Tag Archives: health

New research shows how to make effective political arguments, Stanford sociologist says

Stanford sociologist Robb Willer finds that an effective way to persuade people in politics is to reframe arguments to appeal to the moral values of those holding opposing positions.

BY CLIFTON B. PARKER


In today’s American politics, it might seem impossible to craft effective political messages that reach across the aisle on hot-button issues like same-sex marriage, national health insurance and military spending. But, based on new research by Stanford sociologist Robb Willer, there’s a way to craft messages that could lead to politicians finding common ground.

“We found the most effective arguments are ones in which you find a new way to connect a political position to your target audience’s moral values,” Willer said.

While most people’s natural inclination is to make political arguments grounded in their own moral values, Willer said, these arguments are less persuasive than “reframed” moral arguments.

To be persuasive, reframe political arguments to appeal to the moral values of those holding the opposing political positions, said Matthew Feinberg, assistant professor of organizational behavior at the University of Toronto, who co-authored the study with Willer. Their work was published recently online in the Personality and Social Psychology Bulletin.

Such reframed moral appeals are persuasive because they increase the apparent agreement between a political position and the target audience’s moral values, according to the research, Feinberg said.

In fact, Willer pointed out, the research shows a “potential effective path for building popular support in our highly polarized political world.” Creating bipartisan success on legislative issues – whether in Congress or in state legislatures – requires such a sophisticated approach to building coalitions among groups not always in agreement with each other, he added.

Different moral values

Feinberg and Willer drew upon past research showing that American liberals and conservatives tend to endorse different moral values to different extents. For example, liberals tend to be more concerned with care and equality where conservatives are more concerned with values like group loyalty, respect for authority and purity.

They then conducted four studies testing the idea that moral arguments reframed to fit a target audience’s moral values could be persuasive on even deeply entrenched political issues. In one study, conservative participants recruited via the Internet were presented with passages that supported legalizing same-sex marriage.

Conservative participants were ultimately persuaded by a patriotism-based argument that “same-sex couples are proud and patriotic Americans … [who] contribute to the American economy and society.”

On the other hand, they were significantly less persuaded by a passage that argued for legalized same-sex marriage in terms of fairness and equality.

Feinberg and Willer found similar results for studies targeting conservatives with a pro-national health insurance message and liberals with arguments for high levels of military spending and making English the official language of the United States. In all cases, messages were significantly more persuasive when they fit the values endorsed more by the target audience.

“Morality can be a source of political division, a barrier to building bi-partisan support for policies,” Willer said. “But it can also be a bridge if you can connect your position to your audience’s deeply held moral convictions.”

Values and framing messages

“Moral reframing is not intuitive to people,” Willer said. “When asked to make moral political arguments, people tend to make the ones they believe in and not that of an opposing audience – but the research finds this type of argument unpersuasive.”

To test this, the researchers conducted two additional studies examining the moral arguments people typically make. They asked a panel of self-reported liberals to make arguments that would convince a conservative to support same-sex marriage, and a panel of conservatives to convince liberals to support English being the official language of the United States.

They found that, in both studies, most participants crafted messages with significant moral content, and most of that moral content reflected their own moral values, precisely the sort of arguments their other studies showed were ineffective.

“Our natural tendency is to make political arguments in terms of our own morality,” Feinberg said. “But the most effective arguments are based on the values of whomever you are trying to persuade.”

In all, Willer and Feinberg conducted six online studies involving 1,322 participants.

Source: Stanford News 

Penn Vet-Temple team characterizes genetic mutations linked to a form of blindness

Achromatopsia is a rare, inherited vision disorder that affects the eye’s cone cells, resulting in problems with daytime vision, clarity and color perception. It often strikes people early in life, and currently there is no cure for the condition.

One of the most promising avenues for developing a cure, however, is through gene therapy, and to create those therapies requires animal models of disease that closely replicate the human condition.

In a new study, a collaboration between University of Pennsylvania and Temple University scientists has identified two naturally occurring genetic mutations in dogs that result in achromatopsia. Having identified the mutations responsible, they used structural modeling and molecular dynamics on the Titan supercomputer at Oak Ridge National Laboratory and the Stampede supercomputer at the Texas Advanced Computing Center to simulate how the mutations would impact the resulting protein, showing that the mutations destabilized a molecular channel essential to light signal transduction.

The findings provide new insights into the molecular cause of this form of blindness and also present new opportunities for conducting preclinical assessments of curative gene therapy for achromatopsia in both dogs and humans.

“Our work in the dogs, in vitro and in silico shows us the consequences of these mutations in disrupting the function of these crucial channels,” said Karina Guziewicz, senior author on the study and a senior research investigator at Penn’s School of Veterinary Medicine. “Everything we found suggests that gene therapy will be the best approach to treating this disease, and we are looking forward to taking that next step.”

The study was published in the journal PLOS ONE and coauthored by Penn Vet’s Emily V. Dutrow and Temple’s Naoto Tanaka. Additional coauthors from Penn Vet included Gustavo D. Aguirre, Keiko Miyadera, Shelby L. Reinstein, William R. Crumley and Margret L. Casal. Temple’s team, all from the College of Science and Technology, included Lucie Delemotte, Christopher M. MacDermaid, Michael L. Klein and Jacqueline C. Tanaka. Christopher J. Dixon of Veterinary Vision in the United Kingdom also contributed.

The research began with a German shepherd that was brought to Penn Vet’s Ryan Hospital. The owners were worried about its vision.

“This dog displayed a classical loss of cone vision; it could not see well in daylight but had no problem in dim light conditions,” said Aguirre, professor of medical genetics and ophthalmology at Penn Vet.

The Penn Vet researchers wanted to identify the genetic cause, but the dog had none of the “usual suspects,” the known gene mutations responsible for achromatopsia in dogs. To find the new mutation, the scientists looked at five key genes that play a role in phototransduction, or the process by which light signals are transmitted through the eye to the brain.

They found what they were looking for on the CNGA3 gene, which encodes a cyclic nucleotide channel and plays a key role in transducing visual signals. The change was a “missense” mutation, meaning that the mutation results in the production of a different amino acid. Meanwhile, they heard from colleague Dixon that he had examined Labrador retrievers with similar symptoms. When the Penn team performed the same genetic analysis, they found a different mutation on the same part of the same gene where the shepherd’s mutation was found. Neither mutation had ever been characterized previously in dogs.

“The next step was to take this further and look at the consequences of these particular mutations,” Guziewicz said.

The group had the advantage of using the Titan and Stampede supercomputers, which can simulate models of the atomic structure of proteins and thereby elucidate how the protein might function. That work revealed that both mutations disrupted the function of the channel, making it unstable.

“The computational approach allows us to model, right down to the atomic level, how small changes in protein sequence can have a major impact on signaling,” said MacDermaid, assistant professor of research at Temple’s Institute for Computational Molecular Science. “We can then use these insights to help us understand and refine our experimental and clinical work.”

The Temple researchers recreated these mutated channels and showed that one resulted in a loss of channel function. Further in vitro experiments showed that the second mutation caused the channels to be routed improperly within the cell.

Penn Vet researchers have had success in treating various forms of blindness in dogs with gene therapy, setting the stage to treat human blindness. In human achromatopsia, nearly 100 different mutations have been identified in the CNGA3 gene, including the very same one identified in the German shepherd in this study.

The results, therefore, lay the groundwork for designing gene therapy constructs that can target this form of blindness with the same approach.


The study was supported by the Foundation Fighting Blindness, the National Eye Institute, the National Science Foundation, the European Union Seventh Framework Program, Hope for Vision, the Macula Vision Research Foundation and the Van Sloun Fund for Canine Genetic Research.

Source: University of Pennsylvania 

The rise and fall of cognitive skills:Neuroscientists find that different parts of the brain work best at different ages.

By Anne Trafton


CAMBRIDGE, Mass–Scientists have long known that our ability to think quickly and recall information, also known as fluid intelligence, peaks around age 20 and then begins a slow decline. However, more recent findings, including a new study from neuroscientists at MIT and Massachusetts General Hospital (MGH), suggest that the real picture is much more complex.

The study, which appears in the XX issue of the journal Psychological Science, finds that different components of fluid intelligence peak at different ages, some as late as age 40.

“At any given age, you’re getting better at some things, you’re getting worse at some other things, and you’re at a plateau at some other things. There’s probably not one age at which you’re peak on most things, much less all of them,” says Joshua Hartshorne, a postdoc in MIT’s Department of Brain and Cognitive Sciences and one of the paper’s authors.

“It paints a different picture of the way we change over the lifespan than psychology and neuroscience have traditionally painted,” adds Laura Germine, a postdoc in psychiatric and neurodevelopmental genetics at MGH and the paper’s other author.

Measuring peaks

Until now, it has been difficult to study how cognitive skills change over time because of the challenge of getting large numbers of people older than college students and younger than 65 to come to a psychology laboratory to participate in experiments. Hartshorne and Germine were able to take a broader look at aging and cognition because they have been running large-scale experiments on the Internet, where people of any age can become research subjects.

Their web sites, gameswithwords.org and testmybrain.org, feature cognitive tests designed to be completed in just a few minutes. Through these sites, the researchers have accumulated data from nearly 3 million people in the past several years.

In 2011, Germine published a study showing that the ability to recognize faces improves until the early 30s before gradually starting to decline. This finding did not fit into the theory that fluid intelligence peaks in late adolescence. Around the same time, Hartshorne found that subjects’ performance on a visual short-term memory task also peaked in the early 30s.

Intrigued by these results, the researchers, then graduate students at Harvard University, decided that they needed to explore a different source of data, in case some aspect of collecting data on the Internet was skewing the results. They dug out sets of data, collected decades ago, on adult performance at different ages on the Weschler Adult Intelligence Scale, which is used to measure IQ, and the Weschler Memory Scale. Together, these tests measure about 30 different subsets of intelligence, such as digit memorization, visual search, and assembling puzzles.

Hartshorne and Germine developed a new way to analyze the data that allowed them to compare the age peaks for each task. “We were mapping when these cognitive abilities were peaking, and we saw there was no single peak for all abilities. The peaks were all over the place,” Hartshorne says. “This was the smoking gun.”

However, the dataset was not as large as the researchers would have liked, so they decided to test several of the same cognitive skills with their larger pools of Internet study participants. For the Internet study, the researchers chose four tasks that peaked at different ages, based on the data from the Weschler tests. They also included a test of the ability to perceive others’ emotional state, which is not measured by the Weschler tests.

The researchers gathered data from nearly 50,000 subjects and found a very clear picture showing that each cognitive skill they were testing peaked at a different age. For example, raw speed in processing information appears to peak around age 18 or 19, then immediately starts to decline. Meanwhile, short-term memory continues to improve until around age 25, when it levels off and then begins to drop around age 35.

For the ability to evaluate other people’s emotional states, the peak occurred much later, in the 40s or 50s.

More work will be needed to reveal why each of these skills peaks at different times, the researchers say. However, previous studies have hinted that genetic changes or changes in brain structure may play a role.

“If you go into the data on gene expression or brain structure at different ages, you see these lifespan patterns that we don’t know what to make of. The brain seems to continue to change in dynamic ways through early adulthood and middle age,” Germine says. “The question is: What does it mean? How does it map onto the way you function in the world, or the way you think, or the way you change as you age?”

Accumulated intelligence

The researchers also included a vocabulary test, which serves as a measure of what is known as crystallized intelligence — the accumulation of facts and knowledge. These results confirmed that crystallized intelligence peaks later in life, as previously believed, but the researchers also found something unexpected: While data from the Weschler IQ tests suggested that vocabulary peaks in the late 40s, the new data showed a later peak, in the late 60s or early 70s.

The researchers believe this may be a result of better education, more people having jobs that require a lot of reading, and more opportunities for intellectual stimulation for older people.

Hartshorne and Germine are now gathering more data from their websites and have added new cognitive tasks designed to evaluate social and emotional intelligence, language skills, and executive function. They are also working on making their data public so that other researchers can access it and perform other types of studies and analyses.

“We took the existing theories that were out there and showed that they’re all wrong. The question now is: What is the right one? To get to that answer, we’re going to need to run a lot more studies and collect a lot more data,” Hartshorne says.

The research was funded by the National Institutes of Health, the National Science Foundation, and a National Defense Science and Engineering Graduate Fellowship.

Source: MIT News Office

Rotating night shift work can be hazardous to your health

Possible increase in cardiovascular disease and lung cancer mortality observed in nurses working rotating night shifts, according to report in the American Journal of Preventive Medicine

ELSEVIER HEALTH SCIENCES


Night shift work has been consistently associated with higher risk for cardiovascular disease (CVD) and cancer. In 2007 the World Health Organization classified night shift work as a probable carcinogen due to circadian disruption. In a study in the current issue of the American Journal of Preventive Medicine, researchers found that women working rotating night shifts for five or more years appeared to have a modest increase in all-cause and CVD mortality and those working 15 or more years of rotating night shift work appeared to have a modest increase in lung cancer mortality. These results add to prior evidence of a potentially detrimental effect of rotating night shift work on health and longevity.

Sleep and the circadian system play an important role in cardiovascular health and antitumor activity. There is substantial biological evidence that night shift work enhances the development of cancer and CVD, and contributes to higher mortality.

An international team of researchers investigated possible links between rotating night shift work and all-cause, CVD, and cancer mortality in a study of almost 75,000 registered U.S. nurses. Using data from the Nurses’ Health Study (NHS), the authors analyzed 22 years of follow-up and found that working rotating night shifts for more than five years was associated with an increase in all-cause and CVD mortality. Mortality from all causes appeared to be 11% higher for women with 6-14 or ?15 years of rotating night shift work. CVD mortality appeared to be 19% and 23% higher for those groups, respectively. There was no association between rotating shift work and any cancer mortality, except for lung cancer in those who worked shift work for 15 or more years (25% higher risk).

The NHS, which is based at Brigham and Women’s Hospital, began in 1976, with 121,700 U.S. female nurses aged 30-55 years, who have been followed up with biennial questionnaires. Night shift information was collected in 1988, at which time 85,197 nurses responded. After excluding women with pre-existing CVD or other than non-melanoma skin cancer, 74,862 women were included in this analysis. Defining rotating shift work as working at least three nights per month in addition to days or evenings in that month, respondents were asked how many years they had worked in this way. The prespecified categories were never, 1-2, 3-5, 6-9, 10-14, 15-19, 20-29, and ?30 years.

According to Eva S. Schernhammer, MD, DrPH, currently Associate Professor of Medicine, Harvard Medical School, and Associate Epidemiologist, Department of Medicine, Brigham and Women’s Hospital, Boston, this study “is one of the largest prospective cohort studies worldwide with a high proportion of rotating night shift workers and long follow-up time. A single occupation (nursing) provides more internal validity than a range of different occupational groups, where the association between shift work and disease outcomes could be confounded by occupational differences.”

Comparing this work with previous studies, she continues, “These results add to prior evidence of a potentially detrimental relation of rotating night shift work and health and longevity…To derive practical implications for shift workers and their health, the role of duration and intensity of rotating night shift work and the interplay of shift schedules with individual traits (e.g., chronotype) warrant further exploration.”

Source: American Journal of Preventive Medicine via EurekAlert

Musashi proteins, stained red, appear in the cell cytoplasm, outside the nucleus. At right, the cell nucleus is stained blue.
Image Credit: Yarden Katz/MIT

Proteins drive cancer cells to change states

When RNA-binding proteins are turned on, cancer cells get locked in a proliferative state.

 By Anne Trafton


 

A new study from MIT implicates a family of RNA-binding proteins in the regulation of cancer, particularly in a subtype of breast cancer. These proteins, known as Musashi proteins, can force cells into a state associated with increased proliferation.

Biologists have previously found that this kind of transformation, which often occurs in cancer cells as well as during embryonic development, is controlled by transcription factors — proteins that turn genes on and off. However, the new MIT research reveals that RNA-binding proteins also play an important role. Human cells have about 500 different RNA-binding proteins, which influence gene expression by regulating messenger RNA, the molecule that carries DNA’s instructions to the rest of the cell.

“Recent discoveries show that there’s a lot of RNA-processing that happens in human cells and mammalian cells in general,” says Yarden Katz, a recent MIT PhD recipient and one of the lead authors of the new paper. “RNA is processed at several points within the cell, and this gives opportunities for RNA-binding proteins to regulate RNA at each point. We’re very interested in trying to understand this unexplored class of RNA-binding proteins and how they regulate cell-state transitions.”

Feifei Li of China Agricultural University is also a lead author of the paper, which appears in the journal eLife on Dec. 15. Senior authors of the paper are MIT biology professors Christopher Burge and Rudolf Jaenisch, and Zhengquan Yu of China Agricultural University.

Controlling cell states

Until this study, scientists knew very little about the functions of Musashi proteins. These RNA-binding proteins have traditionally been used to identify neural stem cells, in which they are very abundant. They have also been found in tumors, including in glioblastoma, a very aggressive form of brain cancer.

“Normally they’re marking stem and progenitor cells, but they get turned on in cancers. That was intriguing to us because it suggested they might impose a more undifferentiated state on cancer cells,” Katz says.

To study this possibility, Katz manipulated the levels of Musashi proteins in neural stem cells and measured the effects on other genes. He found that genes affected by Musashi proteins were related to the epithelial-to-mesenchymal transition (EMT), a process by which cells lose their ability to stick together and begin invading other tissues.

EMT has been shown to be important in breast cancer, prompting the team to look into Musashi proteins in cancers of non-neural tissue. They found that Musashi proteins are most highly expressed in a type of breast tumors called luminal B tumors, which are not metastatic but are aggressive and fast-growing.

When the researchers knocked down Musashi proteins in breast cancer cells grown in the lab, the cells were forced out of the epithelial state. Also, if the proteins were artificially boosted in mesenchymal cells, the cells transitioned to an epithelial state. This suggests that Musashi proteins are responsible for maintaining cancer cells in a proliferative, epithelial state.

“These proteins seem to really be regulating this cell-state transition, which we know from other studies is very important, especially in breast cancer,” Katz says.

Musashi proteins, stained red, appear in the cell cytoplasm, outside the nucleus. At right, the cell nucleus is stained blue. Image Credit: Yarden Katz/MIT
Musashi proteins, stained red, appear in the cell cytoplasm, outside the nucleus. At right, the cell nucleus is stained blue.
Image Credit: Yarden Katz , MIT

 

The researchers found that Musashi proteins repress a gene called Jagged1, which in turn regulates the Notch signaling pathway. Notch signaling promotes cell division in neurons during embryonic development and also plays a major role in cancer.

When Jagged1 is repressed, cells are locked in an epithelial state and are much less motile. The researchers found that Musashi proteins also repress Jagged1 during normal mammary-gland development, not just in cancer. When these proteins were overexpressed in normal mammary glands, cells were less able to undergo the type of healthy EMT required for mammary tissue development.

Brenton Graveley, a professor of genetics and developmental biology at the University of Connecticut, says he was surprised to see how much influence Musashi proteins can have by controlling a relatively small number of genes in a cell. “Musashi proteins have been known to be interesting for many years, but until now nobody has really figured out exactly what they’re doing, especially on a genome-wide scale,” he says.

The researchers are now trying to figure out how Musashi proteins, which are normally turned off after embryonic development, get turned back on in cancer cells. “We’ve studied what this protein does, but we know very little about how it’s regulated,” Katz says.

He says it is too early to know if the Musashi proteins might make good targets for cancer drugs, but they could make a good diagnostic marker for what state a cancer cell is in. “It’s more about understanding the cell states of cancer at this stage, and diagnosing them, rather than treating them,” he says.

The research was funded by the National Institutes of Health.

Source : MIT News Office

New way to turn genes on

Technique allows rapid, large-scale studies of gene function.

By Anne Trafton


CAMBRIDGE, MA — Using a gene-editing system originally developed to delete specific genes, MIT researchers have now shown that they can reliably turn on any gene of their choosing in living cells.

This new application for the CRISPR/Cas9 gene-editing system should allow scientists to more easily determine the function of individual genes, according to Feng Zhang, the W.M. Keck Career Development Professor in Biomedical Engineering in MIT’s Departments of Brain and Cognitive Sciences and Biological Engineering, and a member of the Broad Institute and MIT’s McGovern Institute for Brain Research.

This approach also enables rapid functional screens of the entire genome, allowing scientists to identify genes involved in particular diseases. In a study published in the Dec. 10 online edition of Nature, Zhang and colleagues identified several genes that help melanoma cells become resistant to a cancer drug.

Silvana Konermann, a graduate student in Zhang’s lab, and Mark Brigham, a McGovern Institute postdoc, are the paper’s lead authors.

A new function for CRISPR

The CRISPR system relies on cellular machinery that bacteria use to defend themselves from viral infection. Researchers have previously harnessed this cellular system to create gene-editing complexes that include a DNA-cutting enzyme called Cas9 bound to a short RNA guide strand that is programmed to bind to a specific genome sequence, telling Cas9 where to make its cut.

In the past two years, scientists have developed Cas9 as a tool for turning genes off or replacing them with a different version. In the new study, Zhang and colleagues engineered the Cas9 system to turn genes on, rather than knock them out.

Scientists have tried to do this before using proteins that are individually engineered to target DNA at specific sites. However, these proteins are  difficult to work with. “If you use the older generation of tools, getting the technology to do what you actually want is a project on its own,” Konermann says. “It takes a lot of time and is also quite expensive.”

There have also been attempts to use CRISPR to turn on genes by inactivating the part of the Cas9 enzyme that cuts DNA and linking Cas9 to pieces of proteins called activation domains. These domains recruit the cellular machinery necessary to begin reading copying RNA from DNA, a process known as transcription.

However, these efforts have been unable to consistently turn on gene transcription. Zhang and his colleagues, Osamu Nureki and Hiroshi Nishimasu at the University of Tokyo, decided to overhaul the CRISPR-Cas9 system based on an analysis they published earlier this year of the structure formed when Cas9 binds to the guide RNA and its target DNA. “Based on knowing its 3-D shape, we can think about how to rationally improve the system,” Zhang says.

In previous efforts, scientists had tried to attach the activation domains to either end of the Cas9 protein, with limited success. From their structural studies, the MIT team realized that two small loops of the RNA guide poke out from the Cas9 complex and could be better points of attachment because they allow the activation domains to have more flexibility in recruiting transcription machinery.

Using their revamped system, the researchers activated about a dozen genes that had proven difficult or impossible to turn on using the previous generation of Cas9 activators. Each gene showed at least a twofold boost in transcription, and for many genes, the researchers found multiple orders of magnitude increase in activation.

Genome-scale activation screening

Once the researchers had shown that the system was effective at activating genes, they created a library of 70,290 guide RNAs targeting all of the more than 20,000 genes in the human genome.

They screened this library to identify genes that confer resistance to a melanoma drug called PLX-4720. This drug worksDrugs of this type work well in patients whose melanoma cells have a mutation in the BRAF gene, but cancer cells that survive the treatment can grow into new tumors, allowing the cancer to recur.

To discover the genes that help cells become resistant, the researchers delivered CRISPR components to a large population of melanoma cells grown in the lab, with each cell receiving a different guide RNA targeting a different gene. After treating the cells with PLX-4720, they identified several genes that helped the cells to survive — some previously known to be involved in drug resistance, as well as several novel targets.

Studies like this could help researchers discover new cancer drugs that prevent tumors from becoming resistant.

“You could start with a drug that targets the mutated BRAF along with combination therapy that targets genes that allow the cell to survive. If you target both of them at the same time, you could likely prevent the cells from developing resistance mechanisms that enable further growth despite drug treatment,” Konermann says.

Scientists have tried to do large-scale screens like this by delivering single genes carried by viruses, but that does not work with all genes.

Zhang’s lab also plans to use this technique to screen for genes that, when activated, could correct the effects of autism or neurodegenerative diseases such as Alzheimer’s. He also plans to make the necessary reagents available to academic labs that want to use them, through the Addgene repository.

The research was funded by the National Institute of Mental Health; the National Institute of Neurological Disorders and Stroke; the Keck, Searle Scholars, Klingenstein, Vallee, and Simons foundations; and Bob Metcalfe.

Sourse: MIT News

The harlequin filefish can disguise its smell. Image: Tane Sinclair-Taylor

You are what you eat – if you’re a coral reef fish

In a world first study researchers have found a coral-eating fish that disguises its smell to hide from predators.

“For many animals vision is less important than their sense of smell,” says study lead author Dr Rohan Brooker from the ARC Centre of Excellence for Coral Reef Studies (Coral CoE) at James Cook University.

“Because predators often rely on odors to find their prey, even visually camouflaged animals may stick out like a sore thumb if they smell strongly of ‘food’.” Dr Brooker says.

The research, published in the journal Proceedings of the Royal Society B, found that the harlequin filefish changed its smell to match the coral it ate.

“By feeding on corals, the harlequin filefish ends up smelling enough like its food that predators have a hard time distinguishing it from the surrounding coral habitat,” Dr Brooker says.

The harlequin filefish can disguise its smell. Image: Tane Sinclair-Taylor
The harlequin filefish can disguise its smell. Image: Tane Sinclair-Taylor

Study co-author, Professor Philip Munday from the Coral CoE says the ability to chemically camouflage itself is a great advantage for the fish.

“The harlequin filefish shelters among the branches of coral colonies at night, where not only does it look like a coral branch, it also smells like one, enabling it to remain undetected by nocturnal predators.”

Professor Doug Chivers from the University of Saskatchewan, who is also a co-author, agrees.

“A finely-tuned combination of visual and chemical camouflage may be an effective anti-predator strategy that helps the fish to avoid being eaten,” Professor Chivers says.
Not only does the filefish confuse its predators, it matches the odour of the coral so closely that small crabs, which lived on coral branches, couldn’t distinguish it from coral.

Professor Munday says it’s a remarkable example of how closely animals can be adapted to their habitats.

“However, the filefishes’ cover is blown if it shelters in a different species of coral than the one it has been eating. Then, the predators can distinguish it presence and track it down,” Professor Munday says.

The ability to chemically ‘blend in’ occurs in some plant-eating invertebrates, but this is the first time this type of camouflage has been found in higher order animals, such as fish.

“This is very exciting because it opens the possibility of a wide range of different animals also using similar mechanisms, right under our noses,” Dr Brooker says.

Paper

You are what you eat: diet-induced chemical crypsis in a coral-feeding fish by Rohan Brooker, Philip Munday, Doug Chivers and Geoffrey Jones is published in the journal Proceedings of the Royal Society B.

Source : ARC Centre of Excellence Coral Reef Studies

Electrical and computer engineering Professor Barry Van Veen wears an electrode net used to monitor brain activity via EEG signals. His research could help untangle what happens in the brain during sleep and dreaming.

Photo Credit: Nick Berard/UW-Madison

Stanford scientists seek to map origins of mental illness and develop noninvasive treatment

An interdisciplinary team of scientists has convened to map the origins of mental illnesses in the brain and develop noninvasive technologies to treat the conditions. The collaboration could lead to improved treatments for depression, anxiety and post-traumatic stress disorder.

BY AMY ADAMS


Over the years imaging technologies have revealed a lot about what’s happening in our brains, including which parts are active in people with conditions like depression, anxiety or post-traumatic stress disorder. But here’s the secret Amit Etkin wants the world to know about those tantalizing images: they show the result of a brain state, not what caused it.

This is important because until we know how groups of neurons, called circuits, are causing these conditions – not just which are active later – scientists will never be able to treat them in a targeted way.

“You see things activated in brain images but you can’t tell just by watching what is cause and what is effect,” said Amit Etkin, an assistant professor of psychiatry and behavioral sciences. Etkin is co-leader of a new interdisciplinary initiative to understand what brain circuits underlie mental health conditions and then direct noninvasive treatments to those locations.

“Right now, if a patient with a mental illness goes to see their doctor they would likely be given a medication that goes all over the brain and body,” Etkin said. “While medications can work well, they do so for only a portion of people and often only partially.” Medications don’t specifically act on the brain circuits critically affected in that illness or individual.

The Big Idea: treat roots of mental illness

The new initiative, called NeuroCircuit, has the goal of finding the brain circuits that are responsible for mental health conditions and then developing ways of remotely stimulating those circuits and, the team hopes, potentially treating those conditions.

The initiative is part of the Stanford Neurosciences Institute‘s Big Ideas, which bring together teams of researchers from across disciplines to solve major problems in neuroscience and society. Stephen Baccus, an associate professor of neurobiology who co-leads the initiative with Etkin, said that what makes NeuroCircuit a big idea is the merging of teams trying to map circuits responsible for mental health conditions and teams developing new technologies to remotely access those circuits.

“Many psychiatric disorders, especially disorders of mood, probably involve malfunction within specific brain circuits that regulate emotion and motivation, yet our current pharmaceutical treatments affect circuits all over the brain,” said William Newsome, director of the Stanford Neurosciences Institute. “The ultimate goal of NeuroCircuit is more precise treatments, with minimal side effects, for specific psychiatric disorders.”

“The connection between the people who develop the technology and carry out research with the clinical goal, that’s what’s really come out of the Big Ideas,” Baccus said.

Brain control

Etkin has been working with a technology called transcranial magnetic stimulation, or TMS, to map and remotely stimulate parts of the brain. The device, which looks like a pair of doughnuts on a stick, generates a strong magnetic current that stimulates circuits near the surface of the brain.

TMS is currently used as a way of treating depression and anxiety, but Etkin said the brain regions being targeted are the ones available to TMS, not necessarily the ones most likely to treat a person’s condition. They are also not personalized for the individual.

Pairing TMS with another technology that shows which brain regions are active, Etkin and his team can stimulate one part of the brain with TMS and look for a reaction elsewhere. These studies can eventually help map the relationships between brain circuits and identify the circuits that underlie mental health conditions.

In parallel, the team is working to improve TMS to make it more useful as a therapy. TMS currently only reaches the surface of the brain and is not very focused. The goal is to improve the technology so that it can reach structures deeper in the brain in a more targeted way. “Right now they are hitting the only accessible target,” he said. “The parts we really want to hit for depression, anxiety or PTSD are likely deeper in the brain.”

Technology of the future

In parallel with the TMS work, Baccus and a team of engineers, radiologists and physiologists have been developing a way of using ultrasound to stimulate the brain. Ultrasound is widely used to image the body, most famously for producing images of developing babies in the womb. But in recent years scientists have learned that at the right frequency and focus, ultrasound can also stimulate nerves to fire.

In his lab, Baccus has been using ultrasound to stimulate nerve cells of the retina – the light-sensing structure at the back of the eye – as part of an effort to develop a prosthetic retina. He is also teaming up with colleagues to understand how ultrasound might be triggering that stimulation. It appears to compress the nerve cells in a way that could lead to activation, but the connection is far from clear.

Other members of the team are modifying existing ultrasound technology to direct it deep within the brain at a frequency that can stimulate nerves without harming them. If the team is successful, ultrasound could be a more targeted and focused tool than TMS for remotely stimulating circuits that underlie mental health conditions.

The group has been working together for about five years, and in 2012 got funding from Bio-X NeuroVentures, which eventually gave rise to the Stanford Neurosciences Institute, to pursue this technology. Baccus said that before merging with Etkin’s team they had been focusing on the technology without specific brain diseases in mind. “This merger really gives a target and a focus to the technology,” he said.

Etkin and Baccus said that if they are successful, they hope to have both a better understanding of how the brain functions and new tools for treating disabling mental health conditions.

Source: Stanford News

Live longer? Save the planet? Better diet could nail both

New study shows healthier food choices could dramatically decrease environmental costs of agriculture


As cities and incomes increase around the world, so does consumption of refined sugars, refined fats, oils and resource- and land-intense agricultural products such as beef. A new study led by University of Minnesota ecologist David Tilman shows how a shift away from this trajectory and toward healthier traditional Mediterranean, pescatarian or vegetarian diets could not only boost human lifespan and quality of life, but also slash greenhouse gas emissions and save habitat for endangered species.

The study, published in the November 12 online edition of Nature by Tilman and graduate student Michael Clark, synthesized data on environmental costs of food production, diet trends, relationships between diet and health, and population growth. Their integrated analysis painted a striking picture of the human and environmental health costs of our current diet trajectory as well as how strategically modifying food choices could reduce not only incidence of type II diabetes, coronary heart disease and other chronic diseases, but global agricultural greenhouse gas emissions and habitat degradation, as well.

“We showed that the same dietary changes that can add about a decade to our lives can also prevent massive environmental damage,” said Tilman, a professor in the University’s College of Biological Sciences and resident fellow at the Institute on the Environment. “In particular, if the world were to adopt variations on three common diets, health would be greatly increased at the same time global greenhouse gas emissions were reduced by an amount equal to the current greenhouse gas emissions of all cars, trucks, planes, trains and ships. In addition, this dietary shift would prevent the destruction of an area of tropical forests and savannas as large as half of the United States.”

The researchers found that, as incomes increased between 1961 and 2009, people consumed more meat protein, empty calories and total calories per person. When these trends were combined with forecasts of population growth and income growth for the coming decades, the study predicted that diets in 2050 would contain fewer servings of fruits and vegetables, but about 60 percent more empty calories and 25 to 50 percent more pork, poultry, beef, dairy and eggs — a suite of changes that would increase incidence of type II diabetes, coronary heart disease and some cancers. Using life-cycle analyses of various food production systems, the study also calculated that, if current trends prevail, these 2050 diets would also lead to an 80 percent increase in global greenhouse gas emissions from food production as well as habitat destruction due to land clearing for agriculture around the world.

The study then compared health impacts of the global omnivorous diet with those reported for traditional Mediterranean, pescatarian and vegetarian diets. Adopting these alternative diets could reduce incidence of type II diabetes by about 25 percent, cancer by about 10 percent and death from heart disease by about 20 percent relative to the omnivore diet. Additionally, the adoption of these or similar alternative diets would prevent most or all of the increased greenhouse gas emissions and habitat destruction that would otherwise be caused by both current diet trends and increased global population.

The authors acknowledged that numerous factors go into diet choice, but also pointed out that the alternative diets already are part of the lives of countless people around the world. Noting that variations on the diets used in the scenario could potentially show even greater benefit, they concluded that “the evaluation and implementation of dietary solutions to the tightly linked diet-environment-health trilemma is a global challenge, and opportunity, of great environmental and public health importance.”

Tilman is a Regents Professor and McKnight Presidential Chair in Ecology in the College of Biological Sciences’ Department of Ecology, Evolution and Behavior and a resident fellow in the University of Minnesota’s Institute on the Environment, which seeks lasting solutions to Earth’s biggest challenges through research, partnerships and leadership development. Clark is currently a doctoral student in the College of Food, Agricultural and Natural Resource Sciences.

Source: University of Minnesota

In a paper appearing in the Nov. 18 issue of Nature Communications, the researchers demonstrate the use of the particles, which carry distinct sensors for fluorescence and MRI, to track vitamin C in mice. Wherever there is a high concentration of vitamin C, the particles show a strong fluorescent signal but little MRI contrast. If there is not much vitamin C, a stronger MRI signal is visible but fluorescence is very weak.

Illustration: Christine Daniloff/MIT

Two sensors in one

Nanoparticles that enable both MRI and fluorescent imaging could monitor cancer, other diseases.

By Anne Trafton


 

MIT chemists have developed new nanoparticles that can simultaneously perform magnetic resonance imaging (MRI) and fluorescent imaging in living animals. Such particles could help scientists to track specific molecules produced in the body, monitor a tumor’s environment, or determine whether drugs have successfully reached their targets.

 

In a paper appearing in the Nov. 18 issue of Nature Communications, the researchers demonstrate the use of the particles, which carry distinct sensors for fluorescence and MRI, to track vitamin C in mice. Wherever there is a high concentration of vitamin C, the particles show a strong fluorescent signal but little MRI contrast. If there is not much vitamin C, a stronger MRI signal is visible but fluorescence is very weak.

In a paper appearing in the Nov. 18 issue of Nature Communications, the researchers demonstrate the use of the particles, which carry distinct sensors for fluorescence and MRI, to track vitamin C in mice. Wherever there is a high concentration of vitamin C, the particles show a strong fluorescent signal but little MRI contrast. If there is not much vitamin C, a stronger MRI signal is visible but fluorescence is very weak. Illustration: Christine Daniloff/MIT
In a paper appearing in the Nov. 18 issue of Nature Communications, the researchers demonstrate the use of the particles, which carry distinct sensors for fluorescence and MRI, to track vitamin C in mice. Wherever there is a high concentration of vitamin C, the particles show a strong fluorescent signal but little MRI contrast. If there is not much vitamin C, a stronger MRI signal is visible but fluorescence is very weak.
Illustration: Christine Daniloff/MIT

 

Future versions of the particles could be designed to detect reactive oxygen species that often correlate with disease, says Jeremiah Johnson, an assistant professor of chemistry at MIT and senior author of the study. They could also be tailored to detect more than one molecule at a time.

 

“You may be able to learn more about how diseases progress if you have imaging probes that can sense specific biomolecules,” Johnson says.

 

Dual action

 

Johnson and his colleagues designed the particles so they can be assembled from building blocks made of polymer chains carrying either an organic MRI contrast agent called a nitroxide or a fluorescent molecule called Cy5.5.

 

When mixed together in a desired ratio, these building blocks join to form a specific nanosized structure the authors call a branched bottlebrush polymer. For this study, they created particles in which 99 percent of the chains carry nitroxides, and 1 percent carry Cy5.5.

 

Nitroxides are reactive molecules that contain a nitrogen atom bound to an oxygen atom with an unpaired electron. Nitroxides suppress Cy5.5’s fluorescence, but when the nitroxides encounter a molecule such as vitamin C from which they can grab electrons, they become inactive and Cy5.5 fluoresces.

 

Nitroxides typically have a very short half-life in living systems, but University of Nebraska chemistry professor Andrzej Rajca, who is also an author of the new Nature Communications paper, recently discovered that their half-life can be extended by attaching two bulky structures to them.  Furthermore, the authors of the Nature Communications paper show that incorporation of Rajca’s nitroxide in Johnson’s branched bottlebrush polymer architectures leads to even greater improvements in the nitroxide lifetime. With these modifications, nitroxides can circulate for several hours in a mouse’s bloodstream — long enough to obtain useful MRI images.

 

The researchers found that their imaging particles accumulated in the liver, as nanoparticles usually do. The mouse liver produces vitamin C, so once the particles reached the liver, they grabbed electrons from vitamin C, turning off the MRI signal and boosting fluorescence. They also found no MRI signal but a small amount of fluorescence in the brain, which is a destination for much of the vitamin C produced in the liver. In contrast, in the blood and kidneys, where the concentration of vitamin C is low, the MRI contrast was maximal.

 

Mixing and matching

 

The researchers are now working to enhance the signal differences that they get when the sensor encounters a target molecule such as vitamin C. They have also created nanoparticles carrying the fluorescent agent plus up to three different drugs. This allows them to track whether the nanoparticles are delivered to their targeted locations.

 

“That’s the advantage of our platform — we can mix and match and add almost anything we want,” Johnson says.

 

These particles could also be used to evaluate the level of oxygen radicals in a patient’s tumor, which can reveal valuable information about how aggressive the tumor is.

 

“We think we may be able to reveal information about the tumor environment with these kinds of probes, if we can get them there,” Johnson says. “Someday you might be able to inject this in a patient and obtain real-time biochemical information about disease sites and also healthy tissues, which is not always straightforward.”

 

Steven Bottle, a professor of nanotechnology and molecular science at Queensland University of Technology, says the most impressive element of the study is the combination of two powerful imaging techniques into one nanomaterial.

 

“I believe this should deliver a very powerful, metabolically linked, multi-combination imaging modality which should provide a highly useful diagnostic tool with real potential to follow disease progression in vivo,” says Bottle, who was not involved in the study.

 

The research was funded by the National Institutes of Health, the Department of Defense, the National Science Foundation, and the Koch Institute for Integrative Cancer Research.

Source: MIT News