Earth

Oncotarget recently published "Estrogen receptor α polymorphism is associated with dementia in a Brazilian cohort" which reported that the growth of the elderly population is a worldwide phenomenon and it is associated with chronic diseases, including dementia.

In this scenario, the present study aimed to evaluate a possible association of estrogen receptor α polymorphisms with dementia in a Brazilian cohort.

The genotyping for the ERα PvuII and XbaI polymorphisms were performed by polymerase chain reaction-restriction fragment length polymorphism.

The ERα PvuII pp genotype was associated with a higher odds ratio for dementia (OR = 3.42, 95% CI = 1.33–8.77, p = 0.01, in a model including covariates.

A linear regression model identified significant associations of the ERα PvuII genotypes with CDR scale , β = 0.26 and p = 0.001. In conclusion, estrogen receptor α PvuII polymorphism is associated with dementia in a Brazilian cohort.

"In conclusion, estrogen receptor α PvuII polymorphism is associated with dementia in a Brazilian cohort"

Dr. Valerio Garrone Barauna from The Federal University of Espirito Santo-Department of Physiological Sciences said, "One of the most striking features of the current world's demographic dynamics is the process of population aging, that is, the increase in the absolute number and percentage of elderly people in the population as a whole, which has occurred since 1950, but mainly during the 21st century."

One of the most striking features of the current world's demographic dynamics is the process of population aging, that is, the increase in the absolute number and percentage of elderly people in the population as a whole, which has occurred since 1950, but mainly during the 21st century.

In relative terms, the elderly population accounted for 5.1% of the total 1950 population, rose to 6.5% by 2020 and is expected to reach 22.6% by 2100 .

Among the chronic-degenerative conditions that afflict this “new” population, hypertension, diabetes mellitus, osteoporosis, atherosclerosis and dementia, in particular Alzheimer's disease, stand out .

The diagnosis of Alzheimer's disease and other types of dementia, which occur with severe cognitive loss, is based on the observation of clinical data.

Biochemical and genetic studies are important for identifying markers to make diagnosis more assertive, for predicting risk of disease, and/or differential diagnosis between dementias.

The Barauna Research team concluded in their Oncotarget Research Paper that this study has some limitations.

For a better statement about this polymorphism, a larger and more heterogeneous cohort would be needed.

In addition, coexisting multiple factors are important in pathogenesis changes.

The diagnostic research relationships for potential risk factors for dementia versus current clinical application should take into account both genetic and longevity biomarkers with patients.

Diagnostic and prognostic research can no longer be exclusively based on currently used clinical tests, but rather new diagnostic protocols that involve the relevant factors.

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DOI - https://doi.org/10.18632/oncotarget.27744

Full text - https://www.oncotarget.com/article/27744/text/

Correspondence to - Valerio Garrone Barauna - barauna2@gmail.com

Keywords -
dementia,
elderly,
estrogen receptor α,
polymorphism

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Journal

Oncotarget

DOI

10.18632/oncotarget.27744

CHAMPAIGN, Ill. -- Tiny fluorescent semiconductor dots, called quantum dots, are useful in a variety of health and electronic technologies but are made of toxic, expensive metals. Nontoxic and economic carbon-based dots are easy to produce, but they emit less light. A new study that uses ultrafast nanometric imaging found good and bad emitters among populations of carbon dots. This observation suggests that by selecting only super-emitters, carbon nanodots can be purified to replace toxic metal quantum dots in many applications, the researchers said.

The findings, published in the Proceedings of the National Academy of Sciences, brought together researchers from the University of Illinois Urbana-Champaign and the University of Maryland, Baltimore County in a collaborative project through the Beckman Institute for Advanced Science and Technology at Illinois.

"Coming into this study, we did not know if all carbon dots are only mediocre emitters or if some were perfect and others were bad," said Illinois chemistry professor Martin Gruebele, who led the study. "We knew that if we could show that there are good ones and bad ones, maybe we could eventually find a way to pick the perfect ones out of the mix."

Determining whether carbon dots are good or bad light emitters starts with being able to see them, Gruebele said. The dots are less than 10 nanometers in diameter and, when excited, decide whether to fluoresce in a matter of in picoseconds - or one-thousandth of one billionth of a second.

"Using our previously developed single-molecule absorption scanning tunneling microscope, we could only image excited states with no time resolution," Gruebele said. "In this study, however, we can now record quantum dots while in their excited state by combining true nanometer space resolution with femtosecond time resolution."

The team found that the energy excitation takes one of two paths: either emit light or expel the energy as heat before getting a chance to fluorescence.

"We found that in bulk populations, approximately 20% of a given population of carbon nanodots are perfect emitters, while about 80% have a very short light emission state before expelling heat," Gruebele said. "Being able to see that there are different populations tells us that it may be possible to purify carbon dot populations by selecting only the perfect light emitters."

The ability to pick out the perfect dots could make the concept of efficient carbon-based dots a reality, Gruebele said. "Metal quantum dots are often used to monitor the health of living cells, which is far from ideal, and having a nontoxic, economical option would be a significant advancement."

The new imaging technology also allows the researchers to observe why some dots never light up, hinting that there is hope that researchers can someday synthesize perfect light-emitting carbon dots.

"We now know that we have an instrument that identifies the problem," Gruebele said. "Whether we use it to purify groups of carbon dots or to help synthesize perfect light-emitting carbon dots is now just a question of where we want to head next."

About one billion people worldwide are at risk for schistosomiasis -- a debilitating disease caused by parasitic worms that live in fresh water and in intermediate snail hosts. A new study finds that the transmission risk for schistosomiasis peaks when water warms to 21.7 degrees centigrade, and that the most effective interventions should include snail removal measures implemented when the temperature is below that risk threshold.

The Proceedings of the National Academy of Sciences published the results, led by Emory University, the University of South Florida and the University of Florida.

"We've shown how and why temperature matters when it comes to schistosomiasis transmission risk," says Karena Nguyen, a post-doctoral fellow in Emory University's Department of Biology and a first author of the study. "If we really want to maximize human health outcomes, we need to consider disease transmission in the context of regional temperatures and other environmental factors when developing intervention strategies."

The findings indicate that climate change will increase schistosomiasis risk in regions where surface water moves closer to 21.7 degrees centigrade, or 71 degrees Fahrenheit. The researchers also found, however, that implementing snail control measures decreases transmission but raises the temperature for peak transmission risk to 23 degrees centigrade, or 73 degrees Fahrenheit.

Co-first author of the paper is Philipp Boersch-Supan, an expert in ecological systems at the University of Florida and the British Trust for Ornithology.

Nguyen is a member of the lab of David Civitello, Emory assistant professor of biology and a co-author of the PNAS paper. The Civitello lab studies the ecological dynamics of disease, aquatics and agricultural ecology through a combination of experiments, field surveys and models.

"The control of schistosomiasis currently relies on treating infected people," Civitello says. "However, there is renewed awareness that the ecological factors surrounding the disease also need to be considered. Our paper is a beautiful example of the potential power of uniting ecology with human disease interventions and control measures."

Schistosomiasis is one of the most devasting water-based diseases in developing countries, with more than 200 million people infected worldwide, leading to around 200,000 deaths annually. It is caused by Schistosoma parasites that have a complex life cycle.

Freshwater becomes contaminated by the parasite's eggs when infected people urinate or defecate in the water. After the eggs hatch, the parasites enter freshwater snails where they develop and multiply. More mature parasites are able to leave the snails and re-enter the water. These free-swimming parasites can then burrow into the skin of people who are wading, swimming, bathing, washing or doing agricultural work in contaminated water.

Children who are repeatedly infected can develop anemia, malnutrition and learning difficulties. Over the long term, the parasites can also damage the liver, intestine, lungs and bladder.

"Schistosomiasis is treatable -- people can take a drug to get rid of the adult parasites in their bodies," Nguyen says. "But in areas where schistosomiasis is prevalent, people can easily get reinfected by coming in contact with contaminated water. And children, who like to play in water, tend to have the highest burden of the disease."

For the current paper, Nguyen focused on how global climate change and rising water temperatures might affect each stage of the schistosomiasis transmission cycle. It was already established that both the parasites and the snails are sensitive to water temperature, with each stage having an optimum temperature.

"I wanted to build on previous work to see if we could use it to find better predictors for human risk and more effective interventions," Nguyen says.

The researchers integrated an epidemiological model of schistosomiasis and temperature-dependent traits of the parasites and their snail hosts to run different computer-simulated interventions. The results showed that interventions targeting snails were most effective at reducing transmission, and pinpointed the water temperature for when the risk of transmission peaks.

Unexpectedly, the simulations also showed that interventions targeting snail removal actually raised the peak transmission temperature by 1.3 degrees centigrade, while reducing transmission risk.

"That may not sound like a lot," Nguyen says, "but we're talking about water temperature, which takes a lot of energy to warm, so 1.3 degrees is actually a big shift."

Snails naturally start to die off at higher water temperatures. The data in the new paper shows how implementing snail control measures, such as through chemical treatment of the water, amplifies snail mortality at all temperatures. This lowers transmission risk overall, but allows peak transmission risk to occur at higher temperatures.

These insights can guide public health workers to time their interventions, by factoring in regional water temperatures, and how the temperatures fluctuate during different seasons of the year.

"Our findings don't mean that we should stop human treatment for schistosomiasis," Nguyen says. "Instead, it will likely be beneficial to include both the human and ecological components. By combining human drug treatment with snail removal measures, during times when water is below the peak transmission temperature, we may be able to maximize the efficacy of an intervention."

Boston, MA - Financial pollution arises when exorbitant or unnecessary healthcare spending depletes resources needed for the wellbeing of the population. This is the subject of a JAMA Health Forum Insight co-authored by researchers in the Department of Population Medicine at Harvard Pilgrim Health Care Institute and Harvard Medical School. The Insight was published in the March 8, 2021 issue of JAMA Health Forum.

The authors lay out the rationale for "financial pollution" as a metaphor to express the urgency of addressing wasteful health care spending and to guide innovative policymaking. Akin to environmental pollution, financial pollution is human-made, contaminates connected systems, remains largely invisible to many, and disproportionately harms vulnerable populations. The authors highlight approaches that have improved environmental pollution as avenues for reducing financial pollution.

Unlike the term "financial toxicity," which is defined as direct harm that occurs when patients must pay out-of-pocket for substantial shares of health care services, the authors contend that financial pollution is more widespread and insidious, indirectly draining the resources of families through increased health insurance premiums and taxes. This leaves households with fewer resources for education, housing, and child-rearing, ultimately causing a creeping accrual of harm to the population.

"The term 'wasteful healthcare spending' does not sufficiently capture the harm that such spending causes populations," said author Frank Wharam, Associate Professor of Population Medicine at the Harvard Pilgrim Health Care Institute and Harvard Medical School. "'Waste' conjures up images of byproducts that are routed to treatment plants, cleaned, and recycled. In contrast, pollution is waste that hurts people. To express the dangers of wasteful healthcare spending, and to address it urgently, we should call it what it is - financial pollution."

"The current public health, economic, and equity crises demand a new mindset for action," added author Anita Wagner, Associate Professor of Population Medicine at the Harvard Pilgrim Health Care Institute and Harvard Medical School. "We believe naming the problem of financial pollution - about $900 billion in spending each year - and learning from policy approaches to combat environmental pollution can help reduce financial pollution and increase population wellbeing."

When a coastline undergoes massive erosion, like a hurricane flattening a beach and its nearby environments, it has to rebuild itself - relying on the resilience of its natural coastal structures to begin piecing itself back together in a way that will allow it to survive the next large phenomena that comes its way.

Drs. Orencio Duran Vinent, assistant professor, and Ignacio Rodriguez-Iturbe, Distinguished University Professor and Wofford Cain Chair I Professor, in the Department of Ocean Engineering at Texas A&M University, are investigating the resilience of barrier islands and coastal dunes after high-water events and storms. In doing so, they are helping engineers and researchers assess the vulnerability of coastal landscapes.

Their full findings were published as related articles in the Proceedings of the National Academy of Sciences titled "Probabilistic structure of events controlling the after-storm recovery of coastal dunes" and "Stochastic dynamics of barrier island elevation."

"If you understand how dunes grow, then you can take action, for example, in terms of vegetation or artificial barriers, to protect the coastline," Rodriguez-Iturbe said. "But you cannot protect or manage, in this case, dunes and barrier islands if you don't first understand the dynamics taking place."

In general, there are two types of high-water events along the coast: natural disasters like hurricanes and tsunamis, which cause waves that devastate the shoreline, and lesser storm surges, which do not cause widescale damage but still affect the coastal environment. As Duran Vinent explained, it is these smaller, routine events that control the post-storm resiliency of dunes and barrier islands that play a key role in protecting coastal communities by absorbing some of the impact from surges.

"Those events are not really strong enough to erode a mature dune completely, but they are strong enough to prevent one from growing in the first place after a storm that erodes the dunes and the vegetation ecosystem," he said.

With that in mind, the research team first studied the structure and properties of such smaller high-water events from around the world, utilizing buoy and other data to calculate characteristics like beach elevation, wave runup and water level to analyze them.

Their findings were twofold: first, they confirmed that the high-water events happen randomly and unrelatedly to one another. Then the team discovered that high-water events around the world shared the same general characteristics and had the same typical frequency per year with a given intensity when measured at beach level.

"This means that we can actually say something about the typical size of these nuisance flooding events or the typical size and frequency of events affecting the recovery of the coastal environment," Duran Vinent said. "Regardless of location, we have a unified description. And this simplifies the work for policymakers or managers a lot because then they don't need complex calculations."

The team took their newly discovered information and applied it to developing a model that would determine the elevation of a barrier island and, ultimately, whether or not a dune would be able to succeed. Additionally, this model provides a valuable tool in rebuilding coastlines that have been broken down and deteriorated over time, as it gives engineers a way to see how tall a dune or barrier island needs to be in order to prevent frequent overwashes and, thus, ensure ecosystem survival.

"The dynamic between high-water events and the geomorphology of barrier islands is complicated because the impact of any high-water event depends on how big the dunes are," Rodriguez-Iturbe said.

"And then while the dune is growing, you have these high-water events randomly interrupting its growth," Duran Vinent said. "This means that there is a competition between the frequency of the high-water erosional event and how fast the dune is growing."

This competition became the base of their analytical equation developed to determine whether or not a dune would be able to succeed, mathematically mapping in which conditions a barrier island would be resilient or vulnerable.

Dunes on barrier islands are vitally important, Duran Vinent explained, because they prevent water events from breaching the island and protect the vegetation on the back of the island from flooding, allowing a diverse set of vegetation to grow that is otherwise intolerant to seawater.

For cancer cells to metastasize, they must first break free of a tumor's own defenses. Most tumors are sheathed in a protective "basement" membrane -- a thin, pliable film that holds cancer cells in place as they grow and divide. Before spreading to other parts of the body, the cells must breach the basement membrane, a material that itself has been tricky for scientists to characterize.

Now MIT engineers have probed the basement membrane of breast cancer tumors and found that the seemingly delicate coating is as tough as plastic wrap, yet surprisingly elastic like a party balloon, able to inflate to twice its original size.

But while a balloon becomes much easier to blow up after some initial effort, the team found that a basement membrane becomes stiffer as it expands.

This stiff yet elastic quality may help basement membranes control how tumors grow. The fact that the membranes appear to stiffen as they expand suggests that they may restrain a tumor's growth and potential to spread, or metastasize, at least to a certain extent.

The findings, published this week in the Proceedings of the National Academy of Sciences, may open a new route toward preventing tumor metastasis, which is the most common cause of cancer-related deaths.

"Now we can think of ways to add new materials or drugs to further enhance this stiffening effect, and increase the toughness of the membrane to prevent cancer cells from breaking through," says Ming Guo, a lead author of the study and associate professor of mechanical engineering at MIT.

Guo's co-authors include first author Hui Li of Beijing Normal University, Yue Zheng and Shengqiang Cai of the University of California at Santa Diego, and MIT postdoc Yu Long Han.

Blowing up

The basement membrane envelopes not only cancerous growths but also healthy tissues and organs. The film -- a fraction of the thickness of a human hair -- serves as a physical support that holds tissues and organs in place and helps to shape their geometry, while also keeping them separate and distinct.

Guo's group specializes in the study of cell mechanics, with a focus on the behavior of cancer cells and the processes that drive tumors to metastasize. The researchers had been investigating how these cells interact with their surroundings as they migrate through the body.

"A critical question we realized hasn't gotten enough attention is, what about the membrane surrounding tumors?" Guo says. "To get out, cells have to break this layer. What is this layer in terms of material properties? Is it something cells have to work really hard to break? That's what motivated us to look into the basement membrane."

To measure the membrane's properties, scientists have employed atomic force microscopy (AFM), using a tiny mechanical probe to gently push on the membrane's surface. The force required to deform the surface can give researchers an idea of a material's resistance or elasticity. But, as the basement membrane is exceedingly thin and tricky to separate from underlying tissue, Guo says it's difficult to know from AFM measurements what the resistance of the membrane is, apart from the tissue underneath.

Instead, the team used a simple technique, similar to blowing up a balloon, to isolate the membrane and measure its elasticity. They first cultured human breast cancer cells, which naturally secrete proteins to form a membrane around groups of cells known as tumor spheroids. They grew several spheroids of various sizes and inserted a glass microneedle into each tumor. They injected the tumors with fluid at a controlled pressure, causing the membranes to detach from the cells and inflate like a balloon.

The researchers applied various constant pressures to inflate the membranes until they reached a steady state, or could expand no more, then turned the pressure off.

"It's a very simple experiment that can tell you a few things," Guo says. "One is, when you inject pressure to swell this balloon, it gets much bigger than its original size. And as soon as you release the pressure, it gradually shrinks back, which is a classical behavior of an elastic material, similar to a rubber balloon."

Elastic snap

As they inflated each spheroid, the researchers observed that, while a basement membrane's ability to inflate and deflate showed that it was generally elastic like a balloon, the more specific details of this behavior were surprisingly different.

To blow up a latex balloon typically requires a good amount of effort and pressure to start up. Once it gets going and starts to inflate a bit, the balloon suddenly becomes much easier to blow up.

"Typically, once the radius of a balloon increases by about 38 percent, you don't need to blow any harder -- just maintain pressure and the balloon will expand dramatically," Guo says.

This phenomenon, known as snap-through instability, is seen in balloons made of materials that are linearly elastic, meaning their inherent elasticity, or stiffness, does not change as they deform or inflate.

But based on their measurements, the researchers found that the basement membrane instead became stiffer, or more resistant as it inflated, indicating that the material is nonlinearly elastic, and able to change its stiffness as it deforms.

"If snap-through instability were to occur, a tumor would become a disaster -- it would just explode," Guo says. "In this case, it doesn't. That indicates to me that the basement membrane provides a control on growth."

The team plans to measure the membrane's properties at different stages of cancer development, as well as its behavior around healthy tissues and organs. They are also exploring ways to modify the membrane's elasticity to see whether making it stiffer will prevent cancer cells from breaking through.

"We are actively following up on how to modify the mechanics of these membranes, and apply perturbations on breast cancer models, to see if we can delay their invasion or metastasis," Guo says. "This is an analogy to making a stiffer balloon, which we plan to try."

Aging-US published "DNA- and telomere-damage does not limit lifespan: evidence from rapamycin" which reported that failure of rapamycin to extend lifespan in DNA repair mutant and telomerase-knockout mice, while extending lifespan in normal mice, indicates that neither DNA damage nor telomere shortening limits normal lifespan or causes normal aging.

Dr. Mikhail V. Blagosklonny said, "As a provocative title has recently announced, 'rapamycin fails to extend lifespan in DNA repair -deficient mice' [1]. The word 'fails' implies bad news. Rapamycin tried but failed. Yet, it is expected that the anti-aging drug rapamycin should not restore lifespan of short-lived mice that fail to grow and die young from causes other than normal aging [2]. In such growth- retarded mice, rapamycin, an inhibitor of cell growth, further retards weight gain."

While shortening lifespan by 18% in unnatural telomerase- deficient mice, in the same study in natural mice, rapamycin increased lifespan by 39% and healthspan by 58%.

In dozens of independent studies, rapamycin has not failed to extend lifespan in normal mice.

However, while extending lifespan in normal mice, rapamycin may fail to save animals dying young from cellular growth retardation.

The failure of rapamycin to extend lifespan in these short- lived mice, dying from DNA damage, rules out the damage theory of aging and to illustrate this point the author first discusses what limits animal lifespan by providing commentary on 1. Quasi-programmed (hyperfunctional) aging and 2. How molecular damage can become life- limiting

Blagosklonny concluded in his Aging-US Research Output that here he discussed new evidence that normal aging is not caused by accumulation of molecular damage or telomere shortening: while extending normal lifespan in mice, rapamycin failed to do so in mice dying from molecular damage.

Previously, several lines of evidence suggested that molecular damage does not cause normal aging. Their detailed discussion is beyond the focus of this article, so he just mentions some of them, without referencing them.

1. Overexpression of enzymes that decrease damage does not extend lifespan in most studies. Similarly, antioxidants do not extend lifespan in animals and may increase mortality in humans. Furthermore, even data that support damage theory can be explained by other mechanisms. For example, N-Acetyl-L-Cysteine, a commonly used anti- oxidant, can inhibit mTOR.
2. According to calculations, molecular damage, especially mtDNA mutations and telomere shortening, cannot reach a deadly threshold during animal lifetime.
3. Genetic knockout of signaling pathways can extend lifespan without affecting molecular damage. Similarly, pharmacological interventions can extend life without affecting damage accumulation.
4. Dramatic intra- and inter-species differences in lifespan poorly correlate with the rate of molecular damage.
5. Nuclear transfer and nuclear reprogramming both rule out DNA damage as a cause of aging. Following adult somatic cell nuclear transfer, cloned animals are healthy and have normal lifespan.
6. Low levels of molecular damage may increase longevity. This phenomenon is known as hormesis. Regardless of mechanistic explanations, this indicates that molecular damage is not-life-limiting even when moderately increased.
7. Rapamycin increases lifespan in all normal animals tested, indicating that mTORC1-dependent quasi-program is life-limiting.

Once again, damage accumulates and must cause death eventually, but quasi-programmed aging terminates life first. Molecular damage can become life-limiting, when artificially accelerated or, potentially, when quasi-programmed aging is decelerated.

Juvenile white-tailed deer that strike out to find new home ranges -- despite facing more risks -- survive at about the same rate as those that stay home, according to a team of researchers who conducted the first mortality study of male and female dispersal where deer were exposed to threats such as hunting throughout their entire range.

Dispersal occurs when a juvenile leaves the area where it was born and moves to a new location where the young animal establishes its adult home range, explained Duane Diefenbach, Penn State adjunct professor of wildlife ecology. The instinctual dispersal of young deer from the area where they were born to a new home range protects the species' gene pool from inbreeding with close relatives.

Diefenbach's research group in the College of Agricultural Sciences has radio-collared hundreds of Pennsylvania deer over the last 20 years, monitoring their survival, movement and behavior. Earlier research done by his lab, in collaboration with the Pennsylvania Game Commission, revealed that about three of every four young, male white-tailed deer disperse, with yearling female dispersal rates much lower.

Dispersal distances depend on forested cover, Diefenbach and colleagues demonstrated in previous research. But on average in Pennsylvania, males travel more than three miles, typically in direct, straight-line fashion; females that disperse often seemingly wander around before settling down an average of about nine miles from where they started.

"We wanted to know how risky dispersal is," said lead researcher Eric Long, now a professor of biology at Seattle Pacific University, who was a doctoral degree student at Penn State advised by Diefenbach when early stages of the research unfolded. He was surprised to find no detectable increase in death among dispersing deer.

"We expected to find that dispersal results in added mortality because deer are traveling across unfamiliar territory and are more likely to encounter predators or vehicles," Long said. "Going into this research, I expected to have a lot of our dispersers killed by vehicles as they were making the movement. We were surprised at how effective deer are at dispersing, especially when they have to deal with relatively modern risks like roads and hunting."

For this study, researchers captured 398 juvenile male and 276 juvenile female white-tailed deer and compared survival rates of dispersers and nondispersers.

Over three years, 381 males were equipped with very high frequency -- or VHF -- radio-transmitters and were located with telemetry at least weekly; 17 were equipped with global positioning system, or GPS, radio-transmitters that recorded positions at least twice daily. Over six years, 245 females were equipped with VHF transmitters and located at least weekly; 32 were equipped with GPS transmitters that recorded position at least daily.

Juvenile deer were captured in the winter through early spring. At the time of capture, they were seven to 10 months old. For both male and female white-tailed deer, natal dispersal prior to 11 months of age is rare, Long noted, so capture between December and April decreased the likelihood of capturing juveniles that had already dispersed.

Results of the research, recently published in Ecology and Evolution, indicate that for both male and female yearlings, survival rates of dispersers -- males 49.9%, females 64.0% -- did not differ appreciably from those of nondispersers -- males 51.6%, females 70.7%. Only two individuals, both female, were killed by vehicular collision during dispersal movement.

So, why do dispersing juvenile deer fare as well as nondispersers despite facing more risk? Researchers are not sure, but Long suspects that deer with the predisposition to be more adventurous might have a genetic makeup that helps them to avoid threats. Also, he said, there is some evidence to suggest that yearlings in better condition, with bigger bodies, are more likely to disperse than deer in poorer condition.

"It may be that only those deer that are up to the challenge of dispersal even try it," he said. "Bucks, which are more likely to disperse, seem much more efficient at dispersal than females. They don't mess around and wander all over the place like does -- and that likely decreases their risk."

The melting of the Earth's ice cover intensified in the 20th century, with glaciers and sea ice in the Arctic and Antarctic regions melting at alarming speeds. In fact, The Antarctic Peninsula (AP), which is the only landmass of Antarctica extending out past the Antarctic Circle, was found to be one of the most rapidly warming regions on the planet during the second half of the 20th century. This rapid change in climate has raised serious concerns of rising sea levels the world over.

Multiple factors have been associated with the melting of the ice cover: the primary factor being the greenhouse gas emissions from human activities that cause warming up of the atmosphere and the oceans and the consequent ice melting. Apart from this, atmospheric variations, ocean currents, and wind patterns also play a significant role. Now, a collaborative group of scientists from Japan and Australia--led by Assistant Professor Kazutoshi Sato from Kitami Institute of Technology and Associate Professor Jun Inoue from National Institute of Polar Research in Japan--has focused efforts on understanding how fluctuations in these climatic factors affect the warming of the Antarctic. They have documented their findings in a brand-new article published in Nature Communications.

Previous studies have examined the relationship between the wind dynamics over the Southern Ocean (also called SO; located north of Antarctica) and climate variability in tropical oceans. It was found that heating in tropical regions generates atmospheric waves called "Rossby wave trains" from the tropics to the Antarctic region via the SO, which causes heating of the West Antarctic region. Interestingly, Rossby waves are an attempt of nature to balance heat in the atmosphere as they transfer heat from the tropics to the poles and cold air towards the tropics.

On the path of understanding the warming of AP, Dr. Sato points out, "The impacts of climate variabilities over the mid-latitudes of the Southern Hemisphere on this Antarctic warming have yet to be quantified". His team addressed this gap by looking at the climate changes in the Tasman Sea located between Australia and New Zealand and the SO and drew correlations with temperature variations in the AP.

Dr. Sato and his team analyzed the temperature data from six stations in AP and the wind and cyclone patterns over the Tasman sea and the SO from 1979 to 2019. They found that even without unusual heating in the tropics, only the heating in the Tasman Sea modifies the wind patterns over the SO and forces the Rossby waves to move even deeper into the Amundsen sea low, a low-pressure area lying to the west of the AP. This larger pressure gradient causes stronger colder winds towards the poles. The meandering wind stream moves towards the AP, resulting in the warming of this region. Additionally, this effect was found to be prominent in the winter months when the cyclones are more active. "We have shown that warm winter episodes in the Tasman Sea influence warm temperature anomalies over key regions of West Antarctica, including the AP, through a poleward shift of South Pacific cyclone tracks", Dr. Sato summarizes.

The ever-increasing warming of the AP--rather, the whole of Antarctica at large--is a major concern plaguing climatologists all over the world. Commenting on the serious implications of this rapid rise in temperature and sea levels and the importance of the findings of their study, Dr. Inoue says, "Antarctic warming accelerates Antarctic ice sheet melting and contributes to the rise in sea levels across the world. Therefore, knowledge of the mechanisms of the melting of the Antarctic ice sheet would help scientists, policymakers, and administrations to devise measures for people who will be most affected by the rising sea levels."

Dr. Sato and his team concludes by stating that the findings of their study can also aid the future forecast of ice sheet melting in Antarctica and consequent global sea level rise.

Osaka, Japan - Chemotherapy has a damaging effect on hematopoietic stem and progenitor cells (HSPCs) in bone marrow. However, once chemotherapy ends, HSPCs regenerate, a process that has remained unknown—until now. In a new study, researchers from Osaka University have identified the molecular mechanism by which HSPCs recover after injury.

HSPCs reside in the bone marrow and give rise to several types of blood cells, such as red blood cells (which carry oxygen), some white blood cells (which are important for the immune system) and platelets (which are necessary to stop bleeding). Because HSPCs constantly divide to generate new cells, they are particularly sensitive to injury induced by, for example, chemotherapy. Interestingly, HSPCs have the capability to regenerate upon injury.

"The bone marrow is a very active organ because it has to constantly produce new blood cells," says corresponding author of the study Masaru Ishii. "Once it loses its function, such as during chemotherapy, deadly conditions such as anemia, neutropenia and bleeding can occur. In this study, we wanted to understand how hematopoietic stem cells residing in the bone marrow regenerate upon chemotherapy-induced injury to recover their full function."

To achieve their goal, the researchers focused on a specific subset of blood cells that are produced from HSPCs, so-called group 2 innate lymphoid cells (ILC2s). While ILC2s exist in a number of tissues and play an important role in the immune system and tissue repair, those residing in bone marrow are thought to have a distinct role specific to their location. However, the nature of their function was unclear. To unravel the biological role of ILC2s, the researchers treated mice with 5-fluorouracil (5-FU), a chemotherapeutic agent toxic to HSPCs, and transplanted fresh, undamaged HSPCs into these mice, akin to a stem cell transplantation therapy in patients with leukemia. Interestingly, the researchers found that the injured HSPC microenvironment in 5-FU-treated mice promoted the proliferation of the transplanted HSPCs. By analyzing this finding at the molecular level, the researchers found that ILC2s in the bone marrow of treated mice produced granulocyte-macrophage colony-stimulating factor (GM-CSF) to aid in the process of HSPC regeneration.

But how exactly do ILC2s know that they should produce GM-CSF after bone marrow injury? To answer this question, the researchers widened their focus to investigate if there are other cells or molecules that direct ILC2s to the production of GM-CSF. They found that progenitors of antibody-producing B cells in the bone marrow produced interleukin (IL)-33 after injury, which in turn activated ILC2s, demonstrating how multiple molecular players are required to recover the damaged bone marrow. Importantly, the researchers showed that the transfer of isolated ILC2s to 5-FU-treated mice accelerates hematopoietic recovery, while the reduction of ILC2s results in the opposite effect, suggesting that ILC2s may serve as a sensor of bone marrow damage.

"These are striking results that show the bone marrow regenerates after chemotherapy," says first author of the study Takao Sudo. "Our results may contribute to the development of a novel therapeutic approach for chemotherapy-induced myelosuppression."

More Antarctic meltwater is surfacing than was previously known, modifying the climate, preventing sea ice from forming and boosting marine productivity- according to new research from the University of East Anglia (UEA).

For the first time, researchers have been able to obtain full-depth glacial meltwater observations in winter, using instruments attached to the heads of seals living near the Pine Island Glacier, in the remote Amundsen Sea in the west of Antarctica.

The harsh environmental conditions in the Antarctic limit the use of most traditional observation systems, such as ships and airplanes, especially in winter. But oceanographers working with biologists used data collected by tagged seals to measure water temperature and salinity.

The paper, 'Winter seal-based observations reveal glacial meltwater surfacing in the southeastern Amundsen Sea', is published in today the journal Communications: Earth and Environment.

The researchers found a highly variable meltwater distribution with two meltwater-rich layers - one in the upper 250 metres and another at around 450 metres deep - connected by scattered meltwater-rich columns. The hydrographic signature of meltwater is clearest in winter, when its presence can be unambiguously mapped; this analysis is only possible in winter.

The surfacing meltwater provides near-surface heat that helps to maintain areas of open seawater surrounded by sea ice, close to glaciers, and may change the melting rate of these fragile ice shelves. These findings offer important clues to better predicting the future climate system and sea level rise.

Pine Island Glacier is rapidly melting, exporting the glacial meltwater into the ocean. Glacial meltwater is thought to play a role in hydrography and sea ice distribution, but until now little has been known about it.

Yixi Zheng, a postgraduate researcher in UEA's School of Environmental Sciences, is the lead author of the study. She said: "The temperature and salinity of water change everywhere glacial meltwater exists. Just like looking for a 'fingerprint' of glacial meltwater, we use temperature and salinity data to track the glacial meltwater.

"The glacial meltwater distribution is very patchy. It doesn't mix well with the ambient water, instead flowing along two meltwater-rich layers in the upper 250 metres and at around 450 metres, connected by meltwater-rich columns.

"As the glacial meltwater is warmer and fresher than the ambient water, it is lighter than the ambient water and more likely to rise up. It brings heat and nutrients such as iron to the near surface, which may melt the sea ice near glaciers and increase the nutrient level near the surface. This enhances the air-sea interactions, and the meltwater-related nutrient may boost the growth of marine planktons like algae."

The winter processes revealed by the study are likely important for bringing nutrients to the near-surface layer prior to the spring bloom, and for bringing heat to the surface to prevent sea ice from forming. This action helps to maintain the open water areas, called polynyas, in front of glaciers.

Many glaciers around Antarctica are thinning rapidly, due primarily to basal melting (i.e. melting that occurs at the interface between the ocean and the ice shelf glacier). The strongest melt has been reported in west Antarctic glaciers such as the Pine Island Glacier, where the research took place.

The volume of meltwater produced is small in comparison with the volumes of Antarctic shelf seas, but it is believed to exert a disproportionate influence on regional circulation and climate.

The heat from the meltwater is likely to prevent sea ice formation, allowing melting of sea ice and thus increasing the extent of open water areas in front of glaciers.

The strong offshore wind near the glacier front may also transport warm near-surface water further and expand the meltwater-influenced region. These enlarged polynyas (open-water areas surrounded by ice) can then lead to enhanced air-sea fluxes and have further impacts on iceberg calving and glacier melting.

Seven southern elephant seals (Mirounga leonina) and seven Weddell seals (Leptonychotes weddellii) were captured and tagged with CTD-Satellite Relayed Data Loggers around the Amundsen Sea in February 2014. The data were gathered by Marine Mammals Exploring the Oceans Pole to Pole (MEOP). Researchers from the universities of Gothenburg and Rhode Island also contributed.

The scientists say further research is required. The study was based on one year of seal-tag data from the Pine Island Glacier, so it can't be used to calculate trends over time or take into account interannual variability such as the El Nino-Southern Oscillation, which may affect the global water temperature.

Background: Although caregivers of patients with eating disorders usually experience a heavy caregiving burden, the effects of social support on caregivers of patients with eating disorders are unknown. This study aimed to investigate how social support for mothers who are caregivers of patients with an eating disorder improves the mothers' mental status and, consequently, the symptoms and status of the patients.

Methods: Fifty-seven pairs of participants were recruited from four family self-help groups and one university hospital in Japan. Recruitment was conducted from July 2017 to August 2018. Mothers were evaluated for social support using the Japanese version of the Social Provisions Scale-10 item (SPS-10), self-efficacy using the General Self-Efficacy Scale, loneliness using the University of California, Los Angeles Loneliness Scale, listening attitude using the Active Listening Attitude Scale, family functioning using the Family Assessment Device, depression symptoms using the Beck Depression Inventory (Second Edition), and psychological distress using the Kessler Psychological Distress Scale. Patients were evaluated for self-esteem using the Rosenberg Self-Esteem Scale, assertion using the Youth Assertion Scale, and their symptoms using the Eating Disorder Inventory. We divided the mothers and patients into two groups based on the mean score of the SPS-10 of mothers and compared the status of mothers and patients between the high- and low-scoring groups.

Results: High social support for mothers of patients with eating disorders was significantly associated with lower scores for loneliness and depression of these mothers. We found no significant differences in any patient scores based on mothers' level of social support.

Conclusions: For patients with eating disorders, social support for a caregiver cannot be expected to improve their symptoms, but it may help prevent caregiver depression and loneliness.

Autophagy is an intracellular degradation process of cytosolic materials and damaged organelles. Researchers at Ubiquitin Project of TMIMS have been studying the molecular mechanism of mitophagy, the selective autophagy process to eliminate damaged mitochondria. PINK1 (a serine/threonine kinase) and Parkin (a ubiquitin ligating enzyme: E3) work together to ubiquitylate the outer membrane proteins of damaged mitochondria, then ubiquitin chains are recognized as signals for autophagy degradation. Dysfunction of mitophagy causes a decrease in mitochondrial quality with overproduction of ROS, and is linked to neurodegenerative diseases like Parkinson's disease.

In Autophagy machinery, cellular components targeted for degradation are engulfed by phosphatidylinositol-3-phosphate (PI3P)-rich membranes. Membranes are elongated and enclosed to form autophagosomes, which then fuse with lysosomes to degrade the cargo inside. Many proteins function in autophagy machinery and they were initially identified by genetic screens in the budding yeast Saccharomyces cerevisiae, and Caenorhabditis elegans. Essential autophagy proteins are evolutionarily conserved from yeast to humans. However, in mammals, there should be unidentified autophagic proteins, and accessory components, whose single gene deletions only manifest as mild defects in autophagy activity, might be missed by these types of genetic screens.

In this study, by immunoprecipitating WIPI1, the well-known autophagy protein, upon Parkin-mediated mitophagy-inducing conditions, researchers identified human BCAS3 (Breast Carcinoma Amplified Sequence 3) and C16orf70 (chromosome 16 open reading frame 70) as novel autophagic proteins.

While BCAS3 and C16orf70 are dispersed throughout the cytosol under normal condition, they accumulated around the damaged mitochondria after mitophagy induction. They also formed puncta in the cytosol in response to amino-acid starvation, which suggests that BCAS3 and C16orf70 are recruited to the autophagosome in both non-selective and selective autophagy. Researchers then found that BCAS3 and C16orf70 interact each other, and this interaction is required for their accumulation on the autophagosome formation site.

Autophagy efficiencies in response to mitochondrial damage and amino-acid starvation were not affected by BCAS3 and/or C16orf70 gene deletions at least in cultured cells. On the other hand, overexpression of the BCAS3-C16orf70 complex impairs the assembly of several autophagy core proteins. These findings demonstrate important accessory functions of BCAS3 and C16orf70 in autophagy machinery.

Furthermore, in silico structural modeling of BCAS3 followed by mutational analyses in immunocytochemistry and in vitro phosphoinositide-binding assays indicate that BCAS3 directly binds phosphatidylinositol-3-phosphate on the autophagosome membranes.

Frequently occurring chronic skin inflammation like in atopic dermatitis (AD or neurodermatitis) and psoriasis have different causes such as genetic predisposition, stress or allergens. These frequently occurring skin diseases are mostly attributed by biomedical scientists to a disturbed immune system, although the noticeable thickening and flaking of the epidermis, which is the outermost layer of skin, also indicates a disruption of the epithelial cells. A team of researchers from the University Clinic for Dermatology and the Clinical Institute for Laboratory Medicine at MedUni Vienna has now been able to identify new molecular mechanisms as causes that could provide suitable starting points for new therapies.

Using patient samples and animal models, the researchers were able to show that a multifunctional protein called "p62" influences the inflammatory changes in diseased epidermis and that inhibiting p62 leads to an alleviation of chronic inflammation. Sequestosome 1 / p62 is a multifunctional protein that affects the control of signal transduction and cellular balance ("homeostasis)" explains Erwin Wagner, head of the study from the University Clinic for Dermatology and the Clinical Institute for Laboratory Medicine at MedUni Vienna.

The present study therefore examined whether p62 plays a role in the development of atopic dermatitis (AD). Wagner: "For this purpose, AD-like skin lesions were induced by genetic inactivation of a certain gene, called JunB, in keratinocytes - this is the type of cell mainly found in the epidermis - which led to an increase in the expression of p62 in the skin of mice." The contribution of p62 to pathological changes was then determined by the additional genetic inactivation of p62.

New therapy option for AD and related skin diseases

The result: The loss of p62 reduced skin damage, suggesting that the inhibition of p62-dependent signals could improve the clinical picture of atopic dermatitis (AD) and possibly also related skin diseases such as psoriasis. The researchers were also able to detect increased amounts of p62 in skin sections from patients with AD and psoriasis. Further investigations showed that the inactivation of p62 normalized the altered differentiation of epidermal keratinocytes, reduced the thickening of the epidermis and decreased the infiltration of immune cells.

"Both the visible skin lesions were significantly reduced, as was the circulating immunoglobulin E (IgE) in the blood," says Wagner, summarizing the results. High IgE levels are a typical characteristic of AD patients. At the molecular level, in turn, p62 activates certain signalling pathways that play a major role in inflammatory processes. In the absence of p62 or by therapeutic blockade, these signalling pathways are not activated, which underlines the important role of p62 in AD-like inflammation.

Wagner: "These results provide the first in vivo evidence for an inflammatory role of p62 in the skin and suggest that p62-dependent signalling pathways are promising therapeutic targets for ameliorating the skin manifestations of AD and possibly also psoriasis."

Two thirds of children use more than one screen at the same time after school, in the evenings and at weekends as part of increasingly sedentary lifestyles, according to new research at the University of Leicester.

An NIHR study of more than 800 adolescent girls between the ages of 11 and 14 identified worrying trends between screen use and lower physical activity - including higher BMI - as well as less sleep.

The use of concurrent screens (termed 'screen stacking') grew over the course of the week - with 59% of adolescents using two or more screens after school, 65% in the evenings, and 68% at weekends.

Some teens reporting using as many as four screens at one time.

But further analysis showed the use of any screen was still detrimental to the indicators of health and wellbeing. More than 90% owned or had access to a smart phone and using this after school had a knock on effect on their sleep.

Researchers from the Leicester Diabetes Centre at the University measured physical activity and sleep using accelerometers worn on participants' wrists, while those involved in the study self-reported the number of screens they were using at the same time - such as scrolling on a mobile phone while also watching TV - as well as perceptions of self-esteem and physical self-worth.

Dr Deirdre Harrington, Lecturer in Physical Activity for Health led the study during her time at Leicester and now works in the School of Psychological Sciences and Health at the University of Strathclyde. She said:

"Intuitively, we believe there must be negative effects on teenagers of using too many screens at the same time. Our data show it isn't as simple as that.

"This research was done before the COVID-19 lockdown, where much more of our day is spent in front of a screen. More than ever the effects of this on adolescents need to be known - there are positives too, no doubt.

"These adolescents wore an accelerometer 24 hours a day for a week allowing us to capture their daily routines and even estimate their sleep. Uniquely, they also reported how many screens they used at the same time which is not well known."

Melanie Davies, Professor of Diabetes Medicine at the University of Leicester and Co-Director of the Leicester Diabetes Centre based at Leicester General Hospital, said:

"Sadly, this study reminds us that we are in danger of creating a new generation of sedentary children. Increased sedentary time is closely linked to type 2 diabetes, which is increasing in younger age groups.

"The number of young people with type 2 diabetes has gone up by 50% in just five years."