This timid little fish escapes predators by injecting them with opioid-laced venom

This image shows the skull of the venomous species Meiacanthus grammistes.

Credit: Anthony Romilio

Fang blennies are small fish with big teeth. Specifically, they have two large canine teeth that jut out of their lower jaw. Since blenny fish are only about two inches long, these 'fangs' would be less than intimidating if not for the venom within. Blenny fish venom most likely causes a sudden drop in blood pressure in would-be predators, such as grouper fish, that have been bitten by blennies.

When the researchers did a proteomic analysis of extracted fang blenny venom, they found three venom components -- a neuropeptide that occurs in cone snail venom, a lipase similar to one from scorpions, and an opioid peptide. And, surprisingly, when they injected the blenny venom into lab mice, the mice didn't show any signs of pain.

"For the fang blenny venom to be painless in mice was quite a surprise," says study co-author Bryan Fry of University of Queensland. "Fish with venomous dorsal spines produce immediate and blinding pain. The most pain I've ever been in other than the time I broke my back was from a stingray envenomation. 'Sting'ray sounds so benign. They don't sting. They are pure hell."

Fang blenny venom, however, seems to have a very different effect on its victims. Since the researchers used rodents for the pain test, they can't entirely rule out the possibility of blenny venom causing pain in fish, but it seems plausible that the neuropeptide and opioid components may cause a sudden drop in blood pressure, most likely leaving the blenny's attacker disorientated and unable to give chase. "By slowing down potential predators, the fang blennies have a chance to escape," says Fry. "While the feeling of pain is not produced, opioids can produce sensations of extremely unpleasant nausea and dizziness [in mammals]."

Extracting the tiny fish's venom for chemical tests was no easy feat. When blenny fish bite an attacker, they only inject a tiny amount of venom, making it extremely difficult to collect enough for proteomic analyses. The researchers ended up using a quirky but labor-intensive method for extracting blenny venom: they would pluck the little fish out of their tanks, dangle a cotton swab in front of them so that the blenny would bite the cotton swab, and then suspended the cotton swabs in a solution that drew out the venom (after putting the fish back in the tank).

Nonvenomous fang blennies and other small fish capitalize on the venom's success by mimicking venomous fang blennies' colors and patterns. "Predatory fish will not eat those fishes because they think they are venomous and going to cause them harm, but this protection provided also allows some of these mimics to get very close to unsuspecting fish to feed on them, by picking on their scales as a micropredator," says study co-author Nicholas Casewell of the Liverpool School of Tropical Medicine. "All of this mimicry, all of these interactions at the community level, ultimately are stimulated by the venom system that some of these fish have."

Another surprise from the study was the evidence suggesting that fang blenny fangs evolved before the venom. "This is pretty unusual, because often what we've found -- for example, in snakes -- is that some sort of venom secretions evolved first, before the elaborate venom delivery mechanism evolved," says Casewell. Evolution favored the tiny fish with large teeth first and later found a way to enhance them with venom.

"These unassuming little fish have a really quite advanced venom system, and that venom system has a major impact on fishes and other animals in its community," says Casewell.

The researchers went into the study with "no grand hypothesis, just basic wonderment" according to Fry, but they plan to follow up the study by comparing and contrasting the composition of venoms from different blenny species.

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Bad cold? If you're lonely, it may feel worse

Lonelier people report more acute symptomsA new study showed people who feel lonely are likely to report more severe symptoms from the common cold.

Suffering through a cold is annoying enough, but if you're lonely, you're likely to feel even worse, according to Rice University researchers.

A study led by Rice psychologist Chris Fagundes and graduate student Angie LeRoy indicated people who feel lonely are more prone to report a their cold symptoms are more severe than those who have stronger social networks.

"Loneliness puts people at risk for premature mortality and all kinds of other physical illnesses," LeRoy said. "But nothing had been done to look at an acute but temporary illness that we're all vulnerable to, like the common cold."

The study is the subject of a paper published this week in Health Psychology.

The researchers drew a distinction between feeling lonely and actual social isolation.

"This paper is about the quality of your relationships, not the quantity," LeRoy said. "You can be in a crowded room and feel lonely. That perception is what seems to be important when it comes to these cold symptoms."

Carrying out this task meant finding lonely people, isolating them -- and giving them a cold.

A total of 159 people age 18-55, nearly 60 percent of them men, were assessed for their psychological and physical health, given cold-inducing nasal drops and quarantined for five days in hotel rooms.

The participants, scored in advance on the Short Loneliness Scale and the Social Network Index, were monitored during and after the five-day stay. After adjusting for demographics like gender and age, the season, depressive affect and social isolation, the results showed those who felt lonely were no more likely to get a cold than those who weren't.\

But those who were screened in advance for their level of loneliness and became infected -- not all of the participants did -- reported a greater severity of symptoms than those recorded in previous studies used as controls. The size of the participants' social networks appeared to have no bearing on how sick they felt.

"Previous research has shown that different psycho-social factors like feeling rejected or feeling left out or not having strong social bonds with other people do make people feel worse physically, mentally and emotionally," LeRoy said. "So we had that general framework to work with."

The effect may be the same for those under other kinds of stress, Fagundes said. "Anytime you have an illness, it's a stressor, and this phenomenon would probably occur," he said. "A predisposition, whether it's physical or mental, can be exaggerated by a subsequent stressor. In this case, the subsequent stressor is getting sick, but it could be the loss of a loved one, or getting breast cancer, which are subjects we also study.

"What makes this study so novel is the tight experimental design. It's all about a particular predisposition (loneliness) interacting with a particular stressor," he said.

"Doctors should take psychological factors into account at intake on a regular basis," Fagundes said. "It would definitely help them understand the phenomenon when the person comes in sick."

"We think this is important, particularly because of the economic burden associated with the common cold," LeRoy added. "Millions of people miss work each year because of it. And that has to do with how they feel, not necessarily with how much they're blowing their noses."

The findings are also an incentive to be more socially active, she said. "If you build those networks -- consistently working on them and your relationships -- when you do fall ill, it may not feel so bad."

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Abuse accelerates puberty in children

Maltreatment can affect a child's psychological development. New research indicates that the stress of abuse can impact the physical growth and maturation of adolescents as well.Credit: © Roman Bodnarchuk / Fotolia

While it has long been known that maltreatment can affect a child's psychological development, new research indicates that the stress of abuse can impact the physical growth and maturation of adolescents as well.

Jennie Noll, director of the Child Maltreatment Solutions Network and professor of human development and family studies, and Idan Shalev, assistant professor of biobehavioral health, found that young girls who are exposed to childhood sexual abuse are likely to physically mature and hit puberty at rates 8 to twelve months earlier than their non-abused peers. Their results were published recently in the Journal of Adolescent Health.

"Though a year's difference may seem trivial in the grand scheme of a life, this accelerated maturation has been linked to concerning consequences, including behavioral and mental health problems and reproductive cancers," said Noll.

The body is timed so that physical and developmental changes occur in tandem, assuring that as a child physically changes, they have adequate psychological growth to cope with mature contexts. "High-stress situations, such as childhood sexual abuse, can lead to increased stress hormones that jump-start puberty ahead of its standard biological timeline," Noll explained. "When physical maturation surpasses psychosocial growth in this way, the mismatch in timing is known as maladaptation."

In the past, there have been studies loosely linking sexual abuse to maladaptation and accelerated maturation, but the longitudinal work completed by Noll and her team has been the most conclusive and in-depth to date, beginning in 1987 and following subjects throughout each stage of puberty.

Controlling for race, ethnicity, family makeup, obesity, socioeconomic status and nonsexual traumatic experiences, the researchers compared the pubescent trajectories of 84 females with a sexual abuse history and 89 of their non-abused counterparts. Working closely with nurses and Child Protective Services, the subjects were tracked from pre-puberty to full maturity based on a system known as Tanner staging.

Tanner staging is a numeric index of ratings that corresponds with the physical progression of puberty. The study's researchers focused on breast and pubic hair development as two separate mile markers for pubescent change. Subjects were placed somewhere from one (prepubescent) to five (full maturity) on the Tanner index and their Tanner number and age were mapped out and recorded over time.

"We found that young women with sexual abuse histories were far more likely to transition into higher puberty stages an entire year before their non-abused counterparts when it came to pubic hair growth, and a full 8 months earlier in regards to breast development," Noll stated. "Due to increased exposure to estrogens over a longer period of time, premature physical development such as this has been linked to breast and ovarian cancers. Additionally, early puberty is seen as a potential contributor to increased rates of depression, substance abuse, sexual risk taking and teenage pregnancy."

The researchers believe they were able to accurately rule out other variables that may have aided in accelerated puberty, pinpointing child sexual abuse and the stress hormones associated with it as a cause for early maturation in young girls. Their findings add to the body of work highlighting the role of stress in puberty, and it is the hope that the research will lead to increased preventative care and psychosocial aid to young women facing the effects of early maturation.

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Why are primates big-brained? Researchers' answer is food for thought

Brain size in primates is predicted by diet, an analysis by a team of NYU anthropologists indicates. Above, a chimpanzee eating fruit.

Credit: James Higham

Brain size in primates is predicted by diet, an analysis by a team of anthropologists indicates. These results call into question “the social brain hypothesis,” which has posited that humans and other primates are big-brained due to factors pertaining to sociality.

The findings, which appear in the journal Nature Ecology and Evolution, reinforce the notion that both human and non-human primate brain evolution may be driven by differences in feeding rather than in socialization.

"Are humans and other primates big-brained because of social pressures and the need to think about and track our social relationships, as some have argued?" asks James Higham, an assistant professor in NYU's Department of Anthropology and a co-author of the new analysis. "This has come to be the prevailing view, but our findings do not support it -- in fact, our research points to other factors, namely diet."

"Complex foraging strategies, social structures, and cognitive abilities, are likely to have co-evolved throughout primate evolution," adds Alex DeCasien, an NYU doctoral candidate and lead author of the study. "However, if the question is: 'Which factor, diet or sociality, is more important when it comes to determining the brain size of primate species?' then our new examination suggests that factor is diet."

The social brain hypothesis sees social complexity as the primary driver of primate cognitive complexity, suggesting that social pressures ultimately led to the evolution of the large human brain. While some studies have shown positive relationships between relative brain size and group size, other studies which examined the effects of different social or mating systems have revealed highly conflicting results, raising questions about the strength of the social brain hypothesis.

In the Nature Ecology and Evolution study, the researchers, who also included Scott Williams, an assistant professor of anthropology at NYU, examined more than 140 primate species -- or more than three times as many as previous studies -- and incorporated more recent evolutionary trees, or phylogenies. They took into account food consumption across the studied species -- folivores (leaves), frugivores (fruit), frugivores/folivores, and omnivores (addition of animal protein) -- as well as several measures of sociality, such as group size, social system, and mating system.

Their results showed that brain size is predicted by diet rather than by the various measures of sociality -- after controlling for body size and phylogeny. Notably, frugivores and frugivore/folivores exhibit significantly larger brains than folivores and, to a lesser extent, omnivores show significantly larger brains than folivores.

The researchers caution that the results do not reveal an association between brain size and fruit or protein consumption on a within-species level; rather, they note, they are evidence of the cognitive demands required by different species to obtain certain foods.

"Fruit is patchier in space and time in the environment, and the consumption of it often involves extraction from difficult-to-reach-places or protective skins," observes DeCasien. "Together, these factors may lead to the need for relatively greater cognitive complexity and flexibility in frugivorous species."

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Using Latin to analyse other languages

The Latin translation next to the Arabic text helps represent the grammar and contents structure of the original better than a direct German translation would have done.Credit: © RUB, Damian Gorczany

A researcher has figured out why Latin still turned up in many documents in the 17th to 19th centuries, even though it had not been a spoken language for a long time. During that period, Latin served as an instrument for translating languages that had hitherto been little known in Western culture.

Bochum-based philologist Prof Dr Reinhold Glei has figured out why Latin still turned up in many documents in the 17th to 19th centuries, even though it had not been a spoken language for a long time. During that period, Latin served as an instrument for translating languages that had hitherto been little known in Western culture.

Scholars recreated the foreign-language sentences with the aid of Latin, thus crafting a text upon which further analyses could be based. In doing so, translators didn't have to conform to specific linguistic rules of the Latin language, because native speakers no longer existed who might have taken exception to an unusual syntax in Latin.

Arabic, Chinese, Sanskrit: novel sentence structures in those languages posed a challenge to scholars in the Early Modern Period. "Had the foreign-language texts been translated into, for example, German, the translator would have been restricted by the respective grammatical structures. Using Latin, the translators had more freedom," elaborates Glei.

Representing linguistic structures

The philologist refers to this method as epilanguage; the Greek word epi translates as "on" or "above." Latin was superimposed over the foreign language. Thus, translators were able to represent the unfamiliar structures.

Reinhold Glei compiled his results by studying Arabic, Chinese and Persian texts and their respective translations from the period between the 17th and 19th centuries. He analysed, for example, various Quran translations. By comparing excerpts from the Latin translations with the originals, Glei identified to what extent the Latin versions reflected the structure of the original language.

An advantage of using the epilanguage was that it enabled translators to draw up neutral texts, before translating them into their respective vernacular language. "When Christians initially translated the Quran, the texts they created were for the most part ideologically charged. This resulted in corrupted translations," he says. Using Latin as epilanguage did not wholly eradicate the problem, but it was possible to represent the structure of the Arabic language in a more neutral manner.

Future perspectives

Research into epilanguage is still in its early stages. Reinhold Glei intends to analyse additional Latin translations from various languages, in order to gain a better grasp of the function of epilanguage. Glei also wishes to study another world language, namely Ancient Greek, in greater detail. His first impression is: "Ancient Greek appears to occur less frequently as epilanguage. This might be because the language is not dead; it lives on in Modern Greek."

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Scientists reveal hidden structures in bacterial DNA

DNA contains the instructions for life, encoded within genes. Within all cells, DNA is organised into very long lengths known as chromosomes. In animal and plant cells these are double-ended, like pieces of string or shoelaces, but in bacteria they are circular. Whether stringy or circular, these long chromosomes must be organised and packaged inside a cell so that the genes can be switched on or off when they are required.

Working together with colleagues in Spain, Japan and Australia, researchers led by Luis Serrano, ICREA research professor and leader of the Design of Biological Systems laboratory at the Centre for Genomic Regulation, focused their attention on the organisation of DNA within an organism with an extremely small genome -- the pneumonia pathogen Mycoplasma pneumoniae. Its circular chromosome is five times smaller than that of larger bacteria such as the gut bug E. coli.

Using a technique called Hi-C, which reveals the interactions between different pieces of DNA, the researchers created a three-dimensional 'map' of the Mycoplasmachromosome. They then used super-resolution microscopy to prove that this computer-generated map matched up with the real-life chromosome organisation inside bacterial cells.

Notably, the CRG team, which counted with the expertise in Mycoplasma from the Serrano's laboratory and the collaboration of the ICREA research professor Marc Marti-Renom at CNAG-CRG, discovered thatMycoplasma's circular chromosome is consistently organised the same way in all the cells, with a region called the Origin (where DNA copying begins) at one end of the structure and the midpoint of the chromosome located at the opposite end. This is a similar arrangement to that seen in some other larger bacterial species.

The scientists also used the Hi-C technique to study more detailed patterns of organisation within the Mycoplasma genome. In recent years, scientists all over the world have investigated the organisation of chromosomes inside cells from species ranging from larger bacteria to human. Next Generation Sequencing has allowed scientists to 'read' the DNA sequence of any genome, but this doesn't reveal how genetic information is managed and organised in the crowded and bustling biological environment inside a cell. Now, new tools have revealed complex organisational structures within the genomes of larger organisms, with certain regions of chromosomes clustered together to form domains containing genes that are switched on or off together.

However, it was thought that these domains would not be found in Mycoplasma, because its genome is so small and it only makes around 20 different DNA binding proteins responsible for organising the chromosome, compared to the hundreds made by other bacterial species.

Intriguingly, the CRG team found that even the tiny Mycoplasma chromosome is organised into distinct structural domains, each containing genes that are also turned on or off in a co-ordinated way.

Marie Trussart, the lead author on the paper, said: "Studying bacteria with such a small genome was a big technical challenge, especially because we were using super-resolution microscopy, and it took us five years to complete the project. We had suspected that the Mycoplasma genome might have a similar overall organisation to other bacteria, but we were completely surprised to find that it was also organised into domains, which can be considered as regulatory units of chromatin organisation and that we had identified a previously unknown layer of gene regulation. This research shows that the organisation and control of genes cannot be understood by just looking at the linear sequence of DNA in the genome. Indeed, to get the full picture of gene regulation we need to look at the three-dimensional organisation of the chromatin that also coordinates gene activity."

The discovery suggests that this level of organisation and genetic control is common to all living cells, from the largest to the smallest, and can be achieved with little more than a handful of DNA binding proteins and the structural properties of the DNA itself.

The CRG team has been working for a long time to achieve detailed quantitative analyses of Mycoplasma pneumoniae at every level: from genetics to metabolism, including patterns of gene activity and protein composition, and more. They plan to use these findings to inform research focused on controlling and manipulating gene activity in genetically-engineered bacteria, which have many important medical and industrial applications.

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People often use the word 'you' rather than 'I' to cope with negative experiences

Researchers say it may seem contradictory that a means of generalizing to people at large is used when reflecting on one's most personal and idiosyncratic experiences. To cope with negative experiences or to share an insight, people often use the word "you" rather than "I."

"You" is an overlooked word that people use to express norms and rules, new University of Michigan research found.

Researchers conducted nine experiments with 2,489 people to understand why people curiously use "you" not only to refer to specific others, but also to reflect on their own experiences.

"It's something we all do as a way to explain how things work and to find meaning in our lives," said Ariana Orvell, a doctoral student in the Department of Psychology and the study's lead author.

"When people use "you" to make meaning from negative experiences, it allows them to 'normalize' the experience and reflect on it from a distance," said Orvell.

For example, "you win some, you lose some" would indicate that a person has failed in a situation, but by using the word 'you,' they are able to communicate that this could happen to anyone.

"Or saying that 'when you are angry, you say and do things that you will most likely regret' might actually explain a personal situation, but the individual attempts to make it something many people relate to," Orvell said.

In one experiment, researchers asked participants to write about a personal experience: 201 were asked to make meaning from a negative event, 198 were asked to relive a negative event, and 203 were simply asked to write about a neutral experience. Those in the meaning-making group used generic-you more in their essays (46 percent used the word at least once) than those in the Relive group (10 percent used the word at least once) and the neutral group (3 percent used the word at least once). The researchers also found that using generic-you led people to view the event as more distant.

The researchers say it may seem contradictory that a means of generalizing to people at large is used when reflecting on one's most personal and idiosyncratic experiences.

"We suspect that it's the ability to move beyond your own perspective to express shared, universal experiences that allows individuals to derive broader meanings from personal events," Orvell said.

Orvell collaborated on the study with Ethan Kross, psychology professor, and Susan Gelman, Heinz Werner Distinguished University Professor of Psychology and Linguistics.

The findings appear in the latest issue ofScience.

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Scientists identify a new way gut bacteria break down complex sugars

New light has been shed on the functioning of human gut bacteria which could help to develop medicines in the future to improve health and wellbeing.

Scientists have found that single microorganisms in the human gut have the ability to disassemble the most complex of carbohydrates in our diet.

It is the first time such a discovery has been made and it is hoped that this may be used to one day identify new pre- and pro-biotic products to enhance people's health.

Led by Professor Harry Gilbert, from the Institute for Cell and Molecular Biosciences at Newcastle University, UK, the study is published today (Wednesday) in the leading academic journal, Nature.

Bacteria in the large bowel -- the human gut -- has a major impact on health and physiology as they help to disintegrate substances in food that we cannot digest, such as starches and fibre.

The main source of nutrients available to the gut bacteria are carbohydrates from the human diet, which the body is unable to metabolise.

The most complex of these carbohydrates is the plant polysaccharide, 'rhamnogalacturonan II (RG-II)', which can also be found at elevated levels in red wine.

Previously it was thought that only groups of bacteria would be able to metabolise and breakdown RG-II, reflecting its complex structure. However, this research shows that single organisms present in the gut also have the ability to do this.

Professor Gilbert said: "Our research reports how a highly complex biological process in the body is achieved.

"This is an exciting step forward in the understanding of how human gut bacteria work and has implications for future research."

The team of international scientists found that RG-II is metabolised through the action of a type of bacterial enzyme, known as glycoside hydrolases, which target the complex carbohydrates sugars in the large bowel.

The bacteria that can metabolise RG-II contain several genes that encode proteins that previously had no known action until now. The group have shown that seven of these genes produce glycoside hydrolases -- which split the glycosidic linkage that joins sugars together in polysaccharides -- and contribute to the breakdown of RG-II.

Each of these seven glycoside hydrolases are founding members of a novel enzyme family. Three of the glycoside hydrolases that contribute to RG-II degradation break glycosidic linkages that have not previously been shown to be susceptible to biological attack, and these enzymes display novel catalytic functions.

Professor Gilbert said: "This study has potential applications as understanding how this highly complex carbohydrate, which is an integral component of our diet, is utilised offers opportunities for developing new pre- and pro-biotic strategies to improve human health.

"There is much more exciting work to be done in this area. To fully understand the mechanisms by which complex carbohydrates are utilized by human gut bacteria is relevant to medicine as this microbial community has a significant impact on the body."

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Brain 'rewires' itself to enhance other senses in blind people

This is a photo of a participant in a Magnetic Resonance Imaging (MRI) scanner used in this study. (Boston University Medical School Center for Biomedical Imaging)

The brains of those who are born blind make new connections in the absence of visual information, resulting in enhanced, compensatory abilities such as a heightened sense of hearing, smell and touch, as well as cognitive functions (such as memory and language) according to a new study led by Massachusetts Eye and Ear researchers. The report, published online today in PLOS One, describes for the first time the combined structural, functional and anatomical changes in the brain evident in those born with blindness that are not present in normally sighted people.

"Our results demonstrate that the structural and functional neuroplastic brain changes occurring as a result of early ocular blindness may be more widespread than initially thought," said lead author Corinna M. Bauer, Ph.D., a scientist at Schepens Eye Research Institute of Mass. Eye and Ear and an instructor of ophthalmology at Harvard Medical School. "We observed significant changes not only in the occipital cortex (where vision is processed), but also areas implicated in memory, language processing, and sensory motor functions."

The researchers used MRI multimodal brain imaging techniques (specifically, diffusion-based and resting state imaging) to reveal these changes in a group of 12 subjects with early blindness (those born with or who have acquired profound blindness prior to the age of three), and they compared the scans to a group of 16 normally sighted subjects (all subjects were of the same age range). On the scans of those with early blindness, the team observed structural and functional connectivity changes, including evidence of enhanced connections, sending information back and forth between areas of the brain that they did not observe in the normally sighted group.

These connections that appear to be unique in those with profound blindness suggest that the brain "rewires" itself in the absence of visual information to boost other senses. This is possible through the process of neuroplasticity, or the ability of our brains to naturally adapt to our experiences.

The researchers hope that increased understanding of these connections will lead to more effective rehabilitation efforts that will enable blind individuals to better compensate for the absence of visual information.

"Even in the case of being profoundly blind, the brain rewires itself in a manner to use the information at its disposal so that it can interact with the environment in a more effective manner," said senior author Lotfi Merabet, O.D., Ph.D., director of the Laboratory for Visual Neuroplasticity at the Schepens Eye Research Institute of Mass. Eye and Ear and an associate professor of ophthalmology at Harvard Medical School. "If the brain can rewire itself -- perhaps through training and enhancing the use of other modalities like hearing, and touch and language tasks such as braille reading -- there is tremendous potential for the brain to adapt."

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Yellow fever killing thousands of monkeys in Brazil

In a vulnerable forest in southeastern Brazil, where the air was once thick with the guttural chatter of brown howler monkeys, there now exists silence.

Yellow fever, a virus carried by mosquitoes and endemic to Africa and South America, has robbed the private, federally-protected reserve of its brown howlers in an unprecedented wave of death that has swept through the region since late 2016, killing thousands of monkeys.

Karen Strier, a University of Wisconsin-Madison professor of anthropology, has studied the monkeys of this forest since 1983. She visited the reserve -- her long-term study site near the city of Caratinga -- in the state of Minas Gerais, in January of 2017. "It was just silence, a sense of emptiness," she says. "It was like the energy was sucked out of the universe."

Using what in some cases are decades of historical data, Strier and a team of Brazilian scientists focused on studying primates in Brazil's patchwork Atlantic Forest are poised to help understand and manage what happens next. They have never seen monkeys perish in such numbers, so quickly, from disease.

With her Brazilian counterpart Sérgio Lucena Mendes, a professor of animal biology at the Universidade Federal de Espirito Santo, and their former postdoctoral researcher, Carla Possamai, Strier is ready to census the monkeys that remain at the reserve, comparing the new data to prior censuses performed in the forest. They also plan to study how the surviving brown howler monkeys regroup and restructure their societies, since their existing social groups have been destroyed.

Strier's study forest, just 4 square miles in size, is a land-locked island of green surrounded by agricultural and pasture lands. How yellow fever showed up here is a mystery, and the monkeys in the forest have nowhere else to go. Less than 10 percent of Brazil's Atlantic Forest remains intact and much of it exists only as small patches in a fragmented landscape.

"I am very surprised at the speed with which the outbreak is advancing through the landscape and by how the virus can jump from one patch of forest to another, even if they are hundreds of meters apart," says Mendes. "It is also surprising that it is spreading across such a large geographic region."

The way yellow fever has spread also concerns Brazilian health officials. As of mid-March 2017, they have confirmed more than 400 human cases of the disease, mostly in Minas Gerais, causing nearly 150 human deaths. The Brazilian Ministry of Health is investigating another 900 possible cases and concern is mounting that it will spread to cities, threatening many more people.

Brazilian authorities also want to protect the monkeys from people who fear the animals may be spreading the disease. "We need to show that they help inform when the virus arrives in a region, because being more sensitive than humans, they die first," Mendes explains.

A dead monkey is like a canary in a coal mine, alerting public health officials that a pathogen may be present, mobilizing preventative and precautionary efforts. So, what does it mean when so many have perished?

"No one really knows the consequences for the other primates or the forest when nearly the entire population of an abundant species dies from disease in just a few months," says Strier. "We are in a position to learn things we never knew before, with all the background information that we have collected."

Nearly two decades ago, Strier helped expand and secure protection for the primates at her study forest, which include four monkey species: the brown howler, the black capuchin, the buffy-headed marmoset and, Strier's animal of interest, the critically-endangered northern muriqui.

It is too soon to say whether the howler monkey population can recover but Strier remains optimistic, in large part because of a career spent studying and helping conserve the brown howler's main competitor, the muriquis. "The muriquis have shown us that it's possible for small populations of primates to recover if they are well-protected," says Strier.

When she first arrived at her study forest, known as RPPN Feliciano Miguel Abdala, there were just 50 muriquis. By September 2016, there were nearly 340, representing one-third of the species' total known population. The animals reside in just 10 forests in southeastern Brazil and nowhere else in the world. Strier's efforts and those of her colleagues have helped restore their numbers.

She is relieved that, so far, the muriquis appear to be less susceptible to yellow fever. "It was really tense -- scary -- to go into the forest, knowing the howlers were gone but not knowing how bad things might also be for the muriquis," Strier recalls.

Her long-term studies have revealed that muriquis have a lifespan of more than 40 years and she has known some of the individual muriquis in the forest their entire lives. Strier can recognize individuals based on natural differences in their fur and facial markings.

Now, in the face of ecological tragedy, she and her colleagues have an opportunity to study how the muriquis adapt in a forest nearly devoid of their competitors.

"It's like a controlled natural experiment, but one you would never plan to do," Strier says. "My happy hypothesis is that the muriquis are out foraging, feasting on all the best fruits and leaves that the howlers used to eat. Will they eat more of their favorite foods, or travel less? Will their social order change? Will they form smaller groups?"

She has documented that kind of behavioral flexibility before. In the late 1980s and early 90s, the muriquis began splitting into smaller groups. In the early 2000s, as their population grew, they began spending more time on the ground, rather than in the trees, often consuming fallen fruits and even half-eaten "leftovers" under the trees.

"I feel like I am 20 years old again" she says. "I have so many questions that are important to answer, for the primates, their Atlantic forest habitat, and for the people that share their world."

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Did humans create the Sahara desert?

Dunes of the Sahara Desert. (© Andrea / Fotolia)

New research investigating the transition of the Sahara from a lush, green landscape 10,000 years ago to the arid conditions found today, suggests that humans may have played an active role in its desertification.

The desertification of the Sahara has long been a target for scientists trying to understand climate and ecological tipping points. A new paper published in Frontiers in Earth Science by archeologist Dr. David Wright, from Seoul National University, challenges the conclusions of most studies done to date that point to changes in the Earth's orbit or natural changes in vegetation as the major driving forces.

"In East Asia there are long established theories of how Neolithic populations changed the landscape so profoundly that monsoons stopped penetrating so far inland," explains Wright, also noting in his paper that evidence of human-driven ecological and climatic change has been documented in Europe, North America and New Zealand. Wright believed that similar scenarios could also apply to the Sahara.

To test his hypothesis, Wright reviewed archaeological evidence documenting the first appearances of pastoralism across the Saharan region, and compared this with records showing the spread of scrub vegetation, an indicator of an ecological shift towards desert-like conditions. The findings confirmed his thoughts; beginning approximately 8,000 years ago in the regions surrounding the Nile River, pastoral communities began to appear and spread westward, in each case at the same time as an increase in scrub vegetation.

Growing agricultural addiction had a severe effect on the region's ecology. As more vegetation was removed by the introduction of livestock, it increased the albedo (the amount of sunlight that reflects off the earth's surface) of the land, which in turn influenced atmospheric conditions sufficiently to reduce monsoon rainfall. The weakening monsoons caused further desertification and vegetation loss, promoting a feedback loop which eventually spread over the entirety of the modern Sahara.

There is much work still to do to fill in the gaps, but Wright believes that a wealth of information lies hidden beneath the surface: "There were lakes everywhere in the Sahara at this time, and they will have the records of the changing vegetation. We need to drill down into these former lake beds to get the vegetation records, look at the archaeology, and see what people were doing there. It is very difficult to model the effect of vegetation on climate systems. It is our job as archaeologists and ecologists to go out and get the data, to help to make more sophisticated models."

Despite taking place several thousands of years ago, the implications of humans being responsible for environmental and climatic degradation are easy to see. With approximately 15% of the world's population living in desert regions, Wright stresses the importance of his findings: "the implications for how we change ecological systems have a direct impact on whether humans will be able to survive indefinitely in arid environments."

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Cooking at home tonight? It's likely cheaper and healthier, study finds

Cooking at home tonight?

Researchers from the University of Washington School of Public Health have been peeking into kitchens -- via interviews -- for years now. They've just published results showing people who cook at home more often are likely to eat a healthier overall diet.

"By cooking more often at home, you have a better diet at no significant cost increase, while if you go out more, you have a less healthy diet at a higher cost," said Adam Drewnowski, director of the UW's Center for Public Health Nutrition and senior author of "Cooking at home: A strategy to comply with U.S. dietary guidelines at no extra cost," published in the American Journal of Preventive Medicine.

The measurement used to define a healthy diet is called the Healthy Eating Index. It gauges whether a person's diet is giving them the right combination of fruits, vegetables and other elements.

As part of the Seattle Obesity Study, researchers interviewed 437 King County adults, who were asked to remember their last week of eating in and eating out. Researchers supervised the adults answering a questionnaire, with detailed sections on what they ate and where.

The study found that home-cooked dinners were associated with a "greater dietary compliance," meaning the overall weekly diet met more of the federal guidelines for a healthy diet. Households who cooked at home about three times per week showed a score of about 67 on the Healthy Eating Index. Those who cooked at home about six times per week had a score of about 74.

"The differences were significant, even with a relatively small study sample," said Drewnowski, also a professor of epidemiology.

Don't feel bad if you don't have time to cook at home every night. Researchers understand.

Drewnowski realizes that some people in the United States suffer from what epidemiologists call "time poverty."

Roughly half of all food dollars in the United States are spent outside the home, which suggests that cooking at home may not be feasible for a large chunk of the population.

Public health nutritionists suggests that efforts to promote cooking at home should be balanced with efforts to encourage retailers and restaurants to offer healthy, less expensive prepared foods for easy purchase outside of the home.

Other measures of food consumption use calories instead of dollars. The contribution of away-from-home food to total calories rose from 18 percent in the 1970s to 32 percent by the late 1990s, according to the study. Only one in five U.S. residents meets the dietary guidelines set by the U.S. Dept. of Agriculture.

What was surprising to Drewnowski was that the study showed there was no increase in costs for eating a healthier diet. Home cooked meals were associated with diets lower in calories, sugar and fat, but not with higher monthly expenses for food.

One other message of the study was that some common assumptions are wrong about income and education. The study showed no association between income or education and eating at home or eating out. The 437 people chosen for the study were a stratified random sample.

"People have the preconception that a lower income leads to eating more fast foods, but that was not true in our study," Drewnowski said. People who cooked more often at home were likely to have larger households with more children in them.

One of the limitations on the study was that people had to remember everything they ate in the past week, and perhaps some memories are not perfect. But he pointed out that almost all nutritional research is done using self-reported information.

The message of healthier-doesn't-cost-more is one he is sharing immediately with students in his Nutrition 303 class, where one of the assignments is to carefully pencil out how much your typical dinner costs.

"There's a lot of ramen," he joked, in regard to homework papers.

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Emotional intelligence helps make better doctors

Among the qualities that go into making an excellent physician is emotional intelligence.

Emotional intelligence is the ability to recognize and understand emotions in yourself and others and to use this awareness to manage your behavior and relationships.

Emotional intelligence plays a big role in determining a physician's bedside manner. It helps make patients more trusting, which in turn leads to better doctor-patient relationships, increased patient satisfaction and better patient compliance. Emotional intelligence also can help make physicians more resilient to the stresses of the profession and less likely to experience burnout.

Loyola University Medical Center is among the centers that are studying emotional intelligence in physicians as a way to improve patient care and physicians' well-being. In a new study for example, Loyola researchers report that physicians-in-training scored in the high range of emotional intelligence.

The young physicians as a group had a median score of 110 on an emotional intelligence survey, which is considered in the high range. (The average score for the general population is 100.) The physicians scored the highest in the subcategories of impulse control (114), empathy (113) and social responsibility (112) and lowest in assertiveness (102), flexibility (102) and independence (101).

The study by Ramzan Shahid, MD, Jerold Stirling, MD, and William Adams, MA, is published in the Journal of Contemporary Medical Education. Dr. Shahid is an associate professor and director of the pediatric residency program. Dr. Stirling is professor and chair of Loyola's department of pediatrics. Mr. Adams is a biostatistician in the health sciences division of Loyola University Chicago.

There have been previous studies of emotional intelligence among physicians, but most studies have not included pediatric residents. To address this need, the Loyola study enrolled 31 pediatric and 16 med-peds residents at Loyola. (A resident is a physician who, following medical school, practices in a hospital under the supervision of an attending physician. A pediatric residency lasts three years. A med-peds residency, which combines pediatrics and internal medicine, lasts four years.)

The residents completed the Bar-On Emotional Quotient Inventory 2.0, a validated 133-item online survey that assesses emotional intelligence skills.

Residents in their third and fourth years of training scored higher in assertiveness (109) than residents in their first and second years (100). This could be related to the acquisition of new knowledge and skills and increased self-confidence as residents progress in their training.

But first- and second-year residents scored higher in empathy (115.5) than third- and fourth-year senior residents (110). "One could hypothesize: Does a resident's level of assertiveness increase at the cost of losing empathy?" the authors wrote.

There were no differences in emotional intelligence composite scores between males and females or between pediatric and med-peds residents.

The study is titled, "Assessment of emotional intelligence in pediatric and med-peds residents."

Unlike IQ, emotional intelligence can be taught. "Educational interventions to improve resident emotional intelligence scores should focus on the areas of independence, assertiveness and empathy," the authors wrote. "These interventions should help them become assertive but should ensure they do not lose empathy."

The Loyola pediatrics and med-peds residents recently went through an emotional intelligence educational program that consisted of four hours of workshops. Initial data show the intervention has increased residents' emotional intelligence scores, including the subcomponents related to stress management and wellness.

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How cells communicate to move together as a group

When an individual cell needs to move somewhere, it manages just fine on its own. It extends protrusions from its leading edge and retracts the trailing edge to scoot itself along, without having to worry about what the other cells around it are doing. But when cells are joined together in a sheet of tissue, or epithelium, they have to coordinate their movements with their neighbors. It's like walking by yourself versus navigating a crowded room. To push through the crowd, you have to communicate with others by talking ("Pardon me") or tapping them on the shoulder. Cells do the same thing, but instead of verbal cues and hand gestures, they use proteins to signal to each other.

This kind of coordinated migration is important during embryonic development when cells migrate to form organs, during healing when they move to close a wound, and unfortunately during the spread of many cancers. Scientists already knew about some of the proteins involved in this process, but research from the University of Chicago has identified a new signaling system that epithelial cells use to coordinate their individual movements and efficiently move tissues.

In a study published Mar. 13, 2017 in the journal Developmental Cell, cell biologist Sally Horne-Badovinac, PhD, and colleagues describe how two cell membrane proteins work together to coordinate epithelial migration in the fruit fly Drosophila. One, called Fat2, localizes at the trailing edge of cells; the other, called Lar, localizes at the leading edge of cells. As cells migrate, Fat2 signals to Lar in the cell behind it, which causes that cell to extend its leading edge, tucking under the cell in front of it. In response, Lar signals back to Fat2, which retracts its trailing edge. Step-by-step, the neighboring cells work together in this coordinated fashion to move the entire tissue.

"The protrusion of one cell goes underneath edge of the cell ahead, so you get what looks like overlapping shingles on a roof," said Horne-Badovinac, who is an assistant professor of molecular genetics and cell biology and senior author of the study. "This process is understood really well at the single cell level, but when you hook these cells all together in a tight sheet, it becomes something more coordinated."

Horne-Badovinac and her team, which included postdoctoral scholars Kari Barlan, PhD, lead author of the paper, and Marueen Cetera, PhD, now at Princeton University, used a fruit fly model to study the signaling process. As female fly embryos develop, the tissues that form egg chambers elongate and rotate into position. Scientists knew that both Fat2 and Lar were involved in this process, but it wasn't clear that cells were migrating because they were rotating around the circumference of the circular chamber, not moving in a straight line from one point to another.

Using new cell culturing techniques, the researchers could grow the egg chambers separately outside the female flies to study them more closely. They saw that when Fat2 was missing from a patch of cells with normal cells behind it, the normal cells didn't make their usual leading edge protrusions. If Lar was missing in a patch of cells behind a normal patch, the normal cells didn't retract their trailing edges to move.

"It was surprising, because what we knew was that the protein [Fat2] was at the trailing edge of the cell, but we were seeing an effect at the leading edge of the cell. So initially that made absolutely no sense," said Horne-Badovinac. "It required careful analysis along those cloned boundaries to really figure it out."

Horne-Badovinac said she still has a lot of questions about how these proteins interact with each other, and believes that there may be other proteins involved that signal to the cytoskeletal machinery that actually drives cellular movement.

"This is just the tip of the iceberg for figuring out how this signaling system works," she said. "I absolutely love thinking about collective behaviors of cells, how they communicate with one another, and how groups of cells can make decisions to move in uniform in complicated ways. By studying this process in a simple Drosophila system, we might generate information that's going to be useful for understanding wound healing or the spread of cancer."

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For hospitalized patients, spending more on care doesn't buy better health

Hospitalized patients treated by physicians who order more or more expensive tests and procedures are just as likely to be readmitted or to die as patients treated by doctors who order fewer or less expensive tests, according to research led by Harvard Medical School and the Harvard T.H. Chan School of Public Health.

The study, published in JAMA Internal Medicine on March 13, is believed to be the first to examine the impact of individual physicians' spending patterns on patient outcomes.

"If you spend more money on a car or a TV, you tend to get a nicer car or a better TV," said study senior author Anupam B. Jena, the Ruth L. Newhouse Associate Professor of Health Care Policy at Harvard Medical School. "Our findings show that's not the case when it comes to medical care. Spending more doesn't always mean you get better health."

Research on variation in spending and outcomes between geographic regions and between hospitals has produced mixed results, but most evidence suggests that greater spending does not reliably translate into better outcomes.

What has been missing from the picture, the authors said, is how individual physician spending within the same hospital translates into patient health. That insight, the researchers added, is a key piece of the puzzle because individual doctors make most of the clinical decisions that drive spending and affect outcomes.

"Before now, most of the research and efforts aimed at cutting spending and improving the value of care have been aimed at hospitals, health systems and groups of doctors," said the lead author Yusuke Tsugawa, a research associate at the Harvard T.H. Chan School of Public Health. "The differences between hospitals and regions are important, but they're only part of the puzzle. Our findings show how important it is to consider the differences between individual doctors in any effort to improve health care."

The researchers analyzed outcomes among Medicare fee-for-service patients aged 65 years and older who were hospitalized for a nonelective medical condition and treated by an internist between 2011 and 2014.

Health care spending varied more across individual physicians within a single hospital than across hospitals, even after accounting for differences between hospitals and patient populations, the data showed.

Overall, 8.4 percent of the total variation in health care spending could be explained by differences between individual physicians, compared to 7 percent explained by differences between hospitals.

Next, researchers examined the link between physician spending and patient outcomes.

When they compared lower- and higher-spending physicians, the researchers found no difference in 30-day patient mortality, nor did they see a difference in readmissions, two factors regarded as key measures of quality of care.

Jena, who is also a physician at Massachusetts General Hospital, cautioned that it's too soon to say whether the results mean that higher-spending physicians could simply spend less with no ill effects for patients.

"Say you have two painters. One usually takes two hours to paint a room, and one takes six hours. You can ask the slow painter to hurry up, but you might end up with a room that's sloppily painted, or with one of the walls the wrong color," Jena said. "That's obviously a situation we want to avoid in health care."

It could be that some doctors don't fully consider the costs associated with the tests and procedures they order, Jena said, and so policymakers or insurers could create incentives to curb some of the more wasteful spending. On the other hand, Jena said, some doctors might just be less efficient than others and may need additional resources to arrive at a proper diagnosis or an effective treatment. Whatever the causes of the variation, Jena added, these findings underscore the impact of decisions made by individual doctors on health care spending.

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