Tech

Bees are valuable to humans not only because they produce honey, but also because they pollinate wildflowers and food crops. They exclusively eat nectar and pollen. So in areas where intensive agriculture is practised, they suffer from the thin supply of flowers in May and June, when cultivated oilseed rape (colza) and sunflower are not in bloom. During that period, pollen collection, honey production, and colony growth slow. An article published in the Journal of Applied Ecology shows that organic farming can limit this decline. Land on which organic crops are grown offers domesticated bees more resources, especially spontaneous vegetation (unjustly dubbed 'weeds'). After examining data spanning six years for 180 hives in west central France, the researchers found that--compared with bee colonies in areas farmed conventionally--colonies living amid organic farm fields boast 37% more brood, 20% more adult bees, and 53% greater honey production.

The implication is that organically cultivated fields exert unique effects on the bee population. The swell in brood, destined to yield new workers, may be the result of a wider diversity of pollen resources or of lower mortality from local application of pesticides. The surge in honey reserves may reflect availability of melliferous flowers in greater numbers--and over a greater area, corresponding to the range covered by bees in their quest for resources (one to three kilometres in zones where large farm fields are found).

This study was made possible through Ecobee (INRA/CNRS), a unique bee colony monitoring system. Ecobee uses annual data from 50 experimental hives in southwest France to measure the effects of farming practices under real conditions. Previous research conducted by the same team showed that shrinking of brood during the period of flower scarcity resulted in lower colony survival in winter. The present study shows that organic farming can blunt the negative effects of intensive agriculture and increase the survival of bees, which play essential roles as pollinators.

CORVALLIS, Ore. - Researchers at Oregon State University have developed an improved technique for using magnetic nanoclusters to kill hard-to-reach tumors.

Magnetic nanoparticles - tiny pieces of matter as small as one-billionth of a meter - have shown anti-cancer promise for tumors easily accessible by syringe, allowing the particles to be injected directly into the cancerous growth.

Once injected into the tumor, the nanoparticles are exposed to an alternating magnetic field, or AMF. This field causes the nanoparticles to reach temperatures in excess of 100 degrees Fahrenheit, which causes the cancer cells to die.

But for some cancer types such as prostate cancer, or the ovarian cancer used in the Oregon State study, direct injection is difficult. In those types of cases, a "systemic" delivery method - intravenous injection, or injection into the abdominal cavity - would be easier and more effective.

The challenge for researchers has been finding the right kind of nanoparticles - ones that, when administered systemically in clinically appropriate doses, accumulate in the tumor well enough to allow the AMF to heat cancer cells to death.

Olena Taratula and Oleh Taratula of the OSU College of Pharmacy tackled the problem by developing nanoclusters, multiatom collections of nanoparticles, with enhanced heating efficiency. The nanoclusters are hexagon-shaped iron oxide nanoparticles doped with cobalt and manganese and loaded into biodegradable nanocarriers.

Findings were published in ACS Nano.

"There had been many attempts to develop nanoparticles that could be administered systemically in safe doses and still allow for hot enough temperatures inside the tumor," said Olena Taratula, associate professor of pharmaceutical sciences. "Our new nanoplatform is a milestone for treating difficult-to-access tumors with magnetic hyperthermia. This is a proof of concept, and the nanoclusters could potentially be optimized for even greater heating efficiency."

The nanoclusters' ability to reach therapeutically relevant temperatures in tumors following a single, low-dose IV injection opens the door to exploiting the full potential of magnetic hyperthermia in treating cancer, either by itself or with other therapies, she added.

"It's already been shown that magnetic hyperthermia at moderate temperatures increases the susceptibility of cancer cells to chemotherapy, radiation and immunotherapy," Taratula said.

The mouse model in this research involved animals receiving IV nanocluster injections after ovarian tumors had been grafted underneath their skin.

"To advance this technology, future studies need to use orthotopic animal models - models where deep-seated tumors are studied in the location they would actually occur in the body," she said. "In addition, to minimize the heating of healthy tissue, current AMF systems need to be optimized, or new ones developed."

ST. PETERSBURG, FL - It's no secret that massive dust storms in the Saharan Desert occasionally shroud the North Atlantic Ocean with iron, but it turns out these natural blankets aren't the only things to sneeze at. Iron released by human activities contributes as much as 80 percent of the iron falling on the ocean surface, even in the dusty North Atlantic Ocean, and is likely underestimated worldwide, according to a new study in Nature Communications.

"People don't even realize it," said lead author Dr. Tim Conway, Assistant Professor at the USF College of Marine Science, "but we've already been doing an iron fertilization experiment of sorts for many decades."

Burning fossil fuels, biofuels, and forests all release iron, which can be transported as an aerosol over large distances from land into the guts of the North Atlantic and beyond. But human-derived iron aerosols have been nearly impossible to see in the data - until now. The team used the isotope ratios of iron in the atmosphere to 'fingerprint' whether the iron came from Saharan desert dust or human sources such as cars, combustion, or fires.

"Despite much research, iron chemistry is still something of a black box in the ocean," Conway said. Iron, a trace element, is found in exceedingly low amounts in the ocean; one liter of seawater contains 35 grams of salt but only around one billionth of a gram of iron. This makes it very hard to measure. The iron is also hard to sample without risking contamination, especially if working on a rusty ship.

Trying to establish how much atmospheric iron lands on and dissolves in the ocean presents even more challenges, with storms, seasons, and land use all changing how much dust gets blown from the continents. Digesting dust particles in the lab to see how much iron dissolves is also problematic, and has led to estimates of iron that dissolves when it hits the ocean ranging from 0 to 100 percent.

The current study addresses some of these mysteries that remain in iron chemistry, taking our understanding of atmospheric iron supply to the oceans to the next level.

Conway and his colleagues analyzed aerosol samples collected on research cruises to the North Atlantic in 2010 and 2011 on board the R/V Knorr. The cruises were part of GEOTRACES, a global coordinated research program of 35 countries to study trace metals and their isotopes in the ocean.

Samples were taken from an area off West Africa known to collect dust from the Saharan dust storms, and the others were taken off the coasts of New England and Europe where human-derived pollution is expected to be more important. The team then measured iron isotope ratios in the samples in order to determine whether the iron came from a natural or human source.

Iron isotope ratios (56Fe/54Fe) can change in response to chemical reactions, so human-induced processes like burning fossil fuels release iron with a different isotope 'signature' than iron derived from natural materials. Saharan dust particles were previously assumed to have a ratio that looked like the average continental crust, and Conway has suggested that when Saharan dust particles hit the ocean, the iron that dissolves interacts with organic molecules that bind the heavier 56Fe.

"We carried out this research to investigate that idea and fully expected to see continental signals or perhaps more heavy isotopes in the samples from all three regions," said Conway. "What we found was pretty crazy and very light. We weren't expecting this at all," Conway said.

The iron in Saharan air was indeed a match for the continental crust, but was much heavier than the samples from North America and Europe, which were loaded with lighter (more 54Fe), human-derived iron - not iron from the Sahara.

"The fact that we found human-derived iron in the dusty North Atlantic shows how effective this tracer is for anthropogenic iron," Conway said.

Next, they used the iron-isotope tracer work to improve the models used to predict the amount of dust that falls over the global ocean, and were able to show that the iron from human input is much greater than previously thought.

Since the 1990s scientists have proposed the idea of fertilizing the water with iron released from ships to accelerate the growth of phytoplankton. The thinking goes like this:

Iron is a vital micronutrient that phytoplankton need to grow but it's generally scarce in the ocean. When available via dust storm or other source, the phytoplankton slurp up the carbon dioxide during photosynthesis at the ocean's surface. When they die and sink to the ocean bottom, they take the carbon with it - effectively acting as a "carbon sink." So let's add more iron to decrease the carbon dioxide from climate change, say geoengineering enthusiasts.

This geoengineering exercise is still hotly debated today, and the study by Conway and team add fuel to the fire with an unexpected twist.

"It seems we've already been fertilizing the ocean. We just couldn't quantify it," Conway said, although scientists have had a hunch about the human iron input since the mid-2000s.

"We've completely changed the system," he said, and routinely add iron to the ocean when cutting down forests or driving cars. Ironically, because of the way iron works it's therefore possible that these human sources of iron to the ocean may in fact have been acting to mitigate climate change.

"We don't know the magnitude of it yet but it's a fair statement," Conway said.

Results of a two-year update of the world's first comparative trial of mass drug administration against scabies, show that the infection rate is still significantly down. The latest findings are published today in the New England Journal of Medicine.

In 2012, the Murdoch Children's Research Institute, the Kirby Institute and the Fiji Ministry for Health, treated almost everyone on a remote Fijian island (716 people) with the oral anti-parasitic drug ivermectin. Scabies, caused by tiny mites, is a debilitating skin condition leading to severe itching. If untreated it can lead to serious bacterial infections, not only of the skin but internal organ systems including the kidney and heart.

The researchers had previously published their findings at one-year follow up. In the New England Journal of Medicine, the researchers today (June 27) report that 24 months after the treatment, the infection rate was still extremely low, at 3.6 per cent - down 89 per cent on the original figure.

"Mass drug administration has been used to successfully control other important parasitic and bacterial diseases around the world - we have shown it can be used for scabies too, and that its effect is long-lasting," said lead author Dr Lucia Romani from the Kirby Institute at UNSW Sydney.

"The principle of mass drug administration is that regardless of whether or not you know you have scabies, everyone in the community is encouraged to take the medication to kill the mites at the same time and stop them from spreading from person to person."

Professor Andrew Street from the Murdoch Children's Research Institute said the medication, ivermectin, is used against a range of human parasites.

"Ivermectin is recommended by the World Health Organization for the control of common parasitic diseases such as river blindness - over one billion doses have been given and it is known to be very safe," Professor Steer said. "Its creators received the 2015 Noble Prize for Medicine."

Dr Mike Kama, focal person for scabies control in the Fiji Ministry of Health, said in the original trial, the researchers assigned three island communities to different interventions for scabies control: standard care involving treatment of affected individuals and their families using permethrin cream, mass administration of permethrin cream, and mass administration of ivermectin tablets.

"After one year the prevalence of scabies declined in all groups, but by far the most dramatic reduction was in the ivermectin group with a fall in prevalence of 94 per cent," Dr Kama said. "The follow-up study at 24 months shows that this reduction remains sustained over a longer period."

Scabies is widespread in many tropical settings, especially in the Pacific region. The mites thrive in crowded conditions, whether through people living close to each other, or in settings such as schools, or other institutions.

A meta-analysis including 60 million individuals in high-income countries finds significant decreases in HPV infections, anogenital wart diagnoses and precancerous cervical lesions (CIN2+) over 8-9 years after girls-only HPV vaccination.

The new study is the first to show pooled estimates of population-level impact of HPV vaccination on CIN2+ from several countries, the benefit of vaccinating more than one age group, along with substantial herd effects in countries achieving high vaccination coverage. Published in The Lancet, the results provide strong evidence of HPV vaccination working to prevent cervical cancer in real-world settings as both the cause (HPV infection) and precancerous cervical lesions are declining. These results have implications for policy makers around the world as it backs the recently revised WHO position on vaccinating multiple age groups rather than a single cohort when introducing the vaccine.

The HPV vaccination was first licensed in 2007 and since then it has been adopted into 99 countries* and territories. An earlier version of this meta-analysis with data for four years post-vaccination showed substantial decreases in two types of HPV - 16 and 18 - that cause the majority of cervical cancers and anogenital wart diagnoses among women who had received the vaccine along with herd effects among boys and older women. However, the past meta-analysis was unable to assess CIN2+ lesions, which is the most proximal outcome to cervical cancer, as it was too soon after vaccination to be able to estimate the impact.

In addition, since that publication many more countries have introduced vaccination programmes and in 2016 the WHO updated its advice to recommend HPV vaccination of multiple age cohorts of girls - from nine to fourteen.

To update their 2015 review which included 18 studies, the team added 47 new studies published between February 2014 and October 2018 that compared the frequency of one or more HPV endpoints (HPV infections, anogenital wart diagnoses, or histologically confirmed CIN2+) between pre and post-vaccination periods in the general population. In total, their analysis includes 65 articles in 14 high-income countries - including 23 for HPV infection, 29 for anogenital warts and 13 for CIN2+ lesions. It brings together data from over 60 million individuals over eight years.

They found that the two types of HPV that cause 70% of cervical cancers, HPV 16 and 18, were significantly reduced after vaccination. They report a decrease of 83% in girls aged 13-19 and of 66% in women aged 20-24 years after five to eight years of vaccination. An overall 54% reduction was seen in three other types of HPV, 31, 33 and 45 in girls aged 13-19 years.**

There were also significant reductions in anogenital wart diagnoses. After five to eight years of vaccination, they found decreases of 67% in girls aged 15-19, 54% in women aged 20-24 and 31% in women aged 25-29 as well as reductions of 48% in boys aged 15-19 and 32% in men aged 20-24 years.

Five to nine years after vaccination CIN2+ decreased significantly. The team reports a 51% reduction in screened girls aged 15-19 years and a 31% reduction in screened women aged 20-24 years.

The analysis shows the greater and faster impact and herd effects in countries with both multi-cohort vaccination and high vaccination coverage. In such countries after five to eight years of vaccination, anogenital wart diagnoses declined by 88% among girls and 86% in boys aged 15-19 years compared with 44% among girls and 1% among boys from countries with single-cohort or low routine vaccination coverage. In girls aged 15-19 years, CIN2+ decreased by 57% in countries with both multi-cohort vaccination and high vaccination coverage whereas there was no decrease in countries with single-cohort vaccination or low routine coverage.

Mélanie Drolet of the CHU de Quebec-Laval University Research Center says: "Our results provide strong evidence that HPV vaccination works to prevent cervical cancer in real-world settings as both HPV infections that cause most cervical cancers and precancerous cervical lesions are decreasing. We saw that programmes with multiple age cohorts of girls vaccinated and high vaccination coverage have greater direct impact and herd effects. This finding reinforces WHO's recently revised position on HPV vaccination to recommend HPV vaccination of multiple age cohorts of girls aged 9-14 years old when the vaccine is introduced in a country, rather than vaccination of a single cohort." [1]

Professor Marc Brisson of Laval University Canada says: "The landscape of HPV vaccination is rapidly changing, with several countries recently switching from three to two-dose schedules, gender-neutral vaccination, and a newer vaccine that targets more HPV types. It will be crucial to continue monitoring the population-level impact of HPV vaccination to examine the full effect of these changes in strategies and quantify the effect of vaccination in low-income and middle-income countries. Because of our finding, we believe the WHO call for action to eliminate cervical cancer may be possible in many countries if sufficient vaccination coverage can be achieved." [1]

The authors note some limitations, including that causality between HPV vaccination and observed changes in the three endpoints cannot be concluded definitively because the analysis is based on ecological studies. The authors believe the results strongly suggest that the decreases can be largely attributed to HPV vaccination because larger and faster decreases are observed among cohorts targeted for vaccination and in countries with high vaccination coverage, larger decreases are observed with longer follow-up since the introduction of vaccination, and results are consistent across countries and HPV endpoints. In addition, the authors were unable to tease out the specific impact of different programme characteristics (e.g. vaccine used, number of age cohorts vaccinated).

There is a lack of data from low and middle-income countries (LMICs), where the burden of disease is far greater than in high-income countries and results should be extrapolated to those countries with caution. At least 115 countries* and territories include HPV vaccine in their immunisation programmes and almost 40 LMICs are set to join by 2021.

In a linked Comment article, Professor Silvia de Sanjose of PATH, USA, notes that these results will aid the implementation of the vaccine globally during a time of challenges such as high vaccine cost and competing budget priorities, inadequate vaccine supply, and lack of awareness of vaccine impact and vaccine hesitancy - particularly in LMICs.

She says: "Drolet and colleagues can help implementers concentrate on priority targets. Specifically, items like gender-neutral vaccination, number of age cohorts to be included, expansion to adult populations, and number of doses can be modulated on the basis of impact and sustainability. The robust estimates generated should prompt countries to re-evaluate their policies, especially given the global call to eliminate cervical cancer. Finding the optimal number of age cohorts to be vaccinated could also have major budgetary and programmatic advantages, as multiple cohorts of younger individuals would need fewer vaccine doses. The authors emphasise the importance of redoubling our efforts to tackle the fiscal, supply, and programmatic barriers that currently limit HPV vaccine programmes; with these efforts, HPV vaccination could become a hallmark investment of cancer prevention in the 21st century."

LAWRENCE -- Growing up in Liberia during that country's brutal 14-year civil war, Benedictus Freeman and his family fled into the rainforest, where they survived for years eating bush meat and foraging. The rainforest provided Freeman sustenance and protection -- but more than that, the experience ignited a passion in him for understanding and preserving nature.

"At that time, I really didn't know how important the forest would become for me -- I saw the forest as a source of resources like food and shelter," said Freeman, who today is a doctoral student in ecology & evolutionary biology at the University of Kansas and KU Biodiversity Institute. "But I developed an interest in nature there, and eventually I started studying forestry for my undergraduate degree. That actually influenced my decision to get more interested in nature and conservation."

The rainforests that once protected Freeman and his family host one of West Africa's flagship bird species -- the White?breasted Guineafowl (Agelastes meleagrides). Now, Freeman is lead author of a new paper in the peer-reviewed journal Avian Research that projects the geographic distribution of the bird through 2050 as it shifts habitat due to climate change.

"This bird is endemic to West Africa, but it's not fully understood -- it's poorly studied," Freeman said. "Because of this poor history, there's very little understanding about its range. Our study recharacterizes its distribution and helps us to understand to what extent it's distributed across the region. The bird is threatened, and it's of conservation concern. So that's why it was selected for study."

According to Freeman, the vulnerable White-breasted Guineafowl, which has appeared on Liberian postage stamps, serves as an iconic "flagship species," conservation of which could preserve habitat of many lesser-known animals at the same time.

The KU researcher said West Africa suffers from extensive deforestation due to increasing populations, urbanization, agriculture expansion (both substance farming and industrial-scale farming of palm oil), logging and mining. Because of its exclusive dependence on the forest for habitat, the White-breasted Guineafowl is particularly susceptible to habitat loss.

"It occurs within rainforest habitats in West Africa where it feeds like regular birds, like chickens feed, and depends on insects and seeds and things," Freeman said. "The important thing about this bird is that it's a specialist -- it's more restricted to rainforest habitats. There is a sister species (Black Guineafowl, Agelastes niger) of the same bird that occurs on the other side of the Guinean forest, but this one is range-restricted, and it's only found in this region. It's not going to be found anywhere else in the world."

Freeman hopes his research predicting the distribution of the bird in coming decades can help inform policymakers about which areas of rainforest should be prioritized for conservation.

For the new paper, Freeman and his colleagues -- Daniel Jime?nez?Garci?a of Beneme?rita Universidad Auto?noma de Puebla in Mexico, Benjamin Barca of the Royal Society for the Protection of Birds in Sierra Leone and Matthew Grainger of Newcastle University in the United Kingdom -- used occurrence data from the Global Biodiversity Information Facility and datasets about occurrences of the White-breasted Guineafowl in Sapo National Park in Liberia and Gola Rainforest National Park in Sierra Leone, including data collected by Freeman.

The authors used environmental datasets from NASA and other open sources to perform ecological niche modeling, which the researchers said "integrates known occurrences of species and environmental variables (e.g., temperature, precipitation) to characterize potential future geographic distributions of species in response to global climate change."

The team created maps showing current and likely future habitats where the White?breasted Guineafowl could migrate in response to a shifting climate. Unexpectedly, there was good news for the iconic bird in the findings: "The projected impacts of climate change on the geographic distribution of White-breasted Guineafowl were minimal, suggesting stability across the species' range for the present and in the future, at least as regards climate change effects," researchers said. "Low sensitivity to climate change in this species does match the general observation for West African birds."

However, the team found coastal areas where the White?breasted Guineafowl is found today would be degraded by sea-level rise and resulting coastal erosion, destroying some of the species' range.

As for Freeman, this summer he's back in Liberia conducting more fieldwork on birds in some of the same areas his team found to be suitable for the White-breasted Guineafowl.

"We were pleased to document populations at the sites where we worked, and then we were able to collect data on other bird species," he said. "We have some interesting records that might be species not yet known to science, but we need to do some detailed studies."

Freeman aims to finish his doctorate at KU next year, he said. After that, he'll look for opportunities for postdoctoral work.

"I don't know exactly where that's going to be," he said. "But I'm hoping that wherever I get a good job, I can have an opportunity to work in West Africa to do more research. There's a huge capacity gap in that area. There's a need to have homegrown scientists involved with this kind of research specifically. So, my passion is to work there."

DURHAM, N.C. -- Blame junk food or a lack of exercise. But long before the modern obesity epidemic, evolution made us fat too.

"We're the fat primates," said Devi Swain-Lenz, a postdoctoral associate in biology at Duke University.

The fact that humans are chubbier than chimpanzees isn't news to scientists. But new evidence could help explain how we got that way.

Despite having nearly identical DNA sequences, chimps and early humans underwent critical shifts in how DNA is packaged inside their fat cells, Swain-Lenz and her Duke colleagues have found. As a result, the researchers say, this decreased the human body's ability to turn "bad" calorie-storing fat into the "good" calorie-burning kind.

The results were published June 24 in the journal Genome Biology and Evolution.

Compared to our closest animal relatives, even people with six-pack abs and rippling arms have considerable fat reserves, researchers say. While other primates have less than 9% body fat, a healthy range for humans is anywhere from 14% to 31%.

To understand how humans became the fat primate, a team led by Swain-Lenz and Duke biologist Greg Wray compared fat samples from humans, chimps and a more distantly-related monkey species, rhesus macaques. Using a technique called ATAC-seq, they scanned each species' genome for differences in how their fat cell DNA is packaged.

Normally most of the DNA within a cell is condensed into coils and loops and tightly wound around proteins, such that only certain DNA regions are loosely packed enough to be accessible to the cellular machinery that turns genes on and off.

The researchers identified roughly 780 DNA regions that were accessible in chimps and macaques, but had become more bunched up in humans. Examining these regions in detail, the team also noticed a recurring snippet of DNA that helps convert fat from one cell type to another.

Not all fat is created equal, Swain-Lenz explained. Most fat is made up of calorie-storing white fat. It's what makes up the marbling in a steak and builds up around our waistlines. Specialized fat cells called beige and brown fat, on the other hand, can burn calories rather than store them to generate heat and keep us warm.

One of the reasons we're so fat, the research suggests, is because the regions of the genome that help turn white fat to brown were essentially locked up -- tucked away and closed for business -- in humans but not in chimps.

"We've lost some of the ability to shunt fat cells toward beige or brown fat, and we're stuck down the white fat pathway," Swain-Lenz said. It's still possible to activate the body's limited brown fat by doing things like exposing people to cold temperatures, she explained, "but we need to work for it."

Humans, like chimps, need fat to cushion vital organs, insulate us from the cold, and buffer us from starvation. But early humans may have needed to plump up for another reason, the researchers say -- as an additional source of energy to fuel our growing, hungry brains.

In the six to eight million years since humans and chimps went their separate ways, human brains have roughly tripled in size. Chimpanzee brains haven't budged.

The human brain uses more energy, pound for pound, than any other tissue. Steering fat cells toward calorie-storing white fat rather than calorie-burning brown fat, the thinking goes, would have given our ancestors a survival advantage.

Swain-Lenz said another question she gets a lot is: "Are you going to make me skinny?"

"I wish," she said.

Because of brown fat's calorie-burning abilities, numerous researchers are trying to figure out if boosting our body's ability to convert white fat to beige or brown fat could make it easier to slim down.

Swain-Lenz says the differences they found among primates might one day be used to help patients with obesity -- but we're not there yet.

"Maybe we could figure out a group of genes that we need to turn on or off, but we're still very far from that," Swain-Lenz said. "I don't think that it's as simple as flipping a switch. If it were, we would have figured this out a long time ago," she explained.

CINCINNATI--Researchers suggest a possible cell-based therapy to stimulate lung development in fragile premature infants who suffer from a rare condition called Bronchopulmonary Dysplasia (BPD), which in the most severe cases can lead to lifelong breathing problems and even death.

Scientists at Cincinnati Children's Hospital Medical Center report in the American Journal of Respiratory and Critical Care Medicine they studied genetic signatures in donated human neonatal lungs by using single-cell RNA sequencing analysis. They also performed extensive laboratory tests on mouse models of BPD, including computer-assisted bioinformatics analysis.

The tests led to a proposal to develop cell therapy based on what are called c-KIT endothelial progenitor cells. The cells are common in embryonic and neonatal lungs and help in the formation of capillaries and air sacs in the lungs called alveoli. But premature babies with already underdeveloped lungs frequently rely on mechanical breathing assistance, which further interferes with early lung development, according to Vlad Kalinichenko, MD, PhD, a physician/researcher at the Cincinnati Children's Perinatal Institute's Center for Lung Regenerative Medicine and lead study investigator.

"RNA sequencing of human and mouse neonatal lung tissue showed that pulmonary c-KIT endothelial progenitor cells require the c-KIT and FOXF1 proteins to stimulate the development of blood vessels and air sacs," Kalinichenko said. "The cells are highly sensitive to injury by high oxygen concentrations, so lung development in premature babies on mechanical oxygen assistance is impeded. Our findings suggest using c-KIT-positive endothelial cells from donors, or generating them with pluripotent stem cells, might be a way to treat BPD or other pediatric lung disorders associated with loss of alveoli and pulmonary microvasculature."

Kalinichenko and colleagues study extensively the critical role the FOXF1 gene has in lung development. The researchers also explore different situations where mutation of the gene can disrupt the function of the FOXF1 protein, affecting lung development or causing disease.

Preclinical Results Need More Study

This study is the first to suggest the possibility of using donated c-KIT pulmonary endothelial progenitor cells for therapy or those generated with pluripotent stem cells, which can become any cell type in the body and be derived from a patient's own cells. That conclusion was based in part on tests the researchers performed by using c-KIT-positive endothelial progenitor cells to treat neonatal mice that had been exposed to hyperpoxia (over oxygenation) to model the BPD condition in the animals. They found that the infusion of cells in peripheral blood increased the formation of pulmonary blood vessels and air sacs in the animals.

Extensive preclinical testing in larger laboratory animals, such as rats and sheep, will be needed before Kalinichenko and his colleagues would consider recommending the cell-therapy approach be tested in patients, he said. Future work will also include further technical refinement of the therapeutic approach and ongoing efficacy testing in animal models of BPD. It also includes developing a specific cell differentiation protocol for generating c-KIT-positive endothelial progenitor cells from induced pluripotent stem cells derived from patients.

Kalinichenko estimated the additional preclinical development work will require an estimated two to three years before the technology potentially reaches a point where it can be proposed for possible clinical testing.

Many species of wild bumblebees are in decline--and new research shows that diseases spread by domestic honeybees may be a major culprit.

Several of the viruses associated with bumblebees' trouble are moving from managed bees in apiaries to nearby populations of wild bumblebees--"and we show this spillover is likely occurring through flowers that both kinds of bees share," says Samantha Alger, a scientist at the University of Vermont who led the new research.

"Many wild pollinators are in trouble and this finding could help us protect bumblebees," she says. "This has implications for how we manage domestic bees and where we locate them."

The first-of-its-kind study was published June 26 in the journal PLOS ONE.

VIRUS HUNTERS

Around the globe, the importance of wild pollinators has been gaining attention as diseases and declines in managed honeybees threaten key crops. Less well understood is that many of the threats to honeybees (Apis mellifera)--including land degradation, certain pesticides, and diseases--also threaten native bees, such as the rusty patched bumblebee, recently listed under the Endangered Species Act; it has declined by nearly 90% but was once an excellent pollinator of cranberries, plums, apples and other agricultural plants.

The research team--three scientists from the University of Vermont and one from the University of Florida--explored 19 sites across Vermont. They discovered that two well-know RNA viruses found in honeybees--deformed wing virus and black queen cell virus--were higher in bumblebees collected less than 300 meters from commercial beehives. The scientists also discovered that active infections of the deformed wing virus were higher near these commercial apiaries but no deformed wing virus was found in the bumblebees they collected where foraging honeybees and apiaries were absent.

Most impressive, the team detected viruses on 19% of the flowers they sampled from sites near apiaries. "I thought this was going to be like looking for a needle in a haystack. What are the chances that you're going to pick a flower and find a bee virus on it?" says Alger. "Finding this many was surprising." In contrast, the scientists didn't detect any bee viruses on flowers sampled more than one kilometer from commercial beehives.

The UVM scientists--including Alger and co-author Alex Burnham, a doctoral student--and other bee experts have for some years suspected that RNA viruses might move from honeybees to bumblebees through shared flowers. But--with the exception of one small study in a single apiary--the degree to which these viruses can be "horizontally transmitted," the scientists write, with flowers as the bridge, has not been examined until now.

Taken together, these results strongly suggest that "viruses in managed honeybees are spilling over to wild bumblebee populations and that flowers are an important route," says Alison Brody, a professor in UVM's Department of Biology, and senior author on the new PLOS study. "Careful monitoring and treating of diseased honeybee colonies could protect wild bees from these viruses as well as other pathogens or parasites."

JUST LIKE CHICKEN?

Alger--an expert beekeeper and researcher in UVM's Department of Plant & Soil Science and Gund Institute for Environment--is deeply concerned about the long-distance transport of large numbers of honeybees for commercial pollination. "Big operators put hives on flatbed trucks and move them to California to pollinate almonds and then onto Texas for another crop," she says--carrying their diseases wherever they go. And between bouts of work on monoculture farm fields, commercial bees are often taken to more pristine natural habitats "to rest and recover, where there is diverse, better forage," says Alger.

"This research suggests that we might want to keep apiaries outside of areas where there are vulnerable pollinator species, like the rusty patched bumblebees," Alger says, "especially because we have so much more to learn about what these viruses are actually doing to bumblebees."

Honeybees are an important part of modern agriculture, but "they're non-native. They're livestock animals," Alger says. "A huge misconception in the public is that honeybees serve as the iconic image for pollinator conservation. That's ridiculous. It's like making chickens the iconic image of bird conservation."

As animals explore their environment, they learn to master it. By discovering what sounds tend to precede predatorial attack, for example, or what smells predict dinner, they develop a kind of biological clairvoyance--a way to anticipate what's coming next, based on what has already transpired. Now, Rockefeller scientists have found that an animal's education relies not only on what experiences it acquires, but also on when it acquires them.

Studying fruit flies, the researchers showed that a single odor can become either appealing or disgusting to an animal, depending on when the smell is encountered relative to a reward. The study, described in a report in Cell, also reveals that animals can quickly revise these memories, and shows how this process unfolds on a cellular level--insights that likely pertain not just to flies, but to learning across the animal kingdom.

Which came first?

Memory, at its most fundamental level, amounts to a series of associations: Ring a bell before feeding a dog, and eventually the dog will learn to salivate at the sound of the bell alone.

"In this case, the bell comes before the food and is therefore predictive of reward," says Annie Handler, a graduate fellow in the lab of Vanessa Ruta, the Gabrielle H. Reem and Herbert J. Kayden Associate Professor. "But we suspected that there isn't just one order of events that animals find significant. They should also be able extract meaning from cues that follow a reward."

For example, if a dog hears a bell after its meal concludes, then it should develop a negative association with that sound, as it signifies the end of chow. Hoping to better understand how timing affects memory, Ruta and Handler examined the brains and behavior of fruit flies.

Rather than supply the animals with tasty treats, the researchers used a technique called optogenetics to stimulate neurons that normally become active when an animal receives a reward, an approach that allowed them to precisely control the timing of positive feedback. They found that if these neurons were stimulated immediately after an otherwise neutral odor, the flies developed an attraction to that smell. Conversely, if they activated the neurons just before exposing flies to the same odor, the animals began to avoid it.

"The difference in time is only one or two seconds, yet the flies form completely opposing associations," says Handler. "Somewhere in the brain that difference of a second--of whether the odor comes before or after the reward--makes a huge difference."

The fact that brains have a sense of timing may seem intuitive; but exactly how neurons encode the sequence of events on a cellular level is far from obvious. Relatively small and simple, the fly brain offers a unique opportunity to study the neural circuits underlying this phenomenon--and that's exactly what Ruta and Handler did.

Remaking memories

To determine how flies discriminate the timing of events, the researchers monitored changes in a brain region called the mushroom body. Known to be involved in associative learning, this area contains Kenyon cells, which carry odor signals, dopamine neurons, which carry reward signals, and output neurons that regulate a fly's attraction to an odor.

Kenyon cells can be either strongly or weakly connected to output neurons; and dopamine tunes the strength of these connections, or synapses. If a Kenyon cell detecting a specific odor forms a weak connection with an output neuron, the animal becomes attracted to that odor; if this synapse grows stronger, however, the smell will become meaningless, or even aversive to the animal. Analyzing this type of connection, Ruta and Handler identified a signaling pathway that can either strengthen or weaken synapses, depending on the precise moment when dopamine neurons become active.

"This pathway is time sensitive, so whether the dopamine neuron is activated before or after an odor makes a critical difference in the strength of connections between cells in the mushroom body," says Ruta. "And we believe this is the mechanism by which the brain figures out the sequence of events."

By tinkering with this pathway, the researchers also found that they could quickly make strong synapses weak and vice versa, suggesting that memories can be erased just as quickly as they're formed. And when they analyzed fly behavior, they found further evidence of the ability to revise mental associations.

"We performed 50 trials. Each time we switched the timing of the odor relative to the reward; and each time the animal became more or less attracted to the odor, depending on what it had experienced a minute prior," says Handler.

In other words, even if a fly had previously learned to associate an odor with reward, it could quickly unlearn that association if the smell failed to predict reward in future trials. Memories are not set in stone; rather, they're set in synapses, which can be modified as an animal's environment and experiences change. Indeed, this experiment highlights that survival depends not just on the ability to form memories, but also to forget them.

"There are so many things that we could remember on a daily basis, so we hold on to the memories that turn out to be predictive; and we toss out associations that are incorrect or irrelevant," says Ruta. "When you live in a dynamic environment--which both flies and humans do--that seems like a very good strategy."

CAMBRIDGE, MA -- When medical devices are implanted in the body, the immune system often attacks them, producing scar tissue around the device. This buildup of tissue, known as fibrosis, can interfere with the device's function.

MIT researchers have now come up with a novel way to prevent fibrosis from occurring, by incorporating a crystallized immunosuppressant drug into devices. After implantation, the drug is slowly secreted to dampen the immune response in the area immediately surrounding the device.

"We developed a crystallized drug formulation that can target the key players involved in the implant rejection, suppressing them locally and allowing the device to function for more than a year," says Shady Farah, an MIT and Boston Children's Hospital postdoc and co-first author of the study, who is soon starting a new position as an assistant professor of the Wolfson Faculty of Chemical Engineering and the Russell Berrie Nanotechnology Institute at Technion-Israel Institute of Technology.

The researchers showed that these crystals could dramatically improve the performance of encapsulated islet cells, which they are developing as a possible treatment for patients with type 1 diabetes. Such crystals could also be applied to a variety of other implantable medical devices, such as pacemakers, stents, or sensors.

Former MIT postdoc Joshua Doloff, now an assistant professor of Biomedical and Materials Science Engineering and member of the Translational Tissue Engineering Center at Johns Hopkins University School of Medicine, is also a lead author of the paper, which appears in the June 24 issue of Nature Materials. Daniel Anderson, an associate professor in MIT's Department of Chemical Engineering and a member of MIT's Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science (IMES), is the senior author of the paper.

Crystalline drug

Anderson's lab is one of many research groups working on ways to encapsulate islet cells and transplant them into diabetic patients, in hopes that such cells could replace the patients' nonfunctioning pancreatic cells and eliminate the need for daily insulin injections.

Fibrosis is a major obstacle to this approach, because scar tissue can block the islet cells' access to the oxygen and nutrients. In a 2017 study, Anderson and his colleagues showed that systemic administration of a drug that blocks cell receptors for a protein called CSF-1 can prevent fibrosis by suppressing the immune response to implanted devices. This drug targets immune cells called macrophages, which are the primary cells responsible for initiating the inflammation that leads to fibrosis.

"That work was focused on identifying next-generation drug targets, namely which cell and cytokine players were essential for fibrotic response," says Doloff, who was the lead author on that study, which also involved Farah. He adds, "After knowing what we had to target to block fibrosis, and screening drug candidates needed to do so, we still had to find a sophisticated way of achieving local delivery and release for as long as possible."

In the new study, the researchers set out to find a way to load the drug directly into an implantable device, to avoid giving patients drugs that would suppress their entire immune system.

"If you have a small device implanted in your body, you don't want to have your whole body exposed to drugs that are affecting the immune system, and that's why we've been interested in creating ways to release drugs from the device itself," Anderson says.

To achieve that, the researchers decided to try crystallizing the drugs and then incorporating them into the device. This allows the drug molecules to be very tightly packed, allowing the drug-releasing device to be miniaturized. Another advantage is that crystals take a long time to dissolve, allowing for long-term drug delivery. Not every drug can be easily crystallized, but the researchers found that the CSF-1 receptor inhibitor they were using can form crystals and that they could control the size and shape of the crystals, which determines how long it takes for the drug to break down once in the body.

"We showed that the drugs released very slowly and in a controlled fashion," says Farah. "We took those crystals and put them in different types of devices and showed that with the help of those crystals, we can allow the medical device to be protected for a long time, allowing the device to keep functioning."

Encapsulated islet cells

To test whether these drug crystalline formulations could boost the effectiveness of encapsulated islet cells, the researchers incorporated the drug crystals into 0.5-millimeter-diameter spheres of alginate, which they used to encapsulate the cells. When these spheres were transplanted into the abdomen or under the skin of diabetic mice, they remained fibrosis-free for more than a year. During this time, the mice did not need any insulin injections, as the islet cells were able to control their blood sugar levels just as the pancreas normally would.

"In the past three-plus years, our team has published seven papers in Nature journals -- this being the seventh -- elucidating the mechanisms of biocompatibility," says Robert Langer, the David H. Koch Institute Professor at MIT and an author of the paper. "These include an understanding of the key cells and receptors involved, optimal implant geometries and physical locations in the body, and now, in this paper, specific molecules that can confer biocompatibility. Taken together, we hope these papers will open the door to a new generation of biomedical implants to treat diabetes and other diseases."

The researchers believe that it should be possible to create crystals that last longer than those they studied in these experiments, by altering the structure and composition of the drug crystals. Such formulations could also be used to prevent fibrosis of other types of implantable devices. In this study, the researchers showed that crystalline drug could be incorporated into PDMS, a polymer frequently used for medical devices, and could also be used to coat components of a glucose sensor and an electrical muscle stimulation device, which include materials such as plastic and metal.

"It wasn't just useful for our islet cell therapy, but could also be useful to help get a number of different devices to work long-term," Anderson says.

Soft robots can't always compete with the hard. Their rigid brethren dominate assembly lines, perform backflips, dance to Bruno Mars' "Uptown Funk," fly, dive, and walk through volcanoes.

But each year, soft robots gain new abilities. They've learned to jump, squirm, and grip. And, unlike hard robots, they can handle tomatoes without bruising the fruit, resurface unscathed after being run over by a car, and journey through radiation, disaster zones, and outer-space with few scars. For people and animals, they have a "cooperative function": a soft touch.

Recently, researchers in the lab of George M. Whitesides, the Woodford L. and Ann A. Flowers University Professor, have invented soft replacements for the last hard parts required to build a robot. Instead of electricity and wires, pressurized air expands and contracts rubber inflatables to create movement, soft valves take over for the hard, and soft digital logic replicates the same capabilities of an electronic computer.

Now, postdoctoral scholar Daniel J. Preston's latest soft invention gives these robots new, complex movements. As first author on a study published in Science Robotics, he introduces the first soft ring oscillator, which gives soft robots the ability to roll, undulate, sort, meter liquids, and swallow.

"It's another tool in the toolkit to make these smart, soft robots without any electronics, and without any hard valves," Preston says.

Until now, ring oscillators were made with electronic transistors or microfluidics. Electronics always require hard components. Most microfluidics do, too. Many use glass for their pressurized water or air systems and require thin channels that can only handle very low flow rates, limiting operation speeds. Tiny microfluidic systems might achieve higher frequencies than Preston's macroscale pneumatic ring oscillator, but his team already has blueprints to tweak their soft system to achieve greater speeds, if needed.

The soft ring oscillator--like all ring oscillators--relies on inverters ("NOT" digital logic gates). Preston's inverters, for example, manipulate the air pressure in his robot's rubber tubes: If the input is high pressure, the output will be low pressure and vice versa. When three, or any odd number, of gates are connected in a ring, one gate's shift triggers the next, which triggers the next, and on and on.

"The cool response that you get when you combine an odd number of these inverters in a loop is an instability that travels around the loop," Preston says. Like a slinky that collapses in order to spring down a flight of stairs, one movement sparks the next, creating a constant pace without the need for another push.

To test what the soft ring oscillator could do, Preston and his team created five soft robot prototypes. Each uses a single, constant source of air pressure to run three pneumatic actuators (the inverters).

One prototype nudges a ball around a ring. Another undulates a stage to keep beads of two different sizes rolling against the edge. Eventually, all the smaller beads fall through a hole in the side of the stage. They sort themselves out.

"The ring oscillator is really good for things like rolling motions," Preston says. Rolling requires coordination of several actions in time. A single input and output will not suffice. For example, to get their hexagonal foam robot to roll forward, the ring oscillator helps inflate a balloon behind the robot and deflate one in front at the exact same time. The coordinated push-and-release shifts the hexagon forward again and again as the balloons inflate and deflate in perfect sync.

Yet another prototype provides a more tangible purpose. A textile-based sleeve, wrapped around the lower leg and secured with Velcro, exerts coordinated pressure, "pumping" fluid up the leg.

According to recent studies, this "pumping" motion improves symptoms of lymphedema and chronic venous disease better than simple compression. The device could also help nurses, waiters, and police officers prevent deep vein thrombosis, a result of working long shifts on tired feet.

Before they start clinical trials for their sleeve, the team wants to gauge interest. If enough people crave a softer, less expensive way to alleviate and prevent symptoms, the product might just find a big enough market to merit further research.

The low cost of Preston's materials--rubber-like silicone elastomers--make them ideal for more than just inexpensive homecare. Biocompatible, disposable, gentle, and sterile versions could be used for lab experiments, drug delivery, or even medical devices inside the body like this sleeve that helps the heart beat. Preston's final prototype can sort three different colored liquids based on a pre-determined sequence and time, a tool that could prove useful for chemists.

Though all of Preston's prototypes are made with only soft materials, they're not yet untethered: All rely on a constant source of pressurized air. Yet Preston and his colleagues have a few solutions for this, too. For the leg sleeve, patients could provide their own air with a hand-held pump like those used to take blood pressure. And soft robots in the trenches could use mobile carbon dioxide cartridges, strapped on like a backpack, or gas-generating chemical reactions to set the bot in motion.

But Preston expects his new tool to achieve far more than the applications demonstrated in his five prototypes. Since the paper explains how to replicate and customize the design, he hopes other labs will find even more uses. "People can use the soft ring oscillator for a lot of different applications in soft robotics, some of which we may not have even thought of or envisioned yet."

In a study published online in Nature on June 26, research teams led by Dr. YANG Weiwei at the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences (CAS) and Dr. LI Guohui from the Dalian Institute of Chemical Physics of CAS reported a new function of uridine diphosphate glucose (UDP-glucose), a metabolic intermediate in the uronic acid pathway: It impairs lung cancer metastasis by accelerating SNAI1 mRNA decay.

This discovery is important because lung cancer is the leading cancer killer in both China and the world, and cancer metastasis is estimated to be responsible for 95% of cancer deaths. Lung cancer alone kills more than 600,000 people each year in China.

Primary malignant tumors can often be effectively treated by traditional therapies such as surgery, radiation and chemotherapy. However, in most cases, traditional therapies have limited effect on metastatic tumors. Therefore, understanding the molecular mechanisms underlying tumor metastasis helps to provide a biomarker for the early detection of tumor metastasis and a new strategy for intervening in metastasis, thus offering patients a better prognosis.

Deregulated metabolism is the hallmark of cancer. Mutations in oncogenes and tumor suppressor genes cause alterations to multiple intracellular signaling pathways that affect tumor cell metabolism and re-engineer it to allow enhanced survival and growth. The unique biochemical microenvironment further influences the metabolic phenotype of tumor cells, and thus affects tumor progression, response to therapy and patient outcome.

This study reveals a unique function of UDP-glucose in impairing tumor metastasis, presents a new model of metabolite-regulated protein function, and establishes a new connection between metabolism and RNA stability.

Specifically, the researchers demonstrated that upon epidermal growth factor receptor (EGFR) activation, UDP-glucose dehydrogenase (UGDH) is phosphorylated at tyrosine (Y) 473. UGDH is the rate-limiting enzyme in the uronic acid pathway. It catalyzes UDP-glucose to produce UDP-glucuronic acid and participates in the biosynthesis of glycosaminoglycan.

Phosphorylated UGDH binds to HuR and converts UDP-glucose into UDP-glucuronic acid, which attenuates UDP-glucose-mediated inhibition on HuR association with SNAI1 mRNA, thereby enhancing SNAI1 mRNA stability. Increased Snail (encoded by SNAI1) expression in turn initiates the epithelial-mesenchymal transition of tumor cells, thus promoting tumor cell migration and lung cancer metastasis.

In addition, the scientists found that lower UDP-glucose levels are closely related to the metastasis and recurrence of lung cancer. They observed that UDP-glucose levels in metastatic tumors were much lower than in primary tumors. Patients with distant metastasis had much lower UDP-glucose levels than those without distant metastasis, and patients with high UGDH Y473 phosphorylation in tumor tissues had a higher rate of metastasis and worse prognosis.

ANN ARBOR, Michigan -- The Fast and the Furious movie franchise meets the Fast N' Loud television series to define an oncogene that drives 35% of prostate cancers.

A new study from researchers at the University of Michigan Rogel Cancer Center finds that the gene FOXA1 overrides normal biology in three different ways to drive prostate cancer. They refer to the three classes as FAST, FURIOUS, and LOUD to reflect their unique features. The findings are published in Nature.

"It's quite intriguing and complex biology," says senior study author Arul M. Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology and S.P. Hicks Endowed Professor of Pathology at Michigan Medicine.

"We found that the same gene can be turned into an oncogene in three different ways," says Abhijit Parolia, a molecular and cellular pathology graduate student and co-first author on this study. "One moves fast in the nucleus, the second binds to chromatin furiously and the third amplifies itself to be loud. These three alteration classes have different clinical implications for patients."

Class 1 mutations are FAST. They cause the transcription factor to travel more quickly through the DNA, allowing the partnering androgen receptor to activate expression of cancer-promoting genes. Imagine the driver racing forward at high speed. These mutations are seen in early stage prostate cancer and are likely what triggers the disease.

Class 2 mutations are FURIOUS. The mutation causes a portion of the FOXA1 molecule to be cut off. This truncated molecule binds very strongly to the DNA, preventing normal FOXA1 from binding. These mutations are found in lethal hormone-therapy resistant prostate cancer and promote the cancer's spread to distant sites. Think of the mutant as furiously binding DNA and dominantly enabling the cancer's aggressive features.

Class 3 mutations are LOUD. They involve complex rearrangements of the FOXA1 genomic position, creating duplications in which FOXA1 or other oncogenes are overexpressed. In other words, the amplified oncogenes work at top volume to be biologically heard. This can occur in both early stage and metastatic cancer.

Fast and furious mutations are mutually exclusive but loud rearrangements can exist by themselves or mingle with either of the other two.

FOXA1 was previously known to be mutated in prostate cancer, but its biological functions were poorly understood. Scientists were uncertain if FOXA1 was an oncogene that fueled cancer or a tumor suppressor that hit the brakes. The Rogel Cancer Center team now clarified FOXA1's role as a driver oncogene, in addition to classifying the three novel FOXA1 alterations.

The researchers discovered its increased prevalence by using RNA sequencing data from 1,546 prostate cancer samples from multiple collections, including the Rogel Cancer Center's Mi-ONCOSEQ program.

"Oncogenes tend to be easier to develop therapies for as you could theoretically block them with targeted medicines," Chinnaiyan says. "However, FOXA1 is a challenging target because it is a transcription factor, a class of proteins notoriously difficult to inhibit with small molecules. However, scientists are now developing innovative strategies to go after these 'undruggable' targets."

Chinnaiyan says this information can also be used to identify patients with more aggressive disease or begin to understand why patients respond to therapy differently.

The authors also showed that the three classes of FOXA1 alterations are found in breast cancer, presumably impacting the estrogen receptor in a way similar to how it impacts the androgen receptor. FOXA1 alterations are implicated in bladder cancer and some salivary gland cancers as well.

Contrary to popular belief, using social media and the internet regularly could improve mental health among adults and help fend off serious psychological distress, such as depression and anxiety, finds a new Michigan State University study.

Communication technologies and social media platforms make it easier to maintain relationships and access health information, which could explain it, says Keith Hampton, professor of media and information at Michigan State University.

So why the bad rap?

Because until now, adults haven't been the focus of much research on the subject, Hampton said. Instead, most studies on social media have focused on youth and college students, and the effects could be explained by life stages, rather than technology use.

"Taking a snapshot of the anxiety felt by young people today and concluding that a whole generation is at risk because of social media ignores more noteworthy social changes, such as the lingering effects of the Great Recession, the rise in single child families, older and more protective parents, more kids going to college and rising student debt," he said.

So, Hampton set out to study more mature populations, analyzing data from more than 13,000 relationships from adult participants in the Panel Study of Income Dynamics - the world's longest-running household survey. He used 2015 and 2016 data, which included a series of questions about the use of communication technologies and psychological distress.

He found social media users are 63 percent less likely to experience serious psychological distress from one year to the next, including major depression or serious anxiety. Having extended family members on social media further reduced psychological distress, so long as their family member's mental health was not in decline.

The study, published in the Journal of Computer Mediated-Communication, challenges the notion that social media, mobile technologies and the internet contribute to a mental health crisis in the United States.

Other key findings:

Someone who uses a social networking site is 1.63 times more likely to avoid serious psychological distress.

The extent to which communication technologies affect psychological distress varies according to the type and amount of technologies people and their extended family members use.

Changes to the mental health of family members affect the psychological distress experienced by other family, but only if both family members are connected on a social networking site.

"Today, we have these ongoing, little bits of information popping up on our cell phones and Facebook feeds, and that ongoing contact might matter for things like mental health," Hampton said.