Culture

Researchers at the Feinstein Institute for Medical Research, USA have developed an index that identifies the risk for lupus based on the presence and amount of Immunoglobin G (IgG) and Immunoglobin M (IgM) antibodies and levels of C1q, a protein complex associated with protection from lupus, in blood serum. The findings are published in the open access journal Molecular Medicine.

The risk index, which needs to be validated in further studies, could be useful in following at risk individuals over time to identify those that may benefit from early interventions, and to identify diagnosed lupus patients who might be at risk of an impending flare.

Dr Betty Diamond, the corresponding author said: "Lupus - or systematic lupus erythematosus (SLE) - is a multi-organ autoimmune disorder with disproportionally higher prevalence in individuals of West African descent. Understanding risk and why it differs between populations may enable prevention studies. Here we analyzed serum from unique populations with varying degrees of risk in order to identify serologic factors that might correlate with risk of or protection against SLE."

To compare potential biomarkers of SLE among women with different SLE risks, the authors analyzed blood serum samples from five cohorts: 40 Malian women with a history of malaria infection (MAL), 51 African American lupus patients (SLE), 80 healthy African American women (AAHC), 98 unaffected sisters of lupus patients (SIS), and 16 Caucasian healthy controls (CHC).

The authors found that titers of IgM antibodies - which are known to protect against lupus onset - were lowest in the SLE, SIS and AAHC cohorts and higher in the MAL and CCH cohorts. Levels of IgG antibodies - the presence of which precedes lupus onset - were highest in the SLE and MAL cohorts and similar in the CHC, AAHC and SIS cohorts. The SLE cohort was also found to have the lowest C1q levels. C1q promotes immune tolerance, which includes stopping immune cells from attacking the body's own cells as is the case in autoimmune diseases such as lupus. Ninety percent of individuals with hereditary C1q deficiency also have lupus.

Dr Diamond said: "The possibility that a risk index could help identify populations as risk for development of clinical lupus is novel and exciting. The risk index we developed was highest in SLE patients; second highest in unaffected sisters of SLE patients; third highest in healthy African-American women and lowest in healthy Caucasian women and malaria-exposed West African women. Thus, it confirms known lupus risk, as well as our hypothesis that high levels of IgG, low levels of IgM (and the resulting high IgG to IgM ratio) and low levels of C1q predispose to lupus. Our results also confirm the hypothesis that exposure to malaria results in increased levels of protective IgM antibodies and C1q which may delay onset of lupus in genetically predisposed individuals."

The authors caution that their risk index needs to be validated in future longitudinal studies which also need to determine the actual risk of developing SLE for each risk score. However, the observations made in this study may suggest new therapeutic approaches for SLE treatment and could eventually be used in early diagnosis, according to the authors.

In just over 1,000 years, Icelanders have gone through numerous changes in their gene pool, to the extent that Iceland's first settlers, who came to the island from Norway and the British and Irish isles between the years 870 and 930, are much more similar to the inhabitants of their original home countries than to Iceland's present-day inhabitants.

This is one of the main conclusions of a study carried out by an international team of scientists which included members of the Spanish National Research Council (CSIC). For the first time, the researchers, whose results are published in the journal Science, analysed the ancient genomes of 25 individuals who lived in Iceland during the colonisation of the island.

With a population of 330,000, Iceland is a country with its own peculiarities. Genes are no exception: isolation and inbreeding throughout its history make this northern Atlantic island a paradise for genetic studies.

The analysis of ancient skeletal remains- more specifically the teeth belonging to the first generations to populate the island- has shed more light on the genetic evolution which led to a combination of genes coming from Scotland, Ireland and Scandinavia. According to the conclusions of this study, the Norwegian genetic fingerprint of present day Icelanders stands at 70%, while, in the case of the island's original founders, it was 57%.

As CSIC researcher Carles Lalueza-Fox, who works at the Institute of Evolutionary Biology (a joint institute between CSIC and Pompeu Fabra University) explains, "This work takes an in-depth look at the process which makes small, isolated populations go through random changes in their genetic variability over time. Present-day Icelanders have been affected by 1,100 years of profound genetic drift. This means they are more similar to each other, yet different to modern populations of continental Europe."

Gender bias

The work, led by researchers from deCODE Genetics- the biotechnology company based in Reykjavik which claims to have genealogical records going back for up to seven centuries in the history of most families on the island, confirms a gender bias in Iceland's population.

"The settlers of Celtic origin had fewer offspring compared with those of Norwegian origin. This is probably because there were more men of Scandinavian origin compared to more women - who would probably have come to the country as slaves and servants - from Scotland and the rest of Britain," explains Lalueza-Fox.

"We have always known that Icelanders descended from Norwegians and Celts, and the analysis of the ancient genomes from the first colonists allows us to see what they were like, both before mixing started, as well as throughout the whole process," explains Sunna Ebeneserdóttir, a researcher from deCODE Genetics. "It's like having a time machine. Now it is possible to study the actual people who participated in the founding of Iceland," adds Agnar Helgason, also from deCODE Genetics, and another of the study's authors.

Iceland, a genetic laboratory

These results provide a detailed view of the origin of a human population, an aspect, according to scientists, which is key to discovering associations of genotype (genetic information in the form of DNA) and phenotype (the expression of the genotype plus the influence of the mean) to continue making advances in finding ways to diagnose, treat and prevent diseases.

"Iceland is big enough for the diseases that affect Europeans to be represented, yet small enough to easily carry out genetic studies which lead to discovering the roots of these complex pathologies. In the not too distant future, we will be able to study the actual individuals who had a certain mutation 1,000 years ago and make a comparison with current patients", concludes the CSIC researcher.

Boston, MA - The mortality rate in Puerto Rico rose by 62% [95% confidence interval (CI) 11% to 114%] after Hurricane Maria, according to a new study led by researchers from Harvard T.H. Chan School of Public Health. The study was conducted in January and February 2018, in collaboration with colleagues from Carlos Albizu University in Puerto Rico and the University of Colorado School of Medicine.

The researchers concluded that the original estimate of 64 excess deaths due to Hurricane Maria is likely to be a substantial underestimate. The study estimates a death rate of 14.3 deaths per thousand [95% CI 9.8 to 18.9] between September 20 (date of Hurricane Maria) and December 31, 2017, up from a rate of 8.8 deaths per thousand at the same time in 2016. About one third of the reported deaths in the households surveyed in the study were attributed to delayed or prevented access to medical care.

The study was published online May 29, 2018 in the New England Journal of Medicine.

Hurricane Maria made landfall in Puerto Rico on September 20, 2017, inflicting approximately $90 billion worth of damage and displacing thousands of residents. The storm disrupted medical services across the island, and many households were left for weeks without water, electricity, or cell phone coverage.

As with any major natural disaster, assessing the loss of life caused by Hurricane Maria was difficult and contentious. For disaster-related deaths to be confirmed in Puerto Rico, bodies must be transported to San Juan or a medical examiner must travel to the region to verify the death. This makes it difficult to log deaths that were caused by delays in treatment or chronic conditions that worsened in the aftermath of the storm. In December 2017, media reports suggested that the official death toll was significantly underestimated.

To produce an independent estimate of lives lost as a result of the storm, the researchers surveyed 3,299 randomly chosen households across Puerto Rico. Participants were asked about infrastructure damage, displacement, and deaths. Results from the survey showed that there were an estimated 14.3 deaths per 1,000 people between September 20 and December 31, 2017. By comparing this post-hurricane mortality rate with the same time period in 2016, the researchers estimated that there were 4,645 [95% CI, 793 to 8498] additional deaths in the three-month period following Hurricane Maria.

In addition to a significantly higher death toll, the study showed that the average household went approximately 41 days without cell phone service, 68 days without water, and 84 days without electricity following the storm. More than 30% of surveyed households reported interruptions to medical care, with trouble accessing medications and powering respiratory equipment being the most frequently cited challenges.

Household-based surveys such as these are well studied in the scientific literature and offer a cost-effective, rapid approach in the aftermath of a disaster. The researchers have made all of their anonymized data, analysis, and code publicly available for review.

Support for the study came from Harvard T.H. Chan School of Public Health and the University of Colorado School of Medicine, Department of Emergency Medicine, Section of Wilderness and Environmental Medicine.

LA JOLLA--(May 31, 2018) One of the many challenges in treating HIV is that the virus can lie dormant in cells, quietly evading immune detection until it suddenly roars to life without warning and begins replicating furiously. Salk Institute researchers discovered a small molecule called JIB-04 that destroys the HIV protein called Tat, responsible for revving up the virus.

The molecule, while itself too toxic to serve as a therapy for HIV, reveals proteins in host cells that can potentially target Tat and halt this runaway replication process. The work, which appeared in the journal PLOS Pathogens on May 23, 2018, also more broadly illustrates a powerful new laboratory technique that can identify more precisely which proteins bind to drugs--information that is often elusive.

"The level of Tat very much determines whether or not you can reactivate a virus from latency," says senior author Katherine Jones, a professor in Salk's Regulatory Biology Laboratory and holder of the Edwin K. Hunter Chair. "Even though JIB-04 cannot be used clinically, we were able to use it to show an important part of how Tat levels are determined by a pair of enzymes in the host cell. Identifying them offers new targets for potential therapies."

Like all viruses, HIV-1 (the common form of HIV) enters the body and uses the host's own cellular machinery to copy the viral genetic material and spread from cell to cell. Tat kicks copying into high gear when conditions are favorable, revving up the machinery a thousandfold. Jones' team was investigating other HIV proteins when they noticed that one of the compounds they were testing, a small molecule called JIB-04, caused Tat to disappear.

The effect was striking, but how exactly JIB-04 was accomplishing this vanishing act was unclear. Jones enlisted the help of researcher James Moresco, director of Salk's Mass Spectrometry Core, who used a new approach called DiffPOP (short for "differential precipitation of proteins") to identify the protein targets of drug compounds.

"The application of the DiffPOP technique to identify drug/protein interactions enabled the identification of a completely unexpected insight into the biology of HIV," says Moresco. "It is a great example of how collaboration between our labs at Salk, as well as with The Scripps Research Institute, who developed the underlying technology, encourages discovery."

The DiffPOP results showed that JIB-04 was binding to two of the host cells' enzymes (SHMT2 and BRCC36) whose job is to rescue proteins that have been targeted for disposal. Some enzymes flag proteins as cellular "trash"; others remove the flags, thereby saving those proteins from destruction. Jones' team hypothesized that the compound interfered with the ability of these proteins to protect Tat, enabling the cell to destroy Tat and keep the virus in its latent state.

Further tests confirmed their hypothesis: in cells not treated with JIB-04, but in which the two enzymes were disabled through molecular methods, Tat levels also went down. Additionally, in cells that were treated with JIB-04 as well as ones in which the two enzymes were disabled, Tat was flagged for degradation at high levels, which also suggested that the enzymes were responsible for flag removal.

"Based on these phenomena, we think this compound may actually target these two proteins," says Muyu Xu, a research associate at Salk and the paper's first author. "It may have other potential targets, but this pair is one of them. So we concluded that these enzymes might be novel factors that regulate Tat turnover in cells."

Even though HIV has gone from a deadly disease to a chronic condition that can be kept at bay with antiviral therapies, the daily cocktail of drugs is extremely burdensome for people with the disease. The researchers say that understanding the factors that influence Tat's stability are crucial to being able to control the virus.

"As researchers, we'd like to find a way for people not to have to be on these drugs their whole lives," says Jones. "So the idea of inhibiting Tat to get to a functional cure for HIV is very appealing."

New research carried out by the John Innes Centre has delved into the genetic memory systems through which plants pass seasonal information down to their seeds to give them the best chance of reproductive success.

Plants integrate seasonal signals such as temperature and day length and use this memorised information to optimise the timing for key lifecycle stages.

These development transitions include flowering, seed dispersal and seed dormancy a timely tactic employed by "mother" plants to ensure seed germination happens in optimal conditions when seedling survival rate is high.

Seasonal sensing requires the activity of two well characterised genes Flowering Locus C (FLC) and Flowering Locus (FT) the former a temperature sensor that acts as a brake to flowering and the latter a daylength sensor.

Previous studies have indicated that FLC acts on FT in a linear fashion to deliver seasonal information that promotes flowering.

Now this new study led by Professor Steven Penfield of the John Innes Centre, has identified the precise mechanism by which temperature information is passed from mother to seeds.

"What is interesting about these new findings is that the same genes which control the timing of flowering also control seed germination, but act in reverse order," said Professor Penfield.

The study, which appears in the peer reviewed journal Science, shows that the two genes gather temperature information from the environment and share this with progeny during seed set.

"The mother plant uses seasonal information to control the behaviour of the progeny to optimise fitness," explains Professor Penfield

"We discovered some time ago is that the mother generates diversity, and the mechanism the mother uses is variation in temperature because as temperatures vary, plants produce seeds that are slightly different, in size, in number."

In this way, the BBSRC-funded research finds, the mother plant exploits environmental temperature variation to create diversity in seed type and behaviour - a kind of reproductive bet-hedging in which the plant uses temperature information to create a diverse and widely spread offspring.

This mechanistic insight into the model species Arabidopsis thaliana can lead to better crops, say the study authors.

"Greater understanding of how plants communicate seasonal information to their offspring will help efforts to create crops that cope better with climate change," explains Professor Penfield.

"If we understand the mechanism by which plants cause variation in progeny year to year, we can learn how to breed more stable crops," he added.

The full report:

The full findings are in the paper published today in Science: Temperature-responsive vernalisation signalling is rearranged to control plant seed dormancy.

COLUMBUS, Ohio - A strong social network could be the key to preserving memory.

New research from The Ohio State University found that mice housed in groups had better memories and healthier brains than animals that lived in pairs.

The discovery bolsters a body of research in humans and animals that supports the role of social connections in preserving the mind and improving quality of life, said lead researcher Elizabeth Kirby, an assistant professor of behavioral neuroscience and member of the Center for Chronic Brain Injury at Ohio State.

"Our research suggests that merely having a larger social network can positively influence the aging brain," said Kirby, who is a member of the Neurological Institute at Ohio State's Wexner Medical Center. Her research appears in the journal Frontiers in Aging Neuroscience.

"We know that in humans there's a strong correlation between cognitive health and social connections, but we don't know if it's having a group of friends that's protecting people or if it's that people with declining brain health withdraw from their human connections," Kirby said.

This study was designed to answer that hard-to-crack question with an animal model.

Some mice lived in pairs, which Kirby refers to as the "old-couple model." Others were housed for three months with six other roommates, a scenario that allows for "pretty complex interactions."

The mice were 15 months to 18 months old during the experiment - a time of significant natural memory decline in the rodent lifespan.

"It's like mouse post-retirement age. If they drove, they'd be forgetting where the keys are or where they parked the car more often," Kirby said.

In tests of memory, the group-housed mice fared better.

One test challenged the mice to recognize that a toy, such as a plastic car, had moved to a new location. A mouse with good brain health will gravitate toward the novelty of something that has been relocated.

"With the pair-housed mice, they had no idea that the object had moved. The group-housed mice were much better at remembering what they'd seen before and went to the toy in a new location, ignoring another toy that had not moved," Kirby said.

In another common maze-based memory test, mice are placed on a well-lit round table with holes, some of which lead to escape hatches. Their natural tendency is to look for the dark, unexposed and "safe" escape routes.

Both groups of mice improved their escape-route search strategies with practice - but the research team was struck by the differences in the groups' response to repeated tests, Kirby said.

The "couples" mice didn't get faster at the test when it was repeated over the course of a day.

"But over the course of many days, they developed a serial-searching strategy where they checked every hole as quickly as possible. It'd be like walking as quickly as possible through each row of a parking lot to look for your car rather than trying to remember where your car actually is and walk to that spot," Kirby said.

The group-housed mice improved with each trial, though.

"They seemed to try to memorize where the escape hatches are and walk to them directly, which is the behavior we see in healthy young mice," Kirby said. "And that tells us that they're using the hippocampus, an area of the brain that is really important for good memory function."

The serial searching employed by the pair-housed mice is simpler, easier and doesn't use that part of the brain, she said.

In humans, mice and many other animals, brain function in the hippocampus markedly declines with age, even in the absence of dementia. Exercise and social ties are known to preserve memory in this region in people, Kirby said.

After the housing experiment, the researchers examined the brain tissue of the mice and found increased inflammation in the pair-housed mice - biological evidence of eroded cognitive health.

"The group-housed mice had fewer signs of this inflammation, meaning that their brains didn't look as 'old' as those that lived in pairs," Kirby said.

The researchers also looked for evidence of new neuron growth in the hippocampus and found no differences between the groups.

Previous research in this area has primarily focused on mice that have highly enriched environments with lots of toys and opportunities for exercise and compared them with mice without as much to do.

This study goes further by showcasing differences that appear to be due to socialization alone, Kirby said. Future research should explore the molecular explanations for the connection between socialization and improved memory and brain health, she said.

Kirby said that people who are aging would do well to consider how their choices about where to live might impact their ability to be social.

"Something as basic as how long it takes to drive or walk to a friend's house can make a big difference as we get older," she said.

"A lot of people end up isolated not by choice, but by circumstance. 'Over the river and through the woods' might be fun for the kids, but it's probably not so great for Grandma," Kirby said.

Cell biologists have deepened understanding of proteins associated with neurodegenerative diseases. The findings could open up new treatment approaches for disorders including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS), among others.

Researchers in Japan have gained valuable insights into 'stress granules' -- clumps of RNAs and proteins that form when cells are stressed by factors such as heat, toxins and viruses.

As stress granules are linked to a range of neurodegenerative diseases, understanding how they form, and how they can be reduced, is of great interest to the medical world.

Published in the Journal of Cell Science, their study reveals the important role of two enzymes in disassembling stress granules.

These two enzymes, named USP5 and USP13, belong to a group of nearly 100 known deubiquitylases, which are thought to work by cutting ubiquitin chains[1] inside stress granules.

The study is the culmination of over five years of work by the team, including Masayuki Komada, Toshiaki Fukushima and Shunsuke Matsumoto of Tokyo Institute of Technology (Tokyo Tech). First author Xuan Xie, a PhD student at the laboratory led by Komada, has described how they arrived at their 'eureka' moment in an interview with the journal's First Person series.

As a first step, the researchers demonstrated that USP5 and USP13 are preferentially recruited to heat-induced stress granules.

"We found that heat-induced stress granules contain ubiquitin chains, much more so than in stress granules induced by other stressors," explains Fukushima. "This implied that ubiquitin chains may recruit USP5 and USP13 to stress granules."

Importantly, as ubiquitin chains are often found in stress granules in neurodegenerative diseases, the heat-induced stress granules provided a good model for further investigation.

Next, the team compared what happens to heat-shocked cells with and without the two enzymes. The cells were exposed to a temperature of 44°C for one hour, and returned to 37°C for one hour. During the recovery period, in cells lacking USP5 and USP13, the team found that the disassembly of stress granules was delayed.

Specifically, in cells containing USP5 and USP13, the percentage of cells with stress granules fell to 14%, whereas this figure was 60% or more in cells without the two enzymes.

The findings suggest that the presence of USP5 and USP13 is critical to the disassembly of stress granules.

Although the exact mechanisms have yet to be determined, the researchers propose that USP5 hydrolyzes or "cuts" unanchored ubiquitin chains, while USP13 cuts protein-conjugated[2] ubiquitin chains.

"We concluded that both reactions are required for the efficient destabilization of stress granules," says Fukushima.

The study may lead to the development of "artificial deubiquitinating enzymes", which could have a profound impact on future medical treatments.

Developing such innovative enzymes that "possess high activity and show specific localization to stress granules" is a feat that could be achieved in five years, Fukushima adds.

A well preserved, nearly complete skeleton of a new extinct species of pheasant that lived between seven and 11 million years ago adjacent to the northeastern edge of the Tibetan Plateau in China preserves the oldest evidence of a bird having modified and specialized its vocalization sounds (songs or calls).

Everyone is familiar with birds singing and making a variety of sounds, such as roosters crowing at dawn. However, little direct evidence exists for how extinct birds sounded, but this new skeleton from China begins to change that story. The Chinese fossil named Panraogallus hezhengensis preserves a windpipe (trachea) that is extremely long (longer than the bird's body), and it was coiled into several loops outside of the chest cavity (see photo of the fossil and an artist's reconstruction of the whole skeleton with the windpipe).

While the windpipe itself does not produce sounds, birds with a very long windpipe make sounds that are louder and lower in frequency than birds of a similar size with a typical length windpipe. This kind of windpipe elongation is known in about 60 species of birds today including cranes, ibises, and even some Birds of Paradise in New Guinea. However, Panraogallus is the oldest record of its occurrence in birds, and the first record of a super long windpipe in pheasants, a group of birds that is very diverse in China and across Asia today.

It appears that birds evolve these hyper-elongated windpipes in order to sound like a larger-sized bird (who make relatively louder and lower frequency sounds). This change is similar to the evolution of a long windpipe in various mammals for much the same reasons (recently covered in the press). See a recent publication in Nature Communications about the mammalian equivalent.

"This bird's windpipe is special because it coiled around at least twice outside of the chest, and it looks like it might have even looped back towards the leg before returning back up to enter the chest cavity and attach to the lungs," said Chinese paleontologist LI Zhiheng, lead author of the study published in Scientific Reports.

"The discovery of this super long trachea in a pheasant, which don't have long windpipes today, suggests that the story of the evolution of bird song is much more complex than what we think now based only on living species," said coauthor Thomas Stidham, an American paleontologist based at the Chinese Academy of Sciences in Beijing. "The fossil also shows the struggle to sound like the best, biggest, or baddest bird has been going on for millions of years."

The species name of this extinct bird Panraogallus hezhengensis means coiled chicken in reference to the coiled windpipe and its close affinity to living pheasants; and Hezheng, the town in Gansu Province, Western China where the fossil was found. The elevation of Hezheng today is over 2000 meters (more than 6000 feet), and it is adjacent to the high altitude Tibetan Plateau. This bird fossil was found in the yellow and reddish clay that is famous for the many three-toed horse or Hipparion fossils. Based on estimates from the skeleton, the pheasant weighed about 2.5 kilograms or 5.5 pounds, which is close to the average body size of living birds that have elongated windpipes. It appears that this long windpipe may have been present only in males of this extinct species, as in some living bird relatives, and the fossil preserves the bony base where a spur would have attached on the foot like that in chickens and turkeys, suggesting that the fossil bird is a male.

The ancient Hezheng landscape with the tall Tibetan mountains in the background filled with extinct rhinoceroses, three-toed horses, and ostriches, also had the loud call of a male pheasant echoing across the savannah.

Over the last few years, work by LI Zhiheng in the Hezheng fossil deposits has produced other spectacular skeletons including those of an extinct vulture, and an early falcon, that even preserves its last meal of rodents. As of yet, none of those other fossils provide the same clue as to how they sounded in life.

White Americans' fear of losing their socioeconomic standing in the face of demographic change may be driving opposition to welfare programs, even though whites are major beneficiaries of government poverty assistance, according to new research from the University of California, Berkeley, and Stanford University.

While social scientists have long posited that racial resentment fuels opposition to such anti-poverty programs as food stamps, Medicaid and Temporary Aid to Needy Families, this is the first study to show the correlation experimentally, demonstrating a causal relationship between attitudes to welfare and threatened racial status.

"With policymakers proposing cuts to the social safety net, it's important to understand the dynamics that drive the welfare backlash," said study lead author Rachel Wetts, a Ph.D. student in sociology at UC Berkeley. "This research suggests that when whites fear their status is on the decline, they increase opposition to programs intended to benefit poorer members of all racial groups."

The findings, to be published May 30 in the journal Social Forces, highlight a welfare backlash that swelled around the 2008 Great Recession and election of Barack Obama.

Notably, the study found anti-welfare sentiment to be selective insofar as threats to whites' standing led whites to oppose government assistance programs they believed largely benefit minorities, while not affecting their views of programs they thought were more likely to advantage whites.

"Our findings suggest that these threats lead whites to oppose programs they perceive as primarily benefiting racial minorities," said study senior author Robb Willer, a professor of sociology and social psychology at Stanford University.

It is particularly timely in the face of conservative Republican lawmakers' efforts to cut federal spending by putting social safety net programs like Medicaid and the Supplemental Nutrition Assistance Program, formerly known as food stamps, on the chopping block.

In the study, researchers tracked a shift in attitudes to welfare around 2008 when Obama, America's first black president, was elected, and the country was suffering from a major recession whose reverberations continue to impact tens of millions of whites and non-whites alike.

According to census figures, 43 million Americans lived in poverty in 2016. Whites comprised 43 percent of Medicaid recipients, 36 percent of food stamp recipients and 27 percent of the beneficiaries of Temporary Aid to Needy Families.

"Welfare programs are race-blind in that all low-income Americans are eligible to receive them," Willer said. "So opposition to them, especially during tough economic times, threatens the same safety net that helps whites, as well as minorities, endure economic hardship."

HOW THEY CONDUCTED THE STUDY

In three separate studies, researchers analyzed nationally representative survey data of over 7000 adult American men and women. In addition, they conducted two experiments with 400 participants via Amazon's Mechanical Turk, an online marketplace.

First, an examination of attitudes to race and welfare in a nationally-representative survey found that whites' racial resentment rose in 2008, the same year of the Great Recession and election of Barack Obama, suggesting that perceptions of increased political power among minorities were leading whites to sense a threat to their group's status. At the same time, researchers discovered, whites' opposition to welfare increased relative to that of minorities'.

Next, researchers conducted an experiment in which participants were shown one of two graphs highlighting different aspects of U.S. population trends: One emphasized a stable white majority, and the other emphasized the declining white population in the U.S. White participants who saw information highlighting a decline in the white population reported heightened racial resentment and opposition to welfare programs. And, when asked how they would trim the federal budget, they recommended larger cuts to welfare.

In the third experiment, researchers found that when whites saw a threat to their economic advantage over minorities, they were more likely to want to cut social safety net programs, but only if those programs were portrayed as primarily benefiting minorities, not if they were portrayed as benefiting whites.

"Overall, these results suggest whites' perceptions of rising minority power and influence lead them to oppose welfare programs," Wetts said.

The professional ethos of law firms discourages men from taking parental leave, a new Finnish-Canadian study shows. Carried out by the University of Eastern Finland and TÉLUQ University in Quebec, the study found that the professional culture in law firms rests on traditional masculine ideology, with men regarded as the providers for their families. This view does not encourage men to combine their professional career and child care. The findings were reported in the International Journal of the Legal Profession.

The fact that few male lawyers take parental leave is an indication of gender inequality within the legal profession.

"In law firms, family policies and flexible working arrangements are mainly targeted at women, and this has a negative impact on women's career development. If fathers took a more active role in child care, it would facilitate the emergence of a professional culture that is more family-friendly. In the process, it is also likely that this would reduce gender bias in the division of legal tasks and career paths within law firms," Researcher Marta Choroszewicz from the University of Eastern Finland explains.

The study examined male lawyers' motives behind taking or not taking paternity and parental leaves in law firms based in Helsinki, Finland, and in Montreal, Canada. Canadian male lawyers were significantly less keen to take paternity leave than their Finnish colleagues. This is partly explained by Finland's longer paternity leave tradition. Instead of taking paternity leave, Canadian male lawyers preferred taking annual holiday when their child was born.

The greater popularity of paternity leave in Finland is also explained by organisational differences between Finnish and Canadian law firms. In Finland, young lawyers typically work as members of a team, and they for example face lower expectations to attract new clients than their Canadian colleagues. In Canada, the work revolves more around the individual, and even young lawyers are expected to contribute to marketing, networking and new client recruitment.

Preliminary findings from Finland show that there, too, the attitudes to paternity leave vary from one generation to the next. Law firm partners representing the post-Second World War generation and Generation X often did not take paternity leave when their children were small, and they do not necessarily understand the need of today's young male lawyers to participate in early child care. In many law firms, paternity leaves are still regarded as optional, compared to, for example, maternity leaves.

"It is not enough that men's right to parental leave is guaranteed by legislation. We also need organisational solutions, collegial encouragement and examples set by male law firm partners," Choroszewicz points out.

In Finland, the right to paternity leave was enacted in legislation in 1978. In 2013, the length of paternity leave was extended to nine weeks. In Canada, taking paternity leave has been possible since 2006, but only in the province of Quebec, and the length is only half of what it is in Finland.

DALLAS - May 30, 2018 - Building on two decades of research, investigators at UT Southwestern have determined that "cellular housekeeping" can extend the lifespan and healthspan of mammals.

A study jointly led by Drs. Salwa Sebti and Álvaro Fernández, postdoctoral researchers in the Center for Autophagy Research, found that mice with persistently increased levels of autophagy - the process a cell uses to dispose of unwanted or toxic substances that can harm cellular health - live longer and are healthier. The study, published online today, is found in Nature.

"Specifically, they have about a 10 percent extension in lifespan and are less likely to develop age-related spontaneous cancers and age-related pathological changes in the heart and the kidney," said Dr. Beth Levine, Director of the Center for Autophagy Research at UT Southwestern.

Twenty years ago, Dr. Levine and her colleagues discovered beclin 1 - a key gene in the biological process of autophagy. The group's research has since shown that autophagy is important in many aspects of human health, such as preventing neurodegenerative diseases, combating cancer, and fighting infection.

In 2003, Dr. Levine's team found that the genetic machinery required for autophagy was essential for the lifespan extension observed in long-lived mutant roundworms.

"Since then, it has become overwhelmingly clear that autophagy is an important mechanism necessary for the extended lifespan that is observed when model organisms are treated with certain drugs or when they have mutations in certain signaling pathways," said Dr. Levine, also a Professor of Internal Medicine and Microbiology who holds the Charles Cameron Sprague Distinguished Chair in Biomedical Science. "The body's natural ability to perform autophagy declines with aging, which likely contributes to the aging process itself."

Yet a crucial question remained unanswered: Is increased autophagy throughout mammalian life safe and beneficial? In other words, can autophagy extend lifespan and improve healthspan?

To answer this question, Dr. Levine and her UTSW colleagues created a genetically engineered mouse that had persistently increased levels of autophagy. The researchers made a mutation in the autophagy protein Beclin 1 that decreases its binding to another protein, Bcl-2, which normally inhibits Beclin 1's function in autophagy. As the researchers expected, these mice had higher levels of autophagy from birth in all of their organs.

Last summer, Dr. Congcong He, a former trainee in Dr. Levine's laboratory at UT Southwestern who originally made the mice, reported in PLOS Genetics that these mice are partially protected against mouse models of Alzheimer's-like disease. The most recent findings now show that mice with increased cellular housekeeping live longer, healthier lives.

Additionally, in collaboration with Dr. Ming Chang Hu, Associate Professor of Internal Medicine and Pediatrics who holds the Makoto Kuro-o Professorship in Bone and Kidney Research, and Dr. Orson Moe, Professor of Internal Medicine and Physiology who holds The Charles Pak Distinguished Chair in Mineral Metabolism and the Donald W. Seldin Professorship in Clinical Investigation, the Nature study also shows that the mice with increased autophagy are protected from the early death that occurs when the anti-aging hormone klotho is lacking.

"These studies have important implications for human health and for the development of drugs to improve it," said Dr. Levine, who is also a Howard Hughes Medical Institute Investigator. "They show that strategies to increase the cellular housekeeping pathway of autophagy may retard aging and aging-related diseases. The results suggest that it should be safe to increase autophagy on a chronic basis to treat diseases such as neurodegeneration. Furthermore, they reveal a specific target for developing drugs that increase autophagy - namely the disruption of Beclin 1 binding to Bcl-2."

Dr. Levine's group is collaborating with Dr. Jef De Brabander, Professor of Biochemistry and a member of the Harold C. Simmons Comprehensive Cancer Center who holds the Julie and Louis Beecherl, Jr. Chair in Medical Science, and his team to synthesize such drugs. Based on the results reported in the Nature study, drugs acting through this mechanism might be expected to improve the health and prolong the lifespan of human beings.

Conspiracy theories about government officials and the institutions they represent are widespread and rooted deep in U.S. history according to the co-author of two new social psychology studies which predict the likelihood that one will believe conspiracy beliefs or theories.

Joseph A. Vitriol, a postdoctoral research associate at Lehigh, and a co-author on both of the studies, says: "The current political moment is one of volatility and major social change, including increased cultural and ethnic diversity and widespread collective action among members of previously marginalized groups, who are effectively challenging the status quo and seeking change in public policy and political discourse."

He adds, "For many members of the public, particularly individuals who have benefited from existing social and political arrangements, these developments and changes are quite threatening and can motivate compensatory endorsement of conspiracy beliefs or theories."

Vitriol and Jessecae K. Marsh, an associate professor of psychology at Lehigh University, have found new research that inflated confidence in one's understanding of politics and public policy is associated with the tendency to believe in political conspiracies.

That is, people who overestimate how well they understand politics are more likely to believe that hidden actors or clandestine groups are conspiring in wide-ranging activities to influence important world actions, events, and outcomes.

For the research Vitriol and Marsh asked participants to rate how well they thought they understood a series of public policies. They then asked those participants to provide as detailed an explanation as they could for how the policies actually worked.

After generating these explanations, participants re-rated their confidence in their understanding of the policies.

Marsh explains that the act of trying to explain a phenomenon reveals to participants how little they actually understand about the policies, resulting in a reduction in self-reported understanding ratings. "Participants who had high levels of confidence in their understanding of public policies after generating an explanation were more likely to endorse political conspiracies, especially if they also lacked accurate knowledge of political phenomena," she adds.

Vitriol says of the findings, detailed in "The Illusion of Explanatory Depth and Endorsement of Conspiracy Beliefs:" "Our findings might suggest that showing people the limitations of their understanding can lead to more informed, evidence-based opinions and beliefs. The good thing is people can do this on their own-- by proactively seeking out and exposing oneself to information and perspectives that challenges their beliefs, one stands to gain a more objective and credible understanding of the world.

The findings were published on May 12 in the European Journal of Social Psychology.

In a separate study--published in April--Vitriol found that system identity threat, or one's perception that society's fundamental, defining values are under siege due to social change can also predict conspiracy thinking.

Findings of the study--which surveys 3,500 adult, U.S. citizens--also published in the European Journal of Social Psychology, show that people who agreed with statements such as: "In this country, there is a 'real America' distinct from those who don't share the same values" and "America's greatest values are increasingly decaying from within" were more likely to agree with statements such as: "The media is the puppet of those in power" and "Nothing in politics or world affairs happens by accident or coincidence."

The study, "The Role of System Identity Threat in Conspiracy Theory Endorsement", was authored by Vitriol and University of Minnesota, Twin Cities professors Christopher M. Federico and Allison L. Williams and appeared last month in the European Journal of Social Psychology.

Vitriol says: "We found that when one feels that society's fundamental, defining values are under siege, it is a strong predictor of a general tendency toward conspiracy thinking and endorsement of both ideological and non?ideological conspiracy theories."

The findings of both studies offer valuable takeaways.

Vitriol encourages people to practice humility and to rely upon credible, evidence-based perspectives and diverse sources across the ideological spectrum to inform their understanding of current events and public affairs.

He says, "Challenge yourself with information inconsistent with your assumptions and beliefs, learn about the experiences and perspectives that differ from your own, and remember that extraordinary and overly simplistic explanations for complex events may very well be inaccurate, even if it resonates with your intuitions."

BLOOMINGTON, Ind. -- Researchers from three universities have found that extreme price competition in the generic pharmaceutical market -- designed to make medications more affordable -- may be putting more patients at serious health risk, as evidenced by a higher number of product recalls caused by manufacturing-related problems.

The same research, published online today in the Journal of Operations Management, also raises concerns that generic drug makers may be underreporting discretionary recalls due to competitive pressures.

"Extreme price competition in the generic pharmaceutical market has some unexpected risks that regulators and lawmakers may not have foreseen when pushing for cheaper drugs," said George Ball, assistant professor of operations and decision technologies at the Indiana University Kelley School of Business and the study's lead author.

"There's a downside to cheaper drugs: You can't guarantee that they're going to be of the exact same quality," Ball said. "This research demonstrates that regulators and insurers may want to temper their intense public pressure placed upon pharmaceutical companies to bring prices down. Such pressure may come at a cost: poorly manufactured drugs."

Other authors of the paper are Rachna Shah, associate professor of supply chain and operations at the University of Minnesota's Carlson School of Management, and Kaitlin Wowak, assistant professor in the Department of Information, Analytics and Operations at the University of Notre Dame's Mendoza College of Business.

The researchers assessed the impact of the Drug Price Competition and Patent Term Restoration Act -- commonly called the Hatch-Waxman Act -- which was intended to increase competition in the pharmaceutical industry and lower drug prices by expediting the approval process for generic drugs. The process has led to a considerable increase in the number of generic drugs entering the marketplace since its passage in 1984.

It's generally believed that generic drugs are of equivalent quality to the original pioneer drug because they have the same formulation and because generic manufacturers are audited by FDA regulators to the same manufacturing quality standards. But the authors' study of 939 recalls at 64 firms over a 12-year period found that generic drug companies facing more product competition have more serious Class 1 and 2 manufacturing recalls. These are the recall classes designated by the FDA that may cause death or medically reversible harm to the customer.

While generic drug makers are not allowed to change the design of the product, they have considerable leeway regarding manufacturing decisions.

"This may explain why firms producing a higher proportion of generic products may have higher rates of recalls," Shah said. "These decisions may include reducing labor costs, hiring less experienced employees or lowering maintenance costs by servicing manufacturing equipment less often. Firms may also respond to intense competition by purchasing lower-cost ingredients."

Ball, Shah and Wowak used data from the FDA's annual Orange Book, which contains all approved pharmaceutical products for sale in the U.S. and classifies whether a drug is a new drug application (NDA) or an abbreviated new drug application (or a generic). They compared its information with recall data from 2002 to 2014.

"Our results demonstrate that as product competition increases, manufacturing-related recalls increase," Wowak said. "This is particularly evident when firms are encouraged to compete on product price, are free to set prices, and the design of the product is unalterable."

The professors also found that the relationship between product competition and manufacturing-related recalls is not universal but is contingent upon managerial discretion. This finding may indicate that while price competition via more generic drugs leads to more serious manufacturing problems in the production process, it may also encourage managers not to announce recalls when they have discretion.

They believe that their findings suggest the need for changes in processes used by the Food and Drug Administration. These include requiring more detailed and precise documentation about how the generic drug will be produced and how stringently the manufacturing plants that product generic pharmaceuticals are inspected.

Hazardous chemicals such as bromine, antimony and lead are finding their way into food-contact items and other everyday products because manufacturers are using recycled electrical equipment as a source of black plastic, according to a new study.

The substances are among those applied to devices, such as laptops and music systems, as flame retardants and pigments but remain within the products when they reach the end of their useful lives.

Now scientists at the University of Plymouth have shown that a combination of the growing demand for black plastic and the inefficient sorting of end-of-life electrical equipment is causing contaminated material to be introduced into the recyclate.

This is in part because despite black plastics constituting about 15% of the domestic waste stream, this waste material is not readily recycled owing to the low sensitivity of black pigments to near infrared radiation used in conventional plastic sorting facilities.

The study is published in Environmental International and was conducted by Dr Andrew Turner, a Reader in Environmental Science at the University.

As well as posing a threat to human health, he says the study demonstrates there are potentially harmful effects for the marine and coastal environment either through the spread of the products as litter or as microplastics.

For this research, Dr Turner used XRF spectrometry to assess the levels of a range of elements in more than 600 black plastic products such as food-contact items, storage, clothing, toys, jewellery, office items and new and old electronic and electrical equipment.

Bromine, in the form of brominated compounds, is and has been used in electrical plastic housings as a flame retardant, while lead is often encountered in electronic plastics as a contaminant. However, both elements were found extensively in non-electrical black consumer products tested, where they are not needed or desirable.

In many products, including cocktail stirrers, coathangers, various items of plastic jewellery, garden hosing, Christmas decorations and tool handles, concentrations of bromine potentially exceeded legal limits that are designed for electrical items. In other products, including various toys, storage containers and office equipment, concentrations of lead exceeded its legal limit for electrical items.

Speaking about the current study, Dr Turner said: "There are environmental and health impacts arising from the production and use of plastics in general, but black plastics pose greater risks and hazards. This is due to the technical and economic constraints imposed on the efficient sorting and separation of black waste for recycling, coupled with the presence of harmful additives required for production or applications in the electronic and electrical equipment and food packaging sectors."

"Black plastic may be aesthetically pleasing, but this study confirms that the recycling of plastic from electronic waste is introducing harmful chemicals into consumer products. That is something the public would obviously not expect, or wish, to see and there has previously been very little research exploring this. In order to address this, further scientific research is needed. But there is also a need for increased innovation within the recycling industry to ensure harmful substances are eliminated from recycled waste and to increase the recycling of black plastic consumer products."

This research is the latest work by Dr Turner examining the presence of toxic substances within everyday products. He has previously conducted research which showed that decorated drinking glasses can contain harmful levels of lead and cadmium, that the plastic used in second hand toys often fails to meet international safety directives, and that playground paints should be more closely monitored to reduce potential danger to public health.

A portable device common in optometrists' offices may hold the key to faster diagnosis of schizophrenia, predicting relapse and symptom severity and assessing treatment effectiveness, a Rutgers University study finds.

In the study, published in the May 2018 issue of the Journal of Abnormal Psychology, researchers used RETeval, a hand-held device developed to record electrical activity from the retina, to replicate and extend prior studies showing that people with schizophrenia had abnormal electrical activity in the retina. This was the first time a portable device was used for these tests. The results show the device accurately indicated reduced electrical activity in the retina in multiple cell layers in the participants who had schizophrenia, including in cell types that had not been studied before in this disorder.

"Schizophrenia is a devastating disorder, probably the most disabling disorder long term. Although we know quite a bit about it, it's still not that well understood," said Steven Silverstein, professor of psychiatry at Rutgers Robert Wood Johnson Medical School and director of research at Rutgers University Behavioral Health Care (UBHC), who designed the study. "Our study should help generate further research into developing a test that clinicians - like psychologists, psychiatrists or nurses - can use in their offices to diagnose, treat and monitor the condition of people with schizophrenia."

Looking at biomarkers in the eye as a way to understand psychiatric disorders is a new field of study.

"Since the retina is part of the nervous system, what is happening in the retina is likely reflective of what is occurring in the brain," Silverstein said. "For example, we know that certain changes in the retina, like thinning tissue [due to cell loss] or weakening electrical activity, occur alongside loss of brain tissue and reduced brain activity in patients with neurological disorders like multiple sclerosis and Parkinson's disease. We and other researchers are now investigating whether retinal changes are related to brain structure and function changes in schizophrenia."

In the just-published study, the researchers evaluated 50 participants: 25 with schizophrenia and 25 with no diagnosed psychiatric disorder. In the test, the participants closed one eye and placed the other against the RETeval device, which flashed 10 to 20 white or colored lights of various intensity against a white or colored background. A tiny skin electrode was placed on the skin under the eye to record the retina's electrical activity. The participants were tested in normal light and after sitting in the dark for 10 minutes to assess activity in different types of retinal cells. Most individual tests were completed within two minutes.

"Since many of our participants were experiencing severe psychiatric symptoms, such as hallucinations and delusions, we wanted to use a test that was as noninvasive and quick as possible," Silverstein said.

"While the portable device clearly distinguished people with schizophrenia from those without a psychiatric diagnosis, it's too soon to call this a diagnostic tool," said lead author Docia Demmin, a graduate assistant in UBHC's Division of Schizophrenia Research and a doctoral student in Rutgers Department of Psychology. "However, since every prior study has found that people with schizophrenia exhibit reduced retinal wave forms and slowed retinal responses, our research shows that we closing in on an accurate test that is faster, less invasive, inexpensive and more accessible to patients."