Culture

Research conducted by the University of Kent has suggested that the sexual selection hypothesis for infanticide may be the key driver for the high rate of infant killings among a community of chimpanzees in Uganda.

Led by PhD student Adriana Lowe and Dr Nicholas Newton-Fisher from Kent's Living Primates Group, the research team analysed the records of infanticides and failed attempts at infanticide over a 24-year period in the Sonso community of chimpanzees in the Budongo Forest.

While relatively rare, infanticide is well documented in chimpanzees but those in the Sonso community are more prone to practice it than others that have been studied, with infanticide the most common cause of infant death there. However, although various explanations have been proposed, this study is the first to thoroughly investigate the phenomenon.

For the study, the team analysed 33 attacks on 30 victims from a single community of chimpanzees between 1993 and 2017. From this they were able to determine that 11 of the attacks were 'definite' infanticides, four 'almost certain', nine 'suspected', and nine 'attempted'. Most attacks were by adult males, and the victims were often very young: two thirds were under one week old. The team also noted incidents of partial cannibalism.

From their analysis and observations they concluded that the sexual selection hypothesis - the idea that male chimpanzees will kill infants other than their own so they have a better chance of fathering the mother's next infant - was the main reason for the high rates of infanticide. For example, females who lost an infant to infanticide conceived on average around seven times more quickly than if their infant had survived, with the majority of mothers who lost infants going on to reproduce again within the community.

The team found no evidence to suggest that infanticide was part of a male strategy to eliminate future competitors.

Dr Newton-Fisher, who has studied infanticide in the Sonso community since the 1990s, said: 'Sexually-selected infanticide involves the reduction in time until the mother is free to mate again that a male could bring about by killing her present infant. However, we did identify examples of infanticide by females. Although rare, in those cases we suggest that they may use infanticide to drive away rival mothers, who would otherwise compete with them for food.

'We also discovered rare occurrences of partial cannibalism within the community, suggesting meat acquisition was a by-product of the infanticide.'

Chemicals produced by healthy bacteria could be used to assess the health of the gut microbiome and help identify critically-ill children at greatest risk of organ failure, a study published in Critical Care Medicine has found.

The gut microbiome is a trillions-strong community of healthy bacteria that live inside us. They make important contributions to our health, including fermenting the food we eat, making vitamins and regulating our appetite. In critical illness, patients often receive lots of antibiotics, and this may inadvertently damage many healthy gut bacteria.

Children have a less developed microbiome so may be at particular risk following strong antibiotic therapy. If the antibiotics damage healthy gut bacteria, this can result in the loss of important functions of the microbiome and an increase in potentially disease-causing and antibiotic-resistant bugs; in turn, these can cause complications including organ failure.

In this new study, researchers looked at how critical illness affects the functions of the gut microbiome. Researchers examined genetic profiles of gut bacteria and measured levels of chemicals these bacteria produce in 60 critically ill and 55 healthy children. They looked at gut bacterial populations by sequencing the DNA in faecal samples. They then undertook chemical analysis of urine and faecal samples from children participating in the study.

The researchers found that in seriously ill children, the numbers of 'good' bacteria were reduced compared to healthy children. Alongside this, chemicals normally produced by the healthy gut microbiome were dramatically reduced. Levels of some of these chemicals were associated with how sick the children were.

In urine, three bacterial chemicals (called hippurate, formate and 4-cresol sulphate) were dramatically depleted in samples from critically ill patients.

In faeces, the researchers found patients had lost a group of chemicals called short chain fatty acids. These chemicals, normally produced by healthy gut bacteria, have a number of beneficial activities for the body. These include maintaining a healthy gut lining, regulating appetite and supporting the immune system.

The lead investigator, Dr Nazima Pathan, from the Department of Paediatrics at the University of Cambridge and Cambridge University Hospitals NHS Foundation Trust, said: "Trillions of healthy bacteria live in our guts, keeping it healthy as well as supporting our digestion and metabolism. Serious illness may strike a severe blow to the ability of these bacteria to survive and continue their beneficial activities.

"Chemicals produced by healthy gut bacteria are effectively a signature of the presence of a healthy, functioning microbiome. Measuring their levels could offer doctors a way of identifying who needs treatment to restore a healthy microbiome, and for how long."

The researchers say that biochemical measures could complement the assessment of gut microbiome composition and offer an insight into the microbiome's functional capacity. The researchers are working on a rapid assay to help monitor gut health by measuring these chemicals as an indicator of gut health. It could help identify patients who need probiotics to restore the numbers of healthy bacteria in the gut.

Antibodies that exist in the joints before the onset of rheumatoid arthritis can cause pain even in the absence of arthritis, researchers from Karolinska Institutet in Sweden report. The researchers believe that the finding, which is published in the Journal of Experimental Medicine, can represent a general mechanism in autoimmunity and that the results can facilitate the development of new ways of reducing non-inflammatory pain caused by rheumatoid arthritis and other autoimmune diseases.

"We all know that inflammation is painful," says Camilla Svensson, professor at the Department of Physiology and Pharmacology, Karolinska Institutet. "But pain can appear before any sign of inflammation in the joints and can remain a problem after it has healed. Our aim was to find possible mechanisms to explain that."

Rheumatoid arthritis is an autoimmune disease that occurs when immune cells attack the cartilage and bone of the joints. The disease affects roughly one per cent of the Swedish population.

A common early symptom is joint pain, but even before that, the body has started to produce immune antibodies against proteins in the joint. Researchers at Karolinska Institutet have now studied how these autoantibodies can generate pain.

After injecting cartilage-binding autoantibodies into mice, which served as a model for human rheumatoid arthritis, the researchers found that the mice became more sensitive to pain even before they could observe any signs of inflammation in the joints. Antibodies that had been designed not to activate immune cells and trigger inflammation also induced pain-like behaviour in the mice, suggesting increased pain sensitivity in the joints.

The researchers found that the antibodies that caused the behavioural change form so called immune complexes, comprising clusters of antibodies and cartilage proteins in the joints. These complexes activate pain cells via so-called Fc-gamma receptors, which the researchers discovered were present on pain neurons in the tissue.

When they cultivated pain neurons from the mice, the researchers found that the cells were activated when coming into contact with the antibody complexes. The process was dependent upon the Fc-gamma receptors on the neurons but not on the presence of immune cells. Antibodies in complex can thus act as pain-generating molecules in themselves, independently of the activity of the immune cells, as Camilla Svensson, one of the study's two corresponding authors explains:

"Antibodies in these immune complexes can activate the pain neurons directly, and not, as previously thought, as a result of the destructive joint inflammation," she says. "The antibodies can affect the pain neurons also in conditions without any distinct tissue damage or inflammation."

Although the study was conducted in mice, the researchers show that human pain neurons also have antibody receptors that are functionally similar to those they found on the mouse pain neurons, which leads them to believe that their findings are also relevant to humans.

The results can explain the early pain symptoms in rheumatoid arthritis patients. However, joint and muscle pain are also common symptoms of other autoimmune diseases, and since this newly discovered mechanism operates through the constant part - "the shaft" - of the autoantibody, the researchers believe that it can explain non-inflammatory pain caused by other autoimmune diseases too.

"We think that this can be a general pain mechanism in effectively all autoimmune diseases in which these kinds of immune complex form locally in tissue," says Professor Svensson.

More detailed study of what happens in the nerve cell when the antibody complex binds to the receptor could also lead to new targets for reducing the neuronal activity.

"By learning more about the molecular mechanisms of antibody-mediated pain we hope to lay the groundwork for a new way of reducing pain caused by rheumatoid arthritis and other autoimmune diseases," says Rikard Holmdahl, professor at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet, and the study's other corresponding author.

The dentate gyrus (DG) is the input region of the hippocampus and plays an important role in learning and memory. Although emerging evidence suggested that abnormal expression of the polycomb repressive complex 2 protein (PRC2) might cause neurological disease, the underlying molecular mechanisms had not been explored until recently.

Now, in a study published in Stem Cell Reports, a team led by Prof. LIU Changmei from the State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology of the Chinese Academy of Sciences, has shown that the PcG protein EED is essential for the proper formation of the DG.

By generating an EED conditional knockout mouse model, the researchers found that disruption of EED resulted in postnatal lethality, impaired migration of granule cells, loss of the subgranular zone (SGZ), and a severely disrupted secondary radial glial scaffold in the hippocampus.

They then identified Ink4a/Arf (Cdkn2a) and Sox11 as key downstream targets of EED with distinct functions in modulating the proliferation and differentiation of neural stem/progenitor cells (NSPCs) in the DG.

They also for the first time provided functional and molecular evidence supporting the essential role of EED-mediated H3K27 methylation in the reorganization of NSPCs during DG development.

This study establishes EED as an important modulator of hippocampal development and provides novel mechanistic insights into the complex role that EED plays in brain development and neurological diseases.

Fossils of a giant new species from the long-extinct group of sea creatures called trilobites have been found on Kangaroo Island, South Australia.

The finding is adding important insights to our knowledge of the Cambrian 'explosion', the greatest diversification event in the history of life on Earth, when almost all animal groups suddenly appeared over half-a-billion years ago.

Trilobites, which had hard, calcified, armour-like skeletons over their bodies, are related to modern crustaceans and insects. They are one of the most successful fossil animal groups, surviving for about 270 million years (521 to 252 million years ago). Because of their abundance in the fossil record, they are considered a model group for understanding this evolutionary period.

"We decided to name this new species of trilobite Redlichia rex (similar to Tyrannosaurus rex) because of its giant size, as well as its formidable legs with spines used for crushing and shredding food - which may have been other trilobites," says James Holmes, PhD student with the University of Adelaide's School of Biological Sciences, who led the research.

The preservation of trilobite 'soft parts' such as the antennae and legs is extremely rare. The new species was discovered at the Emu Bay Shale on Kangaroo Island, a world-renowned deposit famous for this type of preservation. The findings have been published in the Journal of Systematic Palaeontology by a team of scientists from the University of Adelaide, South Australian Museum and the University of New England.

The new species is about 500 million years old, and is the largest Cambrian trilobite discovered in Australia. It grew to around 30 cm in length, which is almost twice the size of other Australian trilobites of similar age.

"Interestingly, trilobite specimens from the Emu Bay Shale - including Redlichia rex - exhibit injuries that were caused by shell-crushing predators," says senior study author Associate Professor Diego García-Bellido, from the University of Adelaide and the South Australian Museum.

"There are also large specimens of fossilised poo (or coprolites) containing trilobite fragments in this fossil deposit. The large size of injured Redlichia rex specimens and the associated coprolites suggests that either much bigger predators were targeting Redlichia rex, such as Anomalocaris - an even larger shrimp-like creature - or that the new species had cannibalistic tendencies."

One of the major drivers of the Cambrian explosion was likely an evolutionary "arms race" between predators and prey, with each developing more effective measures of defence (such as the evolution of shells) and attack.

"The overall size and crushing legs of Redlichia rex are a likely consequence of the arms race that occurred at this time" says James Holmes. "This giant trilobite was likely the terror of smaller creatures on the Cambrian seafloor."

ANN ARBOR--A new University of Michigan study challenges a popularized view about what's causing the growing gap between the lifespans of more- and less-educated Americans--finding shortcomings in the widespread narrative that the United States is facing an epidemic of "despair."

Some influential studies have argued that growing life expectancy inequality is driven by so-called "deaths of despair," suggesting that economic stagnation has induced less-educated Americans to turn to drugs, alcohol and suicide.

Yet, that explanation is inconsistent with a large body of research on the way many disadvantaged Americans respond to stress, says Arline Geronimus, a professor at U-M's School of Public Health and lead author of the study published in the June issue of the Journal of Health and Social Behavior.

"The assumption that people are giving up neglects the existing research that shows the engaged and tenacious ways people often deal with life challenges," Geronimus said.

Geronimus and her team set out to look at whether the empirical data backed this concept. They used Census and Vital Statistics data to evaluate historically relevant causes of deaths--including opioids, cardiovascular disease, HIV, and lung or other cancers--for non-Hispanic blacks and whites between 1990 and 2015, ranking them by gender and education (less or more educated).

When looking at the deaths of despair (drug overdose, suicide and alcohol-related liver diseases), the researchers found that drug overdoses do contribute to the widening inequality for whites, especially men, but that's not the case for blacks. Also, they found that overdose deaths are less important for growing inequality in women's life expectancy.

For older adults, where the growth in inequality is largest, premature death due to cardiovascular disease and cancers are the main reason for the widening gap--not overdose deaths. The early onset and progression of such chronic diseases can reflect the physiological impact of prolonged and resolute coping with life stressors, Geronimus says.

She points out that suicide rates have contributed little to the growing inequality gap, contrary to the "deaths of despair" theory. Instead, deaths due to cardiovascular disease, non-lung cancers and other internal diseases might help explain important shares of the growing life expectancy gap between those less educated and their highly educated counterparts, Geronimus says.

"These findings suggest that, rather than giving up in the face of hopelessness, less-educated Americans may be losing ground for exactly the opposite reason--because they work so hard, they bear the health consequences of years of stress," she said.

As for the opioid epidemic, Geronimus says researchers should also consider how targeted marketing to white populations, overprescription of legal opioids by physicians, the increasing use of fentanyl in street drugs, and restricted access to life-saving resources have all contributed to the increase in inequality in life expectancy accounted for by opioid deaths in whites.

"The deaths of despair narrative is speculative, overlooks black lives and implies that lack of resilience explains the life expectancy inequities among whites, especially of those who have been socioeconomically disenfranchised," Geronimus said.

"While addressing the opioid epidemic is urgent, we should not lose sight of the widening educational mortality gap attributed to cardiovascular disease, cancers and other internal causes."

Sickle cell disease is a hereditary disorder that affects red blood cells, distorting their natural disc shape into a crescent moon or "sickle" shape. Normal red blood cells move freely through small vessels throughout the body to deliver oxygen. With sickle cell disease, the misshapen red blood cells become hard and sticky, making it difficult for them to move through blood vessels. They eventually block the flow and break apart. This process results in a number of problems including severe chronic pain, stroke, organ damage, spleen dysfunction, heart failure and even death.

Sickle cell disease affects millions of people of many nationalities throughout the world, including both children and adults. A major challenge in managing the disease is the tremendous pain that patients endure from chronic and acute pain episodes called pain crisis. Unfortunately, these pain episodes are unpredictable and patients never know when or where these episodes will take place.

Current methods to detect and monitor sickle cell disease rely mainly on optical microscopy, which is time-consuming, causes delays in capturing important changes, and moreover, does not capture changes in real-time. Morphological changes due to repeated cell sickling events may lead to permanent cell damage. To effectively manage sickle cell disease, time is of the essence.

Researchers from Florida Atlantic University's College of Engineering and Computer Science have developed a rapid and reliable new method to continuously monitor sickle cell disease using a microfluidics-based electrical impedance sensor.

Results of the study, published in the American Chemical Society's journal ACS Sensors, show that this novel technology can characterize the dynamic cell sickling and unsickling processes in sickle blood without the use of microscopic imaging or biochemical markers.

With this method, Sarah E. Du, Ph.D., senior author and an assistant professor in FAU's Department of Ocean and Mechanical Engineering, and co-authors from FAU's College of Engineering and Computer Science and the University of Miami, were able to characterize the rate of cell sickling and the percentage of sickled cells, which are important contributing factors of abnormal blood flow and sickle cell vaso-occlusion. Vaso-occlusion causes acute pain in patients due to altered forms of hemoglobin.

"The combination of electrical impedance measurement and on-chip hypoxia control provides a promising method for rapid assessment of the dynamic processes of cell sickling and unsickling in patients with sickle cell disease," said Du. "In addition, electrical impedance measurement is naturally quantitative, real-time, and offers a convenience in direct or indirect contact with the samples of interest, allowing integrations to microfluidics platform and optical microscopy."

Findings from the study show that simultaneous microscopic imaging of morphological changes in the cell demonstrated the reliability and repeatability of the electrical impedance-based measurements of cell sickling and unsickling processes.

In the study, the researchers also established the correlations between the in vitro measurements and the patients' hematological parameters, such as the levels of sickle hemoglobin (HbS) and fetal hemoglobin (HbF). These findings show a potential clinical relevance because it serves as a proof-of-concept of electrical impedance as a label-free, biophysical marker of cell sickling events as well as a sensitive tool for probing the dynamic cellular and subcellular processes beyond the optical microscopy. The developed electrical impedance sensor may potentially be used for assessing vaso-occlusion risk, disease severity, and therapeutic treatment in sickle cell disease.

"As we move our technology forward, it is our hope to provide patients with sickle cell disease with a portable, standalone sensor that will enable them to conveniently self-monitor the hematological parameters of their disease and evaluate their risk of vaso-occlusion," said Du.

In the United States, sickle cell disease disproportionately affects African Americans as well as Hispanics and those of Middle Eastern descent. Approximately 2 million Americans carry this genetic mutation, which affects about 100,000 individuals in the U.S. The most common and serious problems caused by sickle cell disease are anemia, pain and organ failure, and stroke affects about 10 out of 100 children who have this disease. Currently, the life expectancy for patients with sickle cell disease can reach up to 50 years, a dramatic improvement since 1973, when the average lifespan for the disease was only 14 years.

"Patients with sickle cell disease encounter a number of challenges trying to manage their condition. The inability to monitor their disease in real-time is especially problematic for patients as well as clinicians," said Stella Batalama, Ph.D., dean of FAU's College of Engineering and Computer Science. "Professor Du's cutting-edge research has the potential to provide patients with sickle cell disease worldwide with the same convenience and reliability of monitoring their disease as patients with diabetes who use glucose monitors."

Optoelectronic integration offers a promising strategy to simultaneously obtain the merits of electrons and photons when they serve as information carriers, including high-density communication and high-speed information processing, paving the way for the next-generation integrated circuits (ICs). The ever-increasing demand on bandwidth and information density in ICs call for the micro/nano functional devices capable of being fabricated in three-dimensional (3D) ICs, which is desirable for their improved performance in data processing under lower consumption. In such highly integrated circuits, however, selective electrical modulation of specific micro/nanoscale optical devices, including light sources and waveguides, is a key requirement for yielding more functional and more compact integrated elements, but hindered by the normal used nonlinearity found in electro-optic materials.

Femtosecond laser direct writing (FsLDW), as one of the 3D printing techniques, enables the direct and addressable construction of 3D-integrated optoelectronic devices utilizing organic compounds with two-photon polymerized features. With doping flexibility, the polymerized microstructures can be readily incorporated with organic dye molecules to produce functional devices, like coherent laser sources. Besides, organic polymers possess excellent responsiveness to external stimuli, including temperature. Their large thermo-optic coefficient enables the realization of the electrical tuning of resonant wavelength with high efficiency when they are fabricated into microcavity structures. The incorporation of thermo-responsive polymeric microlaser with underneath electrical microheater in the 3D fabrication manner can be used as an effective hybrid microlaser module with selective electric modulation towards optical-electronic integration.

Very recently, Professor Yong Sheng Zhao's group in the Institute of Chemistry, Chinese Academy of Sciences demonstrated an in situ electrically modulated microlaser module based on 3D-printed dye-doped polymeric microdisks, which is published in Science China Chemistry.

The thermo-optic effect of the polymer matrix enabled the tuning of lasing modes from the microdisk upon heating. The shape designability of FsLDW allows the fabrication of higher-level microstructures to manipulate light signals, including the waveguide coupled microdisks for light remote control and the coupled double-microdisk resonators for laser mode selection. The latter microstructure was further integrated with an underneath electrical microheater.

As a result, the cavity resonant wavelength can be shifted on the basis of resistance heating controlled optical length change through the thermo-optic effect of polymeric matrix material, which enabled an electrical modulation of the output wavelength of the 3D-printed microlaser module.

ANN ARBOR, Mich. - Vaccinating babies against a virus that causes childhood "stomach flu" greatly reduces their chance of getting so sick that they need hospital care, a new study shows.

But the study also reveals a surprise: Getting fully vaccinated against rotavirus in the first months of life is associated with a lower risk of developing Type 1 diabetes later on.

As a group, children who received all recommended doses of rotavirus vaccine had a 33 percent lower risk than unvaccinated children of getting diagnosed with type 1 diabetes - a lifelong disease with no known prevention strategies or cure.

A team from the University of Michigan made the finding using nationwide health insurance data, and published their results in the journal Scientific Reports.

The study provides strong post-market evidence that the vaccine works. Children vaccinated against rotavirus had a 94 percent lower rate of hospitalization for rotavirus infection, and a 31 percent lower rate of hospitalization for any reason, in the first two months after vaccination. Rotavirus hits infants and toddlers hardest; it can cause diarrhea and vomiting that can lead to dehydration or loss of fluids.

Yet the study finds more than a quarter of American children don't get fully vaccinated against rotavirus, and that the rate varies widely across the country. Less than half of children in New England and Pacific states were fully vaccinated. Two-thirds of children in the central part of the country were fully vaccinated.

The Centers for Disease Control and Prevention recommends that infants receive the multi-dose vaccine starting no later than 15 weeks, and finish receiving it before they are eight months old. Infants receive the vaccine in oral drops.

Type 1 diabetes relationship

The paper's authors, led by epidemiologist Mary A.M. Rogers, Ph.D., caution that they cannot show a cause-and-effect relationship between rotavirus vaccination and Type 1 diabetes risk.

"This is an uncommon condition, so it takes large amounts of data to see any trends across a population," says Rogers, an associate professor in the U-M Department of Internal Medicine. "It will take more time and analyses to confirm these findings. But we do see a decline in Type 1 diabetes in young children after the rotavirus vaccine was introduced."

The new result echoes the findings of a study of Australian children published earlier this year, which found a 14 percent reduced risk of Type 1 diabetes after the rotavirus vaccine was introduced in that country. That study, and the new one, suggest that a childhood vaccine may lead to a lower risk of a later chronic condition.

It also fits with laboratory studies showing that rotavirus attacks the same kind of pancreas cells that are affected in people with Type 1 diabetes.

The death of insulin-producing cells, called beta cells, means people with Type 1 diabetes depend on injections of insulin, and multiple daily checks of their blood sugar, for life. If the condition is not managed well, people with Type 1 diabetes may develop problems with their kidneys, heart, eyes, blood vessels and nerves over time.

Data-driven discovery

The U-M team used anonymous insurance data from 1.5 million American children born before and after the modern rotavirus vaccine was introduced in 2006. In nearly all cases, the vaccine was free, with no copayment, to the family of the infant. The total lifetime cost of caring for an individual with Type 1 diabetes has been estimated in the millions of dollars.

The risk was especially lower among children who received all three doses of the pentavalent form of the vaccine than those who received two doses of the monovalent form. The pentavalent rotavirus vaccine protects against 5 types of the rotavirus while the monovalent vaccine protects against 1 type.

Children partially vaccinated - that is, started the vaccine series but never finished it - did not have a lower risk of Type 1 diabetes.

More than 540,000 of the children in the study and born after 2006 received the complete series of rotavirus shots; nearly 141,000 received at least one dose, and more than 246,000 did not.

Another comparison group, born in the five years before the vaccine was available, included nearly 547,000 children.

In absolute terms, Rogers and her colleagues report that eight fewer cases of Type 1 diabetes would be expected to occur for every 100,000 children each year with full vaccination.

Type 1 diabetes, once called "juvenile diabetes," only affects a few children out of every 100,000, so having such a large pool of data can help spot trends, says Rogers, an epidemiologist who worked with internist Catherine Kim, M.D., M.P.H. and statistician Tanima Basu, M.S. Rogers and Kim are members, and Basu is a staff member, of the U-M Institute for Healthcare Policy and Innovation, which provided the data used in the study.

"Five years from now, we will know much more," says Rogers. "The first groups of children to receive the rotavirus vaccine in the United States are now in grade school, when Type 1 diabetes is most often detected. Hopefully, in years to come, we'll have fewer new cases - but based on our study findings, that depends upon parents bringing in their children to get vaccinated."

DURHAM, N.C. - A team led by Duke Health scientists has identified a cellular process that could lead to the development of safer and more effective vaccines that protect pregnant women as well as their newborns from dangerous infections.

Publishing online June 13 in the journal Cell, the researchers describe a previously unidentified route for antibodies to be transferred from the mother to the fetus, illuminating a potential way to capitalize on this process to control when and how certain antibodies are shared.

"It's always been assumed that the types of maternal antibodies that cross over the placenta to the fetus, all antibodies had the same chance of transferring to fetus," said senior author Sallie Permar, M.D., Ph.D., a professor of pediatrics and member of the Duke Human Vaccine Institute.

"This meant there was no way we could direct certain antibodies across the placenta and to the baby," Permar said. "Our study found that there seems to be a code on the antibody that determines which antibodies will more effectively transfer across the placenta."

Permar and colleagues -- including co-senior author Genevieve Fouda, Ph.D., and lead author David Martinez, Ph.D. -- studied two populations of pregnant women in the United States and Malawi who were infected with HIV, which is known to inhibit the transfer of antibodies to the fetus - and not just HIV antibodies. This feature provided a unique circumstance to explore a little-understood process with implications for numerous common pathogens, including tetanus, pertussis, influenza and others.

The researchers identified a sugar molecule that interacts with placental receptors, an interaction that had previously not been known to be involved in the antibody transfer process. The finding was corroborated in healthy women by another research team publishing in the same issue of Cell.

"We have shown that the efficiency of antibody transfer across the placenta is differentially regulated," Permar said. "This insight could improve the design of vaccines for a variety of infectious diseases to improve the transplacental antibody transfer to the fetus."

"Our findings provide a roadmap of how antibodies cross the placenta to the baby," Martinez said. "We hope our results will be useful for developing antibody therapeutics that protect infants against infectious diseases in early life."

WASHINGTON -- People who feel financially vulnerable may be prone to believing incorrectly their success in negotiations must come at the expense of the other party, leading them to ignore the potential for more cooperative and mutually beneficial options, according to research published by the American Psychological Association.

"Our research suggested that those who feel financially disadvantaged often approach economic exchanges, such as negotiations, with the assumption that each party has directly conflicting preferences," said Tianyu He, MA, of INSEAD, Singapore, and lead author of the study. "However, a much more beneficial strategy is a cooperative approach where each side engages in joint problem solving, exploring each party's different preferences. This strategy maximizes the negotiation outcomes for both parties so if financially disadvantaged individuals use this method, they may not continue to perpetuate their situations through poor deals."

The study was published in the Journal of Applied Psychology.

He and her co-authors explored whether having or perceiving financial vulnerability would prompt a zero-sum perception of success, meaning that success for one person can only come at another's expense.

"This idea can also be described as a 'fixed-pie' view, where people go into a negotiation as if each side is arguing over how big a piece of the pie they each get, with one side losing a slice for every slice the other side takes," she explained. "This can cause people to not consider the potential to 'expand the pie,' by looking for cooperative agreements where both sides win."

The researchers first looked at the Integrated Value Survey dataset, an international survey with 191,648 participants across 90 countries from 1981 to 2014. This survey gauged financial vulnerability through multiple measures: reported household income; perception of which income group they felt they were in within their country; satisfaction with their financial situation; and whether respondents lacked food and cash. The survey also measured participants' beliefs that their success must come at the expense of others by using a scale from 1 (e.g., people can only get rich at the expense of others) to 10 (e.g., wealth can grow so there is enough for everyone).

"This provided evidence that when people experienced financial vulnerability, they were more likely to believe their gain depended on the loss of others," said Rellie Derfler-Rozin, PhD, of the University of Maryland and one of the study co-authors.

To test how this relationship might apply to negotiations, the authors conducted four experiments with over 1,000 undergraduate students.

In all four of the experiments, participants were paired up and asked to negotiate four different issues regarding the sale of a car: the price, color, warranty and delivery date.

The authors assigned point values to each potential outcome for each issue (e.g., a one-year warranty gives the seller 600 points and gives the buyer 100 points). The warranty and delivery date scores were weighted in such a way that if players used cooperative strategies (i.e., they worked together to find a mutually acceptable solution), the sum of their points would be greater than if they competed to maximize their individual point totals. The higher the combined point value after the negotiation, the more the participants used an integrative, cooperative strategy as opposed to a zero-sum strategy.

In the first experiment, the students were asked to write about an experience when they did not have enough money or an experience when they did. This was done to put the participants who wrote about not having enough money in a mindset of financial vulnerability in which they would be more inclined to think about concerns related to material resources, said He.

Participants were then put into pairs and engaged in the negotiation. Half of the pairs were told that the two best individual performers in the experiment would receive $50, while the other half were given no financial incentive. Only the pairs who were given a financial incentive showed significant differences in negotiation strategies. The subsequent experiments followed the same procedures as the first experiment except that all pairs were given a financial incentive and financial vulnerability was measured by reported household income.

In all four experiments, the researchers found evidence that financial vulnerability was significantly associated with lower total point values, confirming that participants experiencing financial vulnerability were more likely to approach the situation with a zero-sum mindset and thus less likely to capitalize on opportunities for joint value gain, said He. The authors believe these findings could provide a partial explanation for why it is so difficult for low-income people to improve their economic standing.

"By holding this win-lose mindset, financially disadvantaged people may continue to make poor deals, perpetuating their situation," said Marko Pitesa, PhD, of Singapore Management University, a study-co-author. "Negotiation training programs may be beneficial to help them look for and recognize the potential for cooperative exchanges."

NEW YORK, June 13, 2019 - Many people associate dopamine with reward or attention. Some might think of the part it plays in addiction, or Parkinson's disease, which kills off dopamine-making neurons.

Now scientists at The Graduate Center of The City University of New York and Brooklyn College have discovered yet another role for this neurotransmitter, in the social communication between plainfin midshipman fish. Seasonal changes in dopamine in the female fish's inner ear helps their hearing sensitivity grow in the summer mating season, making them better able to hear the males' mating calls.

Their study was published today in Current Biology.

"Dopamine plays an important role in setting the baseline auditory sensitivity of the fish during a critical moment in their life cycle," said Graduate Center Ph.D. student and lead author Jonathan Perelmuter. "We hope our work will inspire others to consider a role for dopamine in the inner ear in the context of vocal communication."

In the summer these fish migrate from deep waters to the intertidal zone to mate. At night, the males make their call, producing a deep hum to attract females.

A 2014 study also from the lab of Graduate Center and Brooklyn College Professor Paul Forlano found a dopamine pathway from the brain to the fish's inner ear -- the first time this had been seen in a non-mammalian vertebrate. But the pathway's purpose was unclear. Prior studies on dopamine's action in the inner ear looked at rodents in the context of protection from damaging sounds, said Forlano, primary investigator for both studies. A year later, the lab discovered that dopamine in the female fish's inner ears changed with their reproductive state.

Together, these clues led to the latest study. The researchers observed that dopamine decreases hair cell sensitivity in the females' inner ear. It does this, in part, via D2a receptors, a subtype of dopamine receptors. In the summer, D2a receptor expression decreases. As a result, the saccule is less inhibited, and the fish's hearing becomes more sensitive.

Studies from co-author Joseph Sisneros (University of Washington) and the lab of Andrew Bass (Cornell University) have observed seasonal plasticity in the plainfin midshipman fish's inner ear sensitivity as a result of changing hormone levels. Thus, the new paper explains another cause of this yearly change.

Plainfin midshipman fish are a good model for studying auditory-driven behavior and plasticity because the species' survival depends on their hearing abilities. Their seasonal mating behavior also provides more dramatic changes than a species that mates throughout the year.

"Discoveries that are made from studying this simpler system may elucidate fundamental and conserved neural mechanisms of acoustic communication found in other vertebrates more famous for vocalizing such as frogs and birds and primates, including ourselves," Forlano said.

The flow of traffic through our nation's highways and byways is meticulously mapped and studied, but less is known about how materials in cells travel. Now, a team of researchers at the University of Missouri is challenging prior theories about how material leaves the inside of an E.coli cell. This discovery could have important implications for how we treat diseases.

"Proteins are like vehicles that can carry information and materials in cells," said Gavin King, an associate professor of physics in the MU College of Arts and Science and joint associate professor of biochemistry. "We focused on the cells of E.coli, which have two membranes. We observed that when proteins exit the cell's inner membrane, the cell adjusts the way it transfers the protein through the channel depending on the type of protein being transported."

King worked with Linda Randall, professor emerita of biochemistry. Randall verified the transportation function of E.coli cells outside of their natural environment. Once verified, the samples were sent to King where King's team used an atomic force microscope to study the movement of the E.coli proteins. Unlike previous studies where proteins were frozen, the atomic force microscope allows researchers to observe the proteins moving in a fluid environment that closely resembles their natural environment.

"Before our study there were two ways of describing how proteins moved across the cell membrane - either a piston-live movement similar to a car's engine, or a more perpetual motion known as the Brownian ratchet," King said. "Neither model accounted for the differences based on the type of protein being transported. Just as different types of vehicles move differently so do different types of proteins. The maps we made to depict the proteins' movement suggest nature might be more complex than previously thought."

These findings provide basic knowledge on how a cell sends and receives material and information. For instance, a drug can pass through membranes in order to affect a cell, and similarly, some information must pass through membrane channels to exit the cell. While other cells besides E.coli may not have E.coli's exact protein transportation system, King said a similar system exists in all cells.

Wikipedia is one of the most successful online communities in history, yet it struggles to attract and retain editors who are women -- another example of the gender gap online. In a recent University of Washington study, researchers interviewed women "Wikipedians" to examine the lack of female and non-binary editors in Wikipedia. The team identified a common theme: safety.

"People can get harassed when they're editing content in Wikipedia," said co-author Wanda Pratt, a professor in the UW's Information School. "If you're constantly getting negative feedback for doing something, how often are you going to do it?"

The researchers presented their results May 9 at the 2019 ACM CHI conference on Human Factors in Computing Systems in Glasgow, Scotland. In this video, the authors describe their findings.

The team interviewed 25 well-established editors to find out their stories. The conversations revealed that many participants had their edits contested and that some participants felt unsafe within the community.
"In the data we collected, it goes beyond trolling," said first author Amanda Menking, a doctoral student in the iSchool. "There's doxxing, which is exposing people's personal information and where to find them online or in physical space such as their address. Some of the women we talked to received death threats."

But participants also discussed how they managed their safety both conceptually and physically, and how they acted on this understanding to create safe spaces on and off Wikipedia. In order to navigate Wikipedia and related online communities -- for example, Facebook groups -- these women use sophisticated tactics for how they manage their online identities, boundaries and emotions.

The authors suggest solutions for future online environments that encourage equity, inclusivity and safety for historically marginalized users.

"Wikipedia says it's the sum of all human knowledge and it's the encyclopedia anyone can edit. That is a pretty big claim," Menking said. "There's also a responsibility to be held to those claims, that if you say you are the sum of all human knowledge then you need representative humans contributing that information."

As planets form in the swirling gas and dust around young stars, there seems to be a sweet spot where most of the large, Jupiter-like gas giants congregate, centered around the orbit where Jupiter sits today in our own solar system.

The location of this sweet spot is between 3 and 10 times the distance Earth sits from our sun (3-10 astronomical units, or AU). Jupiter is 5.2 AU from our sun.

That's just one of the conclusions of an unprecedented analysis of 300 stars captured by the Gemini Planet Imager, or GPI, a sensitive infrared detector mounted on the 8-meter Gemini South telescope in Chile.

The GPI Exoplanet Survey, or GPIES, is one of two large projects that search for exoplanets directly, by blocking stars' light and photographing the planets themselves, instead of looking for telltale wobbles in the star -- the radial velocity method -- or for planets crossing in front of the star -- the transit technique. The GPI camera is sensitive to the heat given off by recently-formed planets and brown dwarfs, which are more massive than gas giant planets, but still too small to ignite fusion and become stars.

The analysis of the first 300 of more than 500 stars surveyed by GPIES, published June 12 in the The Astronomical Journal, "is a milestone," said Eugene Chiang, a UC Berkeley professor of astronomy and member of the collaboration's theory group. "We now have excellent statistics for how frequently planets occur, their mass distribution and how far they are from their stars. It is the most comprehensive analysis I have seen in this field."

The study complements earlier exoplanet surveys by counting planets between 10 and 100 AU, a range in which the Kepler Space Telescope transit survey and radial velocity observations are unlikely to detect planets. It was led by Eric Nielsen, a research scientist at the Kavli Institute for Particle Astrophysics and Cosmology at Stanford University, and involved more than 100 researchers at 40 institutions worldwide, including the University of California, Berkeley.

One new planet, one new brown dwarf

Since the GPIES survey began five years ago, the team has imaged six planets and three brown dwarfs orbiting these 300 stars. The team estimates that about 9 percent of massive stars have gas giants between 5 and 13 Jupiter masses beyond a distance of 10 AU, and fewer than 1 percent have brown dwarfs between 10 and 100 AU.

The new data set provides important insight into how and where massive objects form within planetary systems.

"As you go out from the central star, giant planets become more frequent. Around 3 to 10 AU, the occurrence rate peaks," Chiang said. "We know it peaks because the Kepler and radial velocity surveys find a rise in the rate, going from hot Jupiters very near the star to Jupiters at a few AU from the star. GPI has filled in the other end, going from 10 to 100 AU, and finding that the occurrence rate drops; the giant planets are more frequently found at 10 than 100. If you combine everything, there is a sweet spot for giant planet occurrence around 3 to 10 AU."

"With future observatories, particularly the Thirty-Meter Telescope and ambitious space-based missions, we will start imaging the planets residing in the sweet spot for sun-like stars," said team member Paul Kalas, a UC Berkeley adjunct professor of astronomy.

The exoplanet survey discovered only one previously unknown planet -- 51 Eridani b, nearly three times the mass of Jupiter -- and one previously unknown brown dwarf -- HR 2562 B, weighing in at about 26 Jupiter masses. None of the giant planets imaged were around sun-like stars. Instead, giant gas planets were discovered only around more massive stars, at least 50 percent larger than our sun, or 1.5 solar masses.

"Given what we and other surveys have seen so far, our solar system doesn't look like other solar systems," said Bruce Macintosh, the principal investigator for GPI and a professor of physics at Stanford. "We don't have as many planets packed in as close to the sun as they do to their stars and we now have tentative evidence that another way in which we might be rare is having these kind of Jupiter-and-up planets."

"The fact that giant planets are more common around stars more massive than sun-like stars is an interesting puzzle," Chiang said.

Because many stars visible in the night sky are massive young stars called A stars, this means that "the stars you can see in the night sky with your eye are more likely to have Jupiter-mass planets around them than the fainter stars that you need a telescope to see," Kalas said. "That is kinda cool."

The analysis also shows that gas giant planets and brown dwarfs, while seemingly on a continuum of increasing mass, may be two distinct populations that formed in different ways. The gas giants, up to about 13 times the mass of Jupiter, appear to have formed by accretion of gas and dust onto smaller objects -- from the bottom up. Brown dwarfs, between 13 and 80 Jupiter masses, formed like stars, by gravitational collapse -- from the top down -- within the same cloud of gas and dust that gave rise to the stars.

"I think this is the clearest evidence we have that these two groups of objects, planets and brown dwarfs, form differently," Chiang said. "They really are apples and oranges."

Direct imaging is the future

The Gemini Planet Imager can sharply image planets around distant stars, thanks to extreme adaptive optics, which rapidly detects turbulence in the atmosphere and reduces blurring by adjusting the shape of a flexible mirror. The instrument detects the heat of bodies still glowing from their own internal energy, such as exoplanets that are large, between 2 and 13 times the mass of Jupiter, and young, less than 100 million years old, compared to our sun's age of 4.6 billion years. Even though it blocks most of the light from the central star, the glare still limits GPI to seeing only planets and brown dwarfs far from the stars they orbit, between about 10 and 100 AU.

The team plans to analyze data on the remaining stars in the survey, hoping for greater insight into the most common types and sizes of planets and brown dwarfs.

Chiang noted that the success of GPIES shows that direct imaging will become increasingly important in the study of exoplanets, especially for understanding their formation.

"Direct imaging is the best way at getting at young planets," he said. "When young planets are forming, their young stars are too active, too jittery, for radial velocity or transit methods to work easily. But with direct imaging, seeing is believing."