinicians involved used DNA samples from almost 12,000 people. Many were from UK patient collections and analysed originally in the Wellcome Trust Case Control Consortium – the largest study ever undertaken into the genetics underlying common diseases – with others coming from European and North American collections.

"We now know of more than thirty genetic regions that affect susceptibility to Crohn's disease," says Dr Jeffrey Barrett from the Wellcome Trust Centre for Human Genetics at the University of Oxford, lead author of the study. "These explain only about a fifth of the genetic risk, which implies that there may be hundreds of genes implicated in the disease, each increasing susceptibility by a small amount.

"Whilst this study shows the power of genome wide association studies to reveal the genetics behind common diseases, it also highlights the complexity of diseases such as Crohn's."

Genome wide association studies have led to an explosion in the number of genes known to be implicated in complex diseases such as diabetes, heart disease and Crohn's disease. The first two Crohn's disease susceptibility genes were discovered in 2001, followed by a third in 2006. The Wellcome Trust Case Control Consortium and parallel studies took that number above ten the following year using genome wide association studies. This number has now almost trebled to thirty-two.

Amongst the findings are loci containing genes known to be implicated in a number of other common diseases including diabetes, rheumatoid arthritis and psoriasis. However, the genetic relationship between Crohn's and these other diseases is not always straightforward. For example, the genetic variant PTPN2 appears to increase susceptibility to both Crohn's disease and type 1 diabetes. But the similarly named PTPN22 increases the risk of developing type 1 diabetes, yet appears to offer protection from Crohn's.

Although some of the disease connections were unsurprising – there is already a known epidemiological correlation between Crohn's disease and psoriasis, for example – the ORMDL3 gene on chromosome 17 provided the most unexpected link. ORMDL3 was already known to be a genetic risk factor for childhood asthma, but until now, no epidemiological link had ever been seen between asthma and Crohn's disease.

"It's too early for us to say how Crohn's disease and many of these other diseases, including asthma, are linked at a biological level," says Dr Miles Parkes, Consultant Gastroenterologist at Addenbrooke's Hospital and the University of Cambridge, who also worked on the study. "However, we are building up a picture of the biology underlying Crohn's disease, and the more we understand about the underlying biology of these diseases, the better equipped we will be to treat them.

"Studies such as this are not about developing diagnostic tests, but about identifying targets for new drugs therapies. Crohn's disease can be a very serious condition, often requiring surgery, and the sooner we can understand the underlying causes, the sooner we will be able to devise new treatments to help our patients."

Some of the most likely candidates for so-called "druggable" targets include the CCR6 gene, which is thought to be part of the signalling machinery that causes white blood cells in the gut to become over-active, leading to inflammation. These particular white blood cells, known as Th17 cells, are also present in inflamed joints, implying that CCR6 may also be relevant to rheumatoid arthritis, and therefore of added interest to the pharmaceutical industry.

"Genetics, and particularly the large scale approach of genome wide association studies, offers much hope for understanding the biological causes of complex diseases," says Dr Mark Walport, Director of the Wellcome Trust. "Studies such as this also highlight the important relationships between different diseases and, as such, may offer valuable insights into the pathways that lead to common symptoms such as inflammation."

###

The collection of samples was supported by the National Association for Colitis and Crohn's Disease.

New York University Rutgers study shows how using mental strategies can alter the brain's reward circuitry

The cognitive strategies humans use to regulate emotions can determine both neurological and physiological responses to potential rewards, a team of New York University and Rutgers University neuroscientists has discovered. The findings, reported in the most recent issue of the journal Nature Neuroscience, shed light on how the regulation of emotions may influence decision making.

Previous research has demonstrated these strategies can alter responses to negative events. However, less understood is whether such strategies can also efficiently regulate expectations of a future reward or a desired outcome. Scientists have already determined that the expectation of a potential reward brings about positive feelings and aids recognizing environmental cues that predict future rewards. Central to this process is the role of the striatum, a multi-faceted structure in the brain that is involved in reward processing—and which is especially engaged when potential rewards are predicted or anticipated.

However, the striatum signal is not always beneficial. Its activity also correlates with drug-specific cravings, most likely increasing urges to partake in risk-seeking behavior in the pursuit of rewards that are detrimental. Therefore, understanding how to regulate or control the positive feelings associated with reward expectation is an important line of inquiry.

The NYU study was conducted by a team of researchers from the laboratory of NYU Professor Elizabeth Phelps, who co-authored the work with Mauricio R. Delgado, now a professor at Rutgers University, and M. Meredith Gillis, an NYU graduate student. They sought to better understand the influence of emotional regulation strategies on the physiological and neural processes relevant to expectations of reward.

The study's subjects were presented with two conditioned stimuli, a blue and a yellow square that either predicted or did not predict a potential monetary reward. Prior to each trial, participants were also given a written cue that instructed them to either respond to the stimulus ("think of the meaning of the blue square, such as a potential reward") or regulate their emotional response to the stimulus ("think of something blue in nature that calms you down, such as the ocean").

Skin conductance responses (SCRs) of the participants were taken at the beginning of each conditioned stimulus. These served as a behavioral measure of physiological reaction potentially related to reward anticipation.

The results showed that the participants' emotion regulation strategies could influence physiological and neural responses relevant to the expectation of reward. Specifically, results from the SCRs revealed that the subjects' emotion regulation strategies decreased arousal that was linked to the anticipation of a potential reward.

"Our findings demonstrated that emotion regulation strategies can successfully curb physiological and neural responses associated with the expectation of reward," said Delgado. "This is a first step to understanding how our thoughts may effectively control positive emotions and eventual urges that may arise, such as drug cravings."

###

The work was supported by the James S. McDonnell Foundation, the Beatrice and Samuel A. Seaver Foundation, and the National Institute on Drug Abuse.

Harvard University Research Team Find New source of heart stem cells discovered

Finding offers hope of eventually being able to regenerate damaged tissue

Harvard Stem Cell Institute(HSCI) researchers at Children’s Hospital Boston are continuing to document the heart’s earliest origins. Now, they have pinpointed a new, previously unrecognized group of stem cells that give rise to cardiomyocytes, or heart muscle cells. These stem cells, located in the surface of the heart, or epicardium, advance the hope of being able to regenerate injured heart tissue.
This finding, published online by the journal Nature, comes on the heels of parallel cardiac stem cell discoveries in 2006, by HSCI scientists at both Children’s and Massachusetts General Hospital (MGH).Then, the Children’s team found that a specific stem cell or progenitor, marked by expression of a gene called Nkx2-5, forms many components of the heart: heart muscle cells, vascular smooth muscle cells, and the endothelial cells lining blood vessels in the heart’s left-sided chambers. The team at MGH found a related progenitor, marked by expression of the Isl1 gene, that produces these same cell-types in the right-sided heart chambers.
Now, researchers at Children’s have shown that heart muscle cells can also be derived from a third type of cardiac progenitor, located within the epicardium and identifiable through its expression of a gene called Wt1. “There’s a lot of interest in finding places to obtain new cardiomyocytes, because in heart failure, you lose cardiomyocytes, so the only way to reverse heart failure is to make more of these cells,” said William Pu, a pediatric cardiologist at Children’s Hospital and HSCI Principal Faculty member who was the study’s senior investigator.
Although epicardial cells are known to give rise to smooth muscle and endothelial cells during coronary vessel formation, nobody previously thought that epicardial cells might turn into cardiomyocytes. “I couldn’t believe it at first, myself,” said Bin Zhou, a research fellow in Pu’s laboratory and the study’s first author.
The results were independently corroborated by researchers from the University of California, San Diego (UCSD). Using a different genetic marker, Tbx18, the UCSD team also showed that cardiomyocytes can be derived from the epicardium: their study will be published in the same issue of Nature.
Pu and Zhou showed that a specific population of cells in the epicardium, marked by Wt1 expression, not only differentiated into cardiomyocytes, but also smooth muscle cells, endothelial cells, and fibroblasts (found in connective tissue).
“If you’re going to regenerate a tissue, you need to regenerate the whole tissue, not just the cardiomyocytes,” said Pu. “This progenitor population contains all the potential to regenerate multiple tissue types within the heart.” In recent years, the scientific literature has described many progenitors for cardiomyocytes, Pu added, but the markers used frequently did not play a direct role in heart development. For example, Sca-1 and c-Kit are markers that most stem cells express throughout the body, with no cardiac or developmental specificity.
“I think our best chance of getting a cell to do what we want is to modify what it was designed to do,” Pu elaborated. “Some of these other progenitors were isolated in the adult heart, but we don’t know what they do in the normal heart, and what they’re related to in the embryo. However, we clearly know what progenitors expressing Wt1, Nkx2-5, and Isl1 do in the fetus: They can make fibroblasts, blood vessels, and cardiomyocytes. Therefore we think we have a good shot, in the adult heart, of recapitulating these events.”
Pu considers his and Zhou’s discovery to be a fortunate accident. They were trying, instead, to study a different gene, GATA4, by deleting it in the epicardium. “The tool we created for that experiment irreversibly marks the cells involved, so you can see where their descendants are headed in normal development,” Pu explained. “Unexpectedly, we saw that these epicardial cells were becoming cardiomyocytes — it was a lucky observation.”
Using an enzyme called Cre recombinase, Pu and Zhou labeled epicardial cells in live mouse embryos with red fluorescent protein (RFP). Each time the Wt1 gene in these cells was activated, RFP lit up. Since the marker is inherited by descendants of the Wt1-expressing cell, the researchers could identify these descendants by looking for RFP.
“If the marker shows up in a cardiomyocyte, then I know that cardiomyocyte came from the Cre-expressing progenitor,” said Pu.
At the moment, scientists are still trying to figure out whether and how the Wt1-expressing progenitors relate to the progenitors reported in 2006.
“What we think is that very early on, our particular progenitor expresses Nkx2-5 and Isl1, but quickly loses expression of both and starts expressing Wt1,” said Pu. “Think of a lineage hierarchy with Nkx2-5 and Isl1 at the top, and Wt1 as a branch. These two lineages separate pretty early, before the heart is present in the embryo. However, the Wt1-expressing progenitor may retain some of the developmental capabilities of the progenitors expressing Nkx2-5 and Isl1.”
Pu and Zhou now want to know whether the epicardium in an adult mouse could be induced to make cardiomyocytes. “If so, obviously this would be much more translatable to human studies,” Pu said. Other ongoing questions are whether this newly discovered progenitor is truly multipotent (able to turn into all other cell types), how multipotency is controlled, and whether this can be used therapeutically to benefit adults with heart failure.
The fact that the Wt1-expressing progenitors can also differentiate into fibroblasts in the developing heart suggests that they can contribute to scar formation in the adult heart after injury, Pu added. “But if we can turn the progenitors away from making scars, and instead turn them towards making cardiomyocytes, that would be pretty exciting.”
Put another way, Pu and Zhou would love to learn what controls a progenitor’s choice — to become a fibroblast, a smooth muscle cell, or a cardiomyocyte — and develop ways of “biasing progenitors to make the choice or choices we want,” says Pu. “We still don’t know how we can manipulate these progenitors, and there’s no way to predict which ones will be useful. But I think having more choices is good, because then hopefully one of them will work.”

© 2008 by the President and Fellows of Harvard College

MIT Research : Media Lab celebrates co-founder Davenport's career

Symposium honors interactive media pioneer's legacy
David Chandler,
MIT News Office
June 25, 2008
Dozens of Media Lab faculty and alums gathered for a daylong symposium Friday, June 20, to celebrate the career of Glorianna Davenport, head of the lab's Media Fabrics group and a longtime innovator in film, video, interactive media and new ways of storytelling.
The event was in honor of Davenport's retirement after more than three decades at MIT, where she initially worked in the Film/Video Section before co-founding the Media Lab in 1985. In 2000, she was a co-founder of Media Lab Europe, based in Dublin. Over the years, dozens of her graduate students have gone on to found innovative companies, and many of them returned to describe their work at the symposium (or "media jam session," as the program described the event).
"I'm a media junkie," Davenport said at the event, held in the Media Lab's Bartos auditorium. "Not so much for the media that's out in the world," she explained, "but for using video to understand what I see."
That concept of using video as a tool for understanding has been a key element of Davenport's work through the years--both in her own creative endeavors, and in the methods she encourages her students to try. "There's no such thing as an unbiased story," she said. "When you play it back, it's never like it was."
That has often been a revelation to people, she said. "Students thought they could be neutral, but in fact the media maker is an improvisational collector."
Among the projects Davenport and her students have worked on were "Elastic Charles," in which a group of people each shot films depicting different aspects of the Charles River, and a three-year New Orleans project that resulted in a set of videodiscs (this was in the pre-DVD era) depicting how the city changed over time.
She has always emphasized the use of film or video cameras as a way of reaching a new understanding of one's environment, and has been especially interested in giving young children a chance to explore the media as a tool for learning.
One of her former students, Hans Peter Brondmo, who has created an online company called Plum.com that provides a way for people to collect and share pictures, video and audio files, documents, and web pages in an online archive, summed up the feelings that many of the event's speakers described in one way or another: "You would never say no," he said to Davenport, "though sometimes you would say something was kind of stupid. You would always inspire and encourage. You were a big inspiration to me."

MIT Research : Solar system's biggest impact scar discovered

MIT scientists solve riddle of Mars' two-faced nature

David Chandler,
MIT News Office
June 25, 2008
A new analysis of the topography and gravity of Mars by researchers at MIT and NASA has solved one of the biggest remaining mysteries in the solar system -- why the planet Mars has two completely different kinds of terrain, in its northern and southern hemispheres. In the process, they have identified what appears to be by far the largest impact scar found anywhere.
The giant basin that covers about 40 percent of the surface of Mars, sometimes called the Borealis Basin, is actually the remains of a colossal impact very early in the solar system's formation, the new analysis shows. The basin, 8,500 km across and 10,600 km long, is larger than the combined area of Asia, Europe and Australia, and about four times wider than the next-biggest impact basins known, the Hellas basin on Mars and the South Pole-Aitken basin on the moon.
The northern-hemisphere basin on Mars is one of the smoothest surfaces found anywhere in the solar system, and some geologists think it may once have contained an ocean in the early days of the planet. The southern hemisphere is high, rough, heavily-cratered terrain, which ranges from 4 to 8 km higher in elevation than the basin floor. Until now, nobody really knew why the two halves were so different.
The new findings are being reported this week in a paper in the journal Nature by MIT postdoctoral researcher Jeffrey Andrews-Hanna, Maria Zuber, MIT's E.A. Griswold Professor of Geophysics, and Bruce Banerdt of NASA-JPL. Accompanying this analysis of the elevations and gravitation of Mars, which shows clear signs of the impact basin, are two other papers that provide a theoretical analysis of the kind of impact that would have been required to create it.
The mystery of how to explain the two-faced nature of the Martian surface has been perplexing planetary scientists ever since the first comprehensive images of the surface were beamed back to Earth from spacecraft in the late 1970s. For many years, there have been two main alternatives: Either some internal process related to the planet's molten subsurface layers, or an ancient impact.
But the impact idea, originally proposed in 1984 by Steven Squyres of Cornell University, now the lead scientist on the Mars Exploration Rovers project, and Don Wilhelms of the U.S. Geological Survey, had quickly fallen into disfavor because the shape of the basin didn't seem to match the expected round shape for a crater, Andrews-Hanna says. "There wasn't any observational evidence" to support the idea, he says.
Since then, other giant impact basins, including the South Pole-Aitken basin on the moon, have been discovered that are elliptical, rather than circular. But it took a complex analysis of the Martian surface, based on both elevation data and data on its gravitational field gathered by many years of spacecraft observations, to reveal the clear elliptical shape of the Borealis Basin on Mars.
One complicating factor was that since the time of the impact -- which must have been at least 3.9 billion years ago -- giant volcanos have formed along one part of the basin rim, and created a huge region of high, rough terrain that obscures the outlines of the basin. It took a combination of the gravity data from the Mars Reconnaissance Orbiter-- which tends to reveal underlying structure -- with the data on current surface elevations from Mars Global Surveyor, to reconstruct a map of Mars elevations as they existed before the volcanos erupted.
With that reconstruction, a very clear elliptical basin shape emerged, Andrews-Hanna says. The match between a perfect ellipse and the traced boundary line between the two topographic regions was startling. And in addition to the elliptical boundary of the basin, there are also signs along part of the rim of a possible second, outer ring -- a typical characteristic of large impact basins. "An impact is really the only mechanism that can produce these large-scale elliptical depressions, these large holes in the ground," Andrews-Hanna says.
"We haven't proved the giant-impact hypothesis," Andrews-Hanna says, "but I think we've shifted the tide. The majority of the evidence is now in favor of the giant impact."When he first presented some of these results at planetary science meetings, "since the idea has been unpopular for so long, I expected people to jump on me," he says. "But people have been very receptive."
In fact, both Andrews-Hanna and Zuber, until they carried out this analysis, had been believers in the alternative theory. "I can't believe I'm involved in this," says Zuber, who is head of MIT's department of Earth, Atmospheric and Planetary Sciences. "I've been a supporter of the internal models for years." But when the evidence from the surface reconstruction became clear, she says, they had to go where the data led. "We thought, people aren't going to buy this, but you've got to say what you've got to say."
And in fact, she says, the peer-reviewers of the paper "were very positive, very constructive, they commented about how careful we were."
And identifying this huge scar of an ancient impact, she says, "is pretty exciting." Until now, nobody had clearly identified signs of any ancient impact in that size range. There are one or two even larger impacts thought to have occurred in the early solar system, a controversial theory that there was one on the innermost planet Mercury, and a widely accepted one that the Earth was struck by a planet as big as Mars, melting the crust and ejecting it into space where some of it clumped together to form our moon.
But in both of those cases, the impacts were so enormous that they completely obliterated all visible signs of the event. It is only through indirect analysis, including study of rocks brought back from the moon by the Apollo astronauts, that these giant ancient impacts have been reconstructed. In terms of impacts that left visible basins, the largest known were the Hellas basin on Mars (about 2,400 by 1,800 km) and the moon's South Pole-Aitken basin (about 2,100 by 1,500 km).
"We knew there must be impacts between these size ranges," Zuber says. "But nobody had identified one." Analysis in the theoretical papers accompanying this one show that the impacting object that produced the huge basin on Mars must have been about 2,000 km across - larger than Pluto -- and struck at an angle of about 45 degrees, creating the oval shape of the basin.
The new finding adds yet another major event to the growing list of large impacts that have been recognized over the last few decades as having shaped the planets and moons of the solar system as we know them today. "The early solar system was a very dangerous place to be a planet," Andrews-Hanna says. "But without those impacts, we wouldn't have the planets as we know them today."
The work was supported by a grant from the Mars Reconnaissance Orbiter project at NASA.