Culture

From the Rocky Mountains to the Alps, the question of whether a deer population migrates can be answered by how springtime comes to the landscapes they occupy.

That's the key finding of a first-of-its-kind study produced by a cross-continental team of researchers working with lead author Ellen Aikens, a recent doctoral student of the U.S. Geological Survey's Wyoming Cooperative Fish and Wildlife Research Unit at the University of Wyoming. The paper was published today (Sept. 7) in Current Biology, a leading journal in the field.

The researchers found that the dynamics of springtime plant growth, specifically whether green-up progresses like a wave or not, explains where migration occurs in many ecosystems. A slow and long spring green-up correlates to a resident strategy.

In contrast, migratory behavior often is found in places where the green-up is shorter in any one place but progresses up in elevation. Migratory behavior emerges as a means for animals to track food in landscapes where pulses of the best forage actually move across the landscape as the spring season unfolds. This wave-like green-up is fleeting, and animals make the most of it by moving sequentially across large landscapes in a behavior that scientists call "green-wave surfing."

The analysis combined vegetation data from satellites with GPS-tracking data from 1,696 individuals across 61 populations of four ungulate species: roe deer and red deer in Europe, and mule deer and elk in North America.

Few other studies have combined movement and vegetation data at this large of a scale to get at the root of what makes deer migrate. This work was made possible through the collaboration of 36 biologists spread out across North America and Europe. The EuroDeer project contributed some of the most crucial datasets on roe deer and red deer movement.

Intriguingly, researchers found that at the species level, migrants and residents received equal foraging benefits regardless of which movement strategy they employed. This finding suggests that the movement tactics of deer populations are fine-tuned to the dynamic way that forage resources move across the landscapes they inhabit.

An important implication is that management and conservation of deer species are best tailored to local patterns of plant growth, and the particular behavioral adaptations that have arisen in each area.

For example, roe deer don't have to move to secure the food they need due to the long springtime season in France or Belgium. However, in the Rocky Mountains or the Alps, to stay put is to be hungry and miss out on the best forage.

"This new research shows that ungulate movement is influenced by altered patterns of forage availability," Aikens says. "Migrations can be lost when changes in the underlying habitat eliminate the need to migrate over long distances."

For example, shortened migrations or increased residency have been caused by food subsidies such as agriculture and supplemental feeding. In such altered landscapes, a switch to a resident strategy may be adaptive in a changing world.

On the other hand, in less-developed areas where animals depend on migration to survive, climate-induced changes in the green wave -- or new barriers to movement such as highways or housing -- can reduce food availability. These changes might be early warning signals of future population declines.

"This research has global implications for the field of animal ecology and should help drive future conservation work," says Matthew Kauffman, director of the Wyoming Cooperative Fish and Wildlife Research Unit and a senior author of the study. "It allows us to understand more fully the types of landscapes where migration is required by ungulates and where conservation of corridors is thus paramount."

COLUMBUS, Ohio - While acetaminophen is helping you deal with your headache, it may also be making you more willing to take risks, a new study suggests.

People who took acetaminophen rated activities like "bungee jumping off a tall bridge" and "speaking your mind about an unpopular issue in a meeting at work" as less risky than people who took a placebo, researchers found.

Use of the drug also led people to take more risks in an experiment where they could earn rewards by inflating a virtual balloon on a computer: Sometimes they went too far and the balloon popped.

"Acetaminophen seems to make people feel less negative emotion when they consider risky activities - they just don't feel as scared," said Baldwin Way, co-author of the study and associate professor of psychology at The Ohio State University.

"With nearly 25 percent of the population in the U.S. taking acetaminophen each week, reduced risk perceptions and increased risk-taking could have important effects on society."

The study extends a series of studies led by Way that have shown acetaminophen - the main ingredient in the pain-reliever Tylenol and nearly 600 other medicines - has psychological effects that most people don't consider when they take it.

Previous research by Way and his colleagues has shown that acetaminophen reduces positive and negative emotions, including hurt feelings, distress over another's suffering and even your own joy.

Way conducted the current study with Alexis Keaveney, a former doctoral student at Ohio State, and Ellen Peters, a former professor at Ohio State who is now at the University of Oregon. The study was published online in the journal Social Cognitive and Affective Neuroscience.

In one study, 189 college students came to a lab and took either 1,000 mg of acetaminophen (the recommended dosage for a headache) or a placebo that looked the same. After waiting for the drug to take effect, the participants rated on a scale of 1 to 7 how risky they thought various activities would be.

Results showed that those under the influence of acetaminophen rated activities like bungee jumping, walking home alone at night in an unsafe area of town, starting a new career in your mid-30s, and taking a skydiving class as less risky than those who took the placebo.

The effects of acetaminophen on risk-taking were also tested in three separate experimental studies.

Across these studies, 545 undergraduate students took part in a task developed in 2002 that is often used by researchers to measure risk-taking behavior. Other researchers have shown that taking more risk on this task predicted risky behaviors outside the laboratory, including alcohol and drug use, driving without a seatbelt and stealing.

In the task, participants click a button on the computer to inflate a balloon on their computer screen. Each time they inflate it they receive virtual money. They can stop at any time and add the money to their "bank," and move on to the next balloon. But there is risk involved.

"As you're pumping the balloon, it is getting bigger and bigger on your computer screen, and you're earning more money with each pump," Way said.

"But as it gets bigger you have this decision to make: Should I keep pumping and see if I can make more money, knowing that if it bursts I lose the money I had made with that balloon?"

For those who took the acetaminophen, the answer was: Keep on pumping. Results showed that those on the drug pumped more times than those on the placebo and had more burst balloons.

"If you're risk-averse, you may pump a few times and then decide to cash out because you don't want the balloon to burst and lose your money," he said.

"But for those who are on acetaminophen, as the balloon gets bigger, we believe they have less anxiety and less negative emotion about how big the balloon is getting and the possibility of it bursting."

The results have a variety of real-life implications, Way said.

For example, acetaminophen is the recommended treatment by the CDC for initial COVID-19 symptoms.

"Perhaps someone with mild COVID-19 symptoms may not think it is as risky to leave their house and meet with people if they're taking acetaminophen," Way said.

Even everyday activities like driving presents people with constant decisions involving risk perception and assessment that could be altered by use of the painkiller.

"We really need more research on the effects of acetaminophen and other over-the-counter drugs on the choices and risks we take," he said.

DALLAS - Sept. 8, 2020 - A program that asks patients to mail in stool samples to screen for colon cancer is an effective way to expand screenings to underserved and underinsured communities and offers an alternative to in-person testing during the pandemic, according to a study conducted by UT Southwestern.

In an article published recently in CA: A Cancer Journal for Clinicians, UT Southwestern physicians identified nine best practices for effective mail-in screening campaigns, which can take the place of invasive, unpopular colonoscopies.

While doctors say that mail-in stool samples bring new meaning to the phrase "dropping something in the mail," they also note that this program is a way to continue cancer screenings while keeping people out of clinics and hospitals during the COVID-19 pandemic.

It's also cost-effective and just as capable of detecting cancer as a colonoscopy.

"This project is succeeding in making cancer screenings less invasive and more widely available. Serendipitously, it now has the added benefit of being yet another way to keep people out of hospitals and clinics during pandemic shutdowns," says Amit Singal, M.D., an author of the study, professor of internal medicine and population and data sciences, medical director of the Liver Tumor Program, and clinical chief of hepatology at UT Southwestern.

More than 53,200 Americans are expected to die of colon cancer in the United States in 2020, according to the National Cancer Institute.

The best practices identified in the article are:

1. Reach out to recipients with texts, telephone calls, and printed mailings before sending them the fecal immunochemical testing kit, or "FIT kit."

2. Ensure the invitation letters are brief and easy to read.

3. Keep instructions simple and address challenges that may lead to failed laboratory processing.

4. Send reminders to recipients who do not return their tests.

5. Use data infrastructure to track each step of the outreach process.

6. Have protocols and procedures, such as patient navigation, in place to promote a colonoscopy if a FIT test shows abnormal results.
7. Use high-quality FIT tests.

8. Ensure the program has a champion, organizational support, and sufficient funding.

9. Push for wide implementation to increase the program's efficacy and efficiency.

The best practices were learned from mailed FIT campaigns throughout the United States, including one that reached more than 108,000 people in 25 North Texas counties including Tarrant County. Another campaign reached more than 15,000 persons at Parkland Health & Hospital System, the Dallas County safety-net health system. Nearly a third of the FIT kits were returned by recipients, and approximately 5 percent of them returned positive.

"What the test enables you to do is say you can do this in the privacy of your own home. A lot of people prefer that," says Keith Argenbright, M.D., director of UT Southwestern's Moncrief Cancer Institute in Fort Worth and a professor in the Harold C. Simmons Comprehensive Cancer Center.

Returned stool samples were tested for a blood antigen associated with colon cancer, and patients who tested positive were told they needed to schedule a diagnostic colonoscopy. Follow-up with patients from Dallas County was performed by UT Southwestern staff, and follow-up with patients from other counties was handled by staff from the Moncrief Cancer Institute, which is part of the Simmons Cancer Center.

Argenbright said oncologists nationwide fear cancer deaths will spike several years from now because many cancers will go undetected as people put off colonoscopies and other screenings during the pandemic.

"We think this is an extremely timely solution to the current pandemic," he says. "Even though screening efforts restarted, patients are still afraid to come in."

Spending long periods of time in space can wreak havoc on space traveler health, including negative effects on metabolism, bone and muscle health, gastrointestinal health, immunity and mental health. This could prevent us pursuing long-distance missions, such as a Mars landing. However, a new review in open-access journal Frontiers in Physiology highlights that promoting a healthy gut microbiome could protect space travelers from the rigors of space travel. Finding out which microbes provide the most benefit and the best way to use them could be key to reaching the red planet in one piece.

If humans are to ever walk on Mars, they will need to endure a long space flight, but space travel can have negative impacts on health, potentially limiting how far we can go. The microgravity environment can result in muscle breakdown and reduced bone mass. It can cause nausea, meaning that sometimes space travelers struggle to eat enough (space food isn't all that nice either). The change in diet aboard a spaceship can disrupt the gut microbiome, leading to further health issues.

These factors can contribute to malnourishment and gastrointestinal problems, such as infection and inflammation. Space travelers can also experience metabolic disturbances, including decreased sensitivity to insulin. Other issues include immune system deficits, mental illness and cognitive decline.

A growing number of studies have focused on gut microbes, and their role in space-related health, prompting Prof. Silvia Turroni of the University of Bologna and Prof. Martina Heer of the University of Bonn to write this latest review.

Their review discusses a variety of studies suggesting that disruptions in the gut microbiome occur during space travel. For instance, one study found that the microbiomes of space travelers on the same mission became more similar to each other during the journey. There was also an increase in bacteria associated with intestinal inflammation and a decrease in those with anti-inflammatory properties.

"Changes in the microbiome are likely to lead to the breakdown of the balanced and complex relationship between microbes and their human host, with potentially severe repercussions on the functionality of body systems," said Turroni.

However, the review reveals that manipulating the gut microbiome may be a powerful way to maintain health on board a spacecraft. "The literature suggests that nutritional countermeasures based on prebiotics and probiotics hold great promise to protect space travelers," said Turroni.

So, what would these microbial treatments involve? They may be as simple as nutritionally balanced meals, with lots of fiber to kickstart microbial metabolism in the gut. Other options could be more targeted, including microbial supplements, such as bacteria that secrete immune-boosting substances, or those that synthesize vitamins required for bone growth.

In fact, there is a huge variety of pro-biotics and nutritional options to protect space travelers from specific issues they may encounter in space. However, there is still plenty of work required to figure out which treatments are most effective and how best to use them for each space traveler.

"The well-being of the gut microbiome of space travelers should be among the primary goals of long-duration exploratory missions," said Heer. "To ensure the success of the mission, we must not overlook the myriad of microorganisms that reside in our gastrointestinal tract and make sure they are in balance."

While future missions to Mars will undoubtedly look for evidence of microbial life on the red planet, this review suggests that it may be our homegrown microbes that get us there.

New research provides insights on the potential causes of racial disparities in deaths following prostate cancer surgery. The findings are published early online in CANCER, a peer-reviewed journal of the American Cancer Society (ACS).

Black men not only have a higher rate of developing prostate cancer compared with white men, but they're also more than twice as likely to die from the disease. Meanwhile, Asian American and Pacific Islanders (AAPIs) have the lowest rates of death from prostate cancer among all races.

To investigate the potential causes behind such disparities, Wanqing Wen, MD, MPH, of Vanderbilt University School of Medicine in Nashville, Tennessee, and his colleagues examined information from the National Cancer Database, which includes cancer registry data from more than 1,500 US facilities. The team sought to quantify the contributions of tumor-related and treatment-related characteristics, as well as factors related to access to care and disparities in prostate cancer survival among different groups.

The analysis included 432,640 white, 63,602 Black, 8,990 AAPI, and 21,458 Hispanic patients who underwent prostate removal between 2001 and 2014. The median follow-up time was 5.5 years, and the 5-year survival rates were 96.2 percent, 94.9 percent, 96.8 percent, and 96.5 percent for whites, Blacks, AAPIs, and Hispanics, respectively.

When the researchers adjusted for age and year of diagnosis, they observed that Blacks had a 51 percent higher death rate than whites, while AAPIs and Hispanics had 22 percent and 6 percent lower rates, respectively. After adjusting for all clinical factors and non-clinical factors, the Black-white survival disparity narrowed to being 20 percent higher for Blacks, while the AAPI-white disparity increased to being 35 percent lower for AAPIs. Adjusting for these factors had little effect on survival disparities between Hispanics and whites.

Of the factors included in the team's adjustments, education, median household income, and insurance status contributed the most to racial disparities. For example, if Blacks and whites had similar education levels, median household income, and insurance status, the survival disparity would decrease from 51 percent to 30 percent.

"Socioeconomic status and insurance status are all changeable factors. Unfortunately, the socioeconomic status inequality in the United States has continued to increase over the past decades," said Dr. Wen. "We hope our study findings can enhance public awareness that the racial survival difference, particularly between Black and white prostate patients, can be narrowed by erasing the racial inequities in socioeconomic status and health care. Effectively disseminating our findings to the public and policy makers is an important step towards this goal."

The hormone, ghrelin, may help protect the elderly population from muscle loss, according to a study being presented at e-ECE 2020. The study found that administering a particular form of ghrelin to older mice helped to restore muscle mass and strength. As muscle-related diseases are a serious health concern in the elderly population, these findings suggest a potential new treatment strategy for muscle loss to enable the aging population to remain fit and healthy.

Age-related skeletal muscle mass loss, in absence of any underlying disease, is defined as sarcopenia, which leads to deterioration of elderly people's quality of life. It causes a decline in muscle mass and functionality, often resulting in poor balance, higher risk of falls or fractures, immobilisation and loss of independence.

Ghrelin is a hormone involved in metabolic regulation and energy balance through activation of appetite, but also plays an important role in protecting against muscle wasting. Both acylated (AG) and unacylated (UnAG) forms are present in the body, but UnAG does not bind to the AG receptor (GHSR-1a), so does not increase appetite. A growing body of evidence indicates that UnAG is acting at an unidentified receptor, which also mediates some common AG and UnAG biological activities, including a strikingly protective effect against muscle wasting. Ghrelin levels decline as we age and may be involved in the development of sarcopenia, but the role of AG versus UnAG in this process has not been investigated previously.

Dr Emanuela Agosti, and her team at the University of Piemonte Orientale in Italy, investigated how unAG affected age-related decline of muscle mass and function, by either deleting the ghrelin gene in mice, or overexpressing unAG. Muscle function as they aged was assessed through a wire hanging test, during which "falling" and "reaching" scores were recorded, to assess whole body strength and endurance. Both the deletion of the ghrelin gene and the lifelong overexpression of UnAG reduced age-associated decline in muscle mass and function. Despite both groups of animals displaying similar aging tendencies in body weight and muscle mass, the mice overexpressing UnAG maintained better muscle structure, performance and metabolism, more typical of muscle in younger mice.

"Understanding the causes and effects of sarcopenia will improve our ability to prevent, detect, and hopefully manage this disease. These findings provide novel understanding and point to UnAG, or analogues, as a possible therapeutic target for future treatment," Dr Agosti comments.

The study indicates that UnAG, or possibly drugs that mimic it, can preserve muscle function and reduce the risk of age-related sarcopenia, without causing weight gain and obesity.

"Due to the worldwide increase in the elderly population, sarcopenia has an important social impact greatly affecting both aged people's quality of life and government health care costs. Therefore, therapeutic strategies aimed at preventing and/or reducing sarcopenia are of pivotal importance." Dr Agosti adds.

Dr Agosti and her colleagues now plan to identify the receptor mediating UnAG biological activities. This will help better define the molecular pathways involved in AG/UnAG actions and to design treatments that may reduce loss of muscle mass in sarcopenia and other similar conditions.

LA JOLLA--(September 8, 2020) Salk scientists have used skin cells called fibroblasts from young and old patients to successfully create blood vessels cells that retain their molecular markers of age. The team's approach, described in the journal eLife on September 8, 2020, revealed clues as to why blood vessels tend to become leaky and hardened with aging, and lets researchers identify new molecular targets to potentially slow aging in vascular cells.

"The vasculature is extremely important for aging but its impact has been underestimated because it has been difficult to study how these cells age," says Martin Hetzer, the paper's senior author and Salk's vice president and chief science officer.

Research into aging vasculature has been hampered by the fact that collecting blood vessel cells from patients is invasive, but when blood vessel cells are created from special stem cells called induced pluripotent stem cells, age-related molecular changes are wiped clean. So, most knowledge about how blood vessel cells age comes from observations of how the blood vessels themselves change over time: veins and arteries become less elastic, thickening and stiffening. These changes can contribute to blood pressure increases and a heightened risk of heart disease with age.

In 2015, Hetzer was part of the team led by Salk President Rusty Gage to show that fibroblasts could be directly reprogrammed into neurons, skipping the induced pluripotent stem cell stage that erased the cells' aging signatures. The resulting brain cells retained their markers of age, letting researchers study how neurons change with age.

In the new work, Hetzer and his colleagues applied the same direct-conversion approach to create two types of vasculature cells: vascular endothelial cells, which make up the inner lining of blood vessels, and the smooth muscle cells that surround these endothelial cells.

"We are among the first to use this technique to study the aging of the vascular system," says Roberta Schulte, the Hetzer lab coordinator and co-first author of the paper. "The idea of developing both of these cell types from fibroblasts was out there, but we tweaked the techniques to suit our needs."

The researchers used skin cells collected from three young donors, aged 19 to 30 years old, three older donors, 62 to 87 years old, and 8 patients with Hutchinson-Gilford progeria syndrome (HGPS), a disorder of accelerated, premature aging often used to study aging.

The resulting induced vascular endothelial cells (iVECs) and induced smooth muscle cells (iSMCs) showed clear signatures of age. 21 genes were expressed at different levels in the iSMCs from old and young people, including genes related to the calcification of blood vessels. 9 genes were expressed differently according to age in the iVECs, including genes related to inflammation. In patients with HGPS, some genes reflected the same expression patterns usually seen in older people, while other patterns were unique. In particular, levels of BMP-4 protein, which is known to play a role in the calcification of blood vessel, were slightly higher in aged cells compared to younger cells, but more significantly higher in smooth muscle cells from progeria patients. This suggests that the protein is particularly important in accelerated aging.

The results not only hinted at how and why blood vessels change with age, but confirmed that the direct-conversion method of creating vascular endothelial and smooth muscle cells from patient fibroblasts allowed the cells to retain any age-related changes.

"One of the biggest theoretical implications of this study is that we now know we can longitudinally study a single patient during aging or during the course of a treatment and study how their vasculature is changing and how we might be able to target that," says Simone Bersini, a Salk postdoctoral fellow and co-first author of the paper.

To test the utility of the new observations, the researchers tested whether blocking BMP4--which had been present at higher levels in smooth muscle cells developed from people with HGPS--could help treat aging blood vessels. In smooth muscle cells from donors with vascular disease, antibodies blocking BMP4 lowered levels of vascular leakiness--one of the changes that occurs in vessels with aging.

The findings point toward new therapeutic targets for treating both progeria and the normal age-related changes that can occur in the human vascular system. They also illustrate that the direct conversion of fibroblasts to other mature cell types--previously successful in neurons and, now, in vascular cells--is likely useful for studying a wide range of aging processes in the body.

"By repeating what was done with neurons, we've demonstrated that this direct reprogramming is a powerful tool that can likely be applied to many cell types to study aging mechanisms in all sorts of other human tissues," says Hetzer, holder of the Jesse and Caryl Philips Foundation Chair.

The team is planning future studies to probe the exact molecular mechanisms by which some of the genes they found to change with age control the changes seen in the vasculature.

African wild dogs have a vestigial first digit and muscular adaptations for life on the run

Anatomists identify a vestigial first digit in the forelimb of the African wild dog and document anatomical adaptations to its unique lifestyle of long-distance running and exhaustive predation

African wild dogs (Lycaon pictus) are known for their unique hunting style, often referred to as "exhaustive predation", in which they chase their prey to exhaustion, rather than hunting using speed, strength, or stealth. They are also unique among the dog clade in having only four full digits on their front paws. Until recently, it was unclear how these unique behavioral and anatomical features would affect their forelimb morphology.

The African wild dog, also known as the African painted dog or Cape hunting dog, is native to southern and eastern Africa, and classified as Endangered by the International Union for the Conservation of Nature (IUCN). They use sophisticated, coordinated hunting behaviors in which some packs decide as a group to hunt and communicate their vote via "sneezing". They also have a nomadic lifestyle with packs traveling up to 50 km per day and geographically extensive home ranges of 560 to 3000 km2. African wild dogs also differ from other canid (dog) species in the absence of a fully formed first digit (tetradactyly), which may allow for increased speed and stride length, facilitating long-distance pursuit of prey.

In a recent study published in PeerJ, a team of anatomists discovered a small, vestigial first metacarpal deep to the skin of the African wild dog. Surprisingly, this species is not fully tetradactyl as previously thought, but instead has a rudimentary digit 1. Prior to this study, the vestigial first digit of the African wild dog had never been described. The unexpected reduced digit results in a reconfiguration of some of the associated forelimb muscles to assist with proprioceptive functions (the body's perception of its own position and movement). According to Heather F. Smith, the study's lead author, "We now not only know that this vestigial digit exists, but how its presence completely reorganizes and repurposes the muscles typically associated with the first digit."

The authors have also discovered a stout ligament in the wrist which may act as a strut, assisting with passive flexion and rebound of the forefoot. This taut ligament provides non-muscular propulsion during push-off of the forepaw, which may help sustain endurance running and prevent the wrist muscles from tiring. This morphology is similar in function to the suspensory ligaments of the horse "spring foot", which provides passive "spring" action by absorbing and transferring forces experienced during locomotion.

Several other muscular adaptations to long-distance endurance running in the forelimb muscles have also been identified, including relatively reduced wrist rotator muscles and thick ligaments binding the radius and ulna (the two forearm bones), resulting in greater wrist and forearm stability. Several muscles associated with joint stability elastic energy storage during locomotion are also expanded compared to other species.

According to Smith, "This is the first in-depth study of African wild dog forelimb anatomy, and it demonstrates multiple adaptive mechanisms of endurance running, including reconfiguration of forelimb muscles, ligaments, and even bones, which function synchronously to facilitate the highly cursorial lifestyle of this fascinating species".

Probiotics may help children and adolescents with obesity lose weight when taken alongside a calorie-controlled diet, according to a study being presented at e-ECE 2020. The study found that obese children who were put on a calorie-restricted diet and given probiotics Bifidobacterium breve BR03 and Bifidobacterium breve B632, lost more weight and had improved insulin sensitivity compared with children on a diet only. These findings suggest that probiotic supplements and a calorie-controlled diet may help manage obesity in the younger population and reduce future health risks, such as heart disease and diabetes.

Obesity is a global health concern and can lead to a number of life-threatening conditions, such as diabetes and heart disease. Treatment and prevention is a serious public health challenge, especially in children and adolescents. Bifidobacteria are a group of probiotic bacteria that are part of the natural gut microbiome and help with preventing infection from other bacteria, such as E.coli, and digestion of carbohydrates and dietary fibre. During digestion, they release chemicals called short-chain fatty acids, which play an important role in gut health and controlling hunger. Low numbers of Bifodobacteria may impair digestion, affect food intake and energy expenditure, leading to body weight gain and obesity.

Previous studies suggested that probiotic supplementation with Bifidobacteria could help restore the composition of the gut microbiome, which may aid weight loss and could be a potential approach for obesity management. However, current research uses mixtures of different strains of probiotics and does not examine the effects of administering Bifidobacteria alone.

Dr Flavia Prodam and her team at the University of Piemonte Orientale, aimed to assess the impact of Bifidobacteria probiotic treatment in children and adolescents with obesity on a controlled diet, on weight loss and gut microbiota composition. 100 obese children and adolescents (6-18 years) were put on a calorie-controlled diet and randomly given either probiotics Bifidobacterium breve BR03 and Bifidobacterium breve B632, or a placebo for 8 weeks. Clinical, biochemical and stool sample analyses were carried out to determine the effect of probiotic supplementation on weight gain, gut microbiota and metabolism.

The results suggested that children who had taken probiotics had a reduction in waist circumference, BMI, insulin resistance and E.coli in their gut. These beneficial effects demonstrate the potential of probiotics in helping to treat obesity in children and adolescents, when undergoing dietary restrictions.

"Probiotic supplements are frequently given to people without proper evidence data. These findings start to give evidence of the efficacy and safety of two probiotic strains in treating obesity in a younger population," Dr Prodam comments.

The study suggests that supplementation with probiotics could modify the gut microbiome environment and beneficially affect metabolism, helping obese children or adolescents who are also undergoing a restricted diet to lose weight. However, larger studies over a longer period of time are needed to investigate this.

Dr Prodam explains, "The next step for our research is to identify patients that could benefit from this probiotic treatment, with a view to creating a more personalised weight-loss strategy. We also want to decipher more clearly the role of diet and probiotics on microbiome composition. This could help us to understand how the microbiota is different in young people with obesity."

If you have not been hearing much of the French Gilets Jaunes or of the Italian Sardines in the last few months, it's because "the social and psychological unrest arising from the epidemic tends to crowd-out the conflicts of the pre-epidemic period, but, at the same time it constitutes the fertile ground on which global protest may return more aggressively once the epidemic is over," writes Massimo Morelli, Professor of Political Science at Bocconi, in a paper recently published in Peace Economics, Peace Science and Public Policy.

Professor Morelli and Roberto Censolo (University of Ferrara) argue that we can get an informed opinion about the possible effects of COVID-19 on protest and future social unrest by looking at the great plagues of the past, so they analyze 57 epidemic episodes between the Black Death (1346-1353) and the Spanish Flu (1919-1920). They state that while the epidemic lasts the status quo and incumbent governments tend to consolidate, but warn that a sharp increase in social instability in the aftermath of the epidemic should be expected.

Revolts not evidently connected with the disease are infrequent within an epidemic period, but epidemics can sow other seeds of conflict. Government conspiracy, "the filth of the poor", foreigners and immigrants have often been singled out as the cause of an epidemic. "Overall, the historical evidence shows that the epidemics display a potential disarranging effect on civil society along three dimensions," the authors write. "First, the policy measures tend to conflict with the interest of people, generating a dangerous friction between society and institutions. Second, to the extent that an epidemic impacts differently on society in terms of mortality and economic welfare, it may exacerbate inequality. Third, the psychological shock can induce irrational narratives on the causes and the spread of the disease, which may result in social or racial discrimination and even xenophobia." Focusing on five cholera epidemics, Morelli and Censolo count 39 rebellions in the 10 years preceding an epidemic and 71 rebellions in the 10 years following it.

On the other hand, the authors note that, in the short-term, the necessary restrictions of freedom during an epidemic may be strategically exploited by governments to reinforce power.

Scientists from King's College London have discovered an unexpected tissue reparative role for a rare immune cell type in the gut that could tip toward fibrosis or cancer if dysregulated. The breakthrough will have important implications for treating patients who suffer from inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis.

In a paper published today in Nature Materials, the team of researchers from King's College London found that type-1 innate lymphoid cells (ILC1) can promote tissue repair, but when they accumulate in inflamed tissues, can also contribute to IBD co-morbidities such as cancer and fibrosis. It was previously assumed that these cells drove inflammation, so these findings could inspire completely new therapeutic approaches for those suffering from IBD.

To understand the impact of ILC1 on the gut, the academics combined ILC1 with intestinal organoids, miniature versions of the normal intestine that are grown in a dish. Whilst they intended to harness this system to study ILC1-driven inflammation in organoids, they instead found that ILC1 secreted additional proteins that promoted both growth of the intestinal barrier and remodelling of the supporting structure beneath it; a response closely resembling wound healing. However, ILC1's healing response was only half the story; the team also found that accumulation of ILC1 could trigger fibrotic lesions or exacerbate tumour growth, two common complications of IBD that severely impact a patient's quality of life.

Lead author King's College London PhD student Geraldine Jowett admits this finding came as somewhat of a surprise. "Even though the signals we identified were established biomarkers that had previously been associated with IBD, it was exciting, unexpected, and important to discover that these signals were actually coming from ILC1." she said.

Jowett explains: "It's a matter of balance: On the one hand ILC1s' ability to secrete this protein could suggest that we have been thinking about them the wrong way, and that encouraging this healing response could provide hope for the two thirds of patients who currently don't respond to anti-inflammatory treatments.

"On the other hand, ILC1 may only be beneficial in small doses, and could actually make things worse for IBD patients if they become dysregulated, leading to tumour growth or fibrotic scar tissue formation, outcomes we would want to avoid at all costs."

This discovery has the potential to inspire new strategies for therapeutic intervention, such as allowing physicians to identify patients that are at high risk for developing IBD co-morbidities that require invasive surgery.

The team's findings may also have implications for COVD-19 patients, as ILC1 are more typically known as the key first responders to viral infections in the lung and the gut. Even young, asymptomatic patients infected with SARS-CoV2 have presented with early signs of lung fibrosis. Since ILC1 are enriched during chronic viral infections, it is possible that ILC1 also accumulate and play a role in driving fibrosis in the lungs of COVID-19 patients, providing a potential therapeutic target for the urgent research efforts currently underway.

The team's findings required the authors to develop a complex culture system, as ILC1 are so rare in the gut that they can be hard to study. To accomplish this, they cultured ILC1 alongside human stem cell-derived intestinal organoids in a dish. They then encapsulated the tissues in a synthetic soft material called a hydrogel, allowing them to mimic the 3D environment of normal intestinal tissue.

Pinning down how the ILC1 could drive fibrosis was particularly challenging and required the team's expertise in materials science. "Culturing cells in a dish can be so artificial that the results become irrelevant for disease pathology, so it was critical that we performed our key experiments within an environment that could appropriately respond to the biological cues that drive fibrosis," explains Dr Eileen Gentleman, co-senior author on the study.

The new hydrogels the team developed for this study were designed using complex computational models, which were key to creating materials that were soft enough to support the organoids, and uniform enough to allow for reproducible measurements of the changes in stiffness created by ILC1.

King's College London Mucosal Immunologist and co-senior author Dr Joana Neves remarks: "Many environmental and genetic factors can contribute to IBD, so by combining ILC1 from patients with IBD with this synthetic culture system we were able to provide that extra layer of certainty that it was the ILC1 themselves that were driving the wound healing response, without interference from patients' diets, mutations, or treatment regimens."

Thus, the reductionist system developed by this team provides a powerful template for studying the impact of rare cell types on complex processes of development and teasing apart components of multifactorial diseases.

The study was a collaboration of different departments at King's College London, as well as other UK and international partners. Dr Chris Lorenz, Interim Head of Physics at King's explains their involvement: "Our coarse-grain molecular dynamics simulations provided a detailed description of how changes in the chemistry of the underlying polymeric building blocks affected the structural properties of the resulting hydrogels. As a result, we were able to inform the design of the hydrogels made by Eileen's group such that in the end the softness and uniformity of the hydrogels were optimised."

The COVID-19 pandemic has had an adverse impact on the global economy. Researchers around the globe have been working hard to find ways to stop the spread of the disease either in the form of drugs or SOP changes that revolve around guidelines given by the WHO for maintaining hygiene and social distancing norms. The challenge of stopping the spread is especially challenging as many individuals who are exposed to the novel SARS coronavirus do not show the symptoms of COVID-19 and risk exposing non-infected individuals.

Researchers are now using GIS and IT systems to find ways to monitor populations and the movement of infected individuals to track the spread of the disease and efficiently tackle problems arising due to exposure to the novel coronavirus.

A team of researchers based in Hong Kong have devised a system to track asymptomatic individuals through the use of anonymous transit smart cards and terminals. The proposed system is connected to a central database of infected individuals maintained by the medical authorities. The location and movement of individuals is tracked by this system and it issues an alert in case they check in at a location where others are visiting. Non-infected individuals are flagged as asymptomatic carriers if they have been detected at a location where infected individuals have also been present. Through a combination of metrics such as gathering size and infection rates, the system calculates an index (called the alert level) by comparing the changes in the number of persons listed as infected individuals and asymptomatic individuals over the previous days. The alert level is designed to give an idea of the severity of the spread of the infection. The alerts issued by the system can be used to issue warnings to non-infected persons about a possible risk of COVID-19 infection in a specific location and also to block the entry of suspected carriers at a terminal.

The system has received recognition as a top solution for tourism destinations from the UN World Tourism Organization (UNWTO) in the recent Healing for Destinations tourism solutions contest. The system is in use in elderly homes, wet markets, public schools and restaurants in Hong Kong.

"The spread of COVID-19 is a mathematical problem." Explains Keith Lau, who is one of the principal researchers on the project. "By monitoring asymptomatic individuals and limiting the participation of individuals in large gatherings, we can see a reduction in exponential growth of cases, and this is reflected in our data. Our system makes it easy for local authorities to identify problems during pandemics such as the COVID-19 pandemic and invest their resources appropriately to minimize impacts on economic trade."

Pioneering scientists at the Francis Crick Institute, Great Ormond Street Hospital (GOSH) and UCL Great Ormond Street Institute of Child Health (ICH) have grown human intestinal grafts using stem cells from patient tissue that could one day lead to personalised transplants for children with intestinal failure, according to a study published in Nature Medicine today (Monday 7th September).

Children with intestinal failure cannot absorb the nutrients that are essential for their overall health and development. This may be due to a disease or injury to their small intestine.

In these cases, children can be fed intravenously via a process called parenteral nutrition, however this is associated with severe complications such as line infections and liver failure. If complications arise or in severe cases these children may need a transplant. However, there is a shortage of suitable donor organs and problems can arise after surgery, such as the body rejecting the transplant.

In their proof-of-concept study, the research team showed how intestinal stem cells and small intestinal or colonic tissue taken from patients can be used to grow the important inner layer of small intestine in the laboratory with the capacity to digest and absorb peptides and digest sucrose in food.

This is the first step in efforts to engineer all the layers of the intestine for transplantation. The researchers hope that one day, laboratory grown organs could offer a safe and longer-lasting alternative to traditional donor transplants.

"It's urgent that we find new ways to care for children without a working intestine because, as they grow older, complications from parental nutrition can arise," says Dr Vivian Li, senior author and group leader of the Stem Cell and Cancer Biology Laboratory at the Crick.

"We've set out a process to grow one layer of intestine in the laboratory, moving us a step closer to being able to offer these patients a form of regenerative medicine, which uses materials created from their own tissue. This would reduce some of the risks that transplant patients face, such as their immune system attacking the transplant."

The researchers took small biopsies of intestine from 12 children who either had intestinal failure or were at risk of developing the condition. In the lab, they then stimulated the biopsy cells to grow into "mini-guts", also known as intestinal organoids, generating over 10 million intestinal stem cells from each patient over the course of 4 weeks.

The researchers also collected small intestine and colon tissue, that would otherwise have been discarded, from other children undergoing essential surgery to remove parts of their gut. Using laboratory techniques, cells were removed from these tissues leaving behind a skeleton structure which formed scaffolds.

The researchers placed the "mini-guts" onto these scaffolds, where they grew on this structure to form a living graft. Due to specific culture conditions, the stem cells changed into many of the different types of cells that exist in the small intestine. The grafts were able to digest and absorb peptides, the building blocks of proteins, as well as digest sucrose into glucose sugars.

"Although this research is in the lab right now, we're concentrating on making this a realistic and safe treatment option," explains senior author NIHR Professor Paolo De Coppi, Consultant Paediatric Surgeon at GOSH and Head of Surgery, Stem Cells & Regenerative Medicine Section at the UCL Great Ormond Street Institute of Child Health (ICH).

"What's significant here is we've shown that scaffolds can be created using tissue from the colon, not only tissue from the small intestine. In practice, it is often easier to obtain tissue from the colon, so this could make the approach much more feasible. It's an important step forward in regenerative medicine and we're optimistic about what this means for patients, but more research lies ahead before we can safely and effectively translate this approach to treatment."

As well as proving that biopsies taken from children could be used to grow functioning intestinal grafts, the researchers also demonstrated that the grafts survive and mature when transplanted into mice.

"By applying our basic science knowledge of intestinal stem cell biology, we have developed a time efficient and clinically relevant method for rebuilding human small intestine grafts for transplantation," says Laween Meran, lead author, Gastroenterology Registrar and Clinical Research Training Fellow at the Stem Cell and Cancer Biology Laboratory at the Crick and the ICH.

"Now that we've shown the grafts are successful on a small scale, the next crucial steps will be to start growing the other layers of the intestine such as muscle and blood vessels, whilst also scaling up our methods to create viable grafts relevant to individual patient needs".

Australian rodents skulls all correspond to one simple, size-dependent shape that is more than ten million years old but it turns out this lack of change is the secret behind their survivor reputation.

A new study, co-led by scientists from Flinders University and The University of Queensland, has revealed that the skulls of rodents resemble each other in any given size, meaning little adaptation seems to be necessary for a rodent to survive in a variety of habitats.

Flinders University Associate Professor Vera Weisbecker, who supervised the study says everyone knows rodents all look similar, but researchers expected far more variety in the details of their skull shape when compared to what was found.

"It seems intuitive that a group of animals that displays a wide variety of shapes should be more successful in evolution. However, Australian rodents demonstrate that shape diversity doesn't always mean evolutionary success. So it really does show if the skull ain't broke, don't fix it."

Dr Ariel Marcy, from The University of Queensland, says rodents first entered Australia around four million years ago, and quickly adapted to the diversity of habitats available on our continent.

"Because well-adapted skulls are key to the survival of mammals, we expected to find a lot of locally adapted skull shapes."

"What we found was the opposite of what we expected: there was low variation in the skull shape of rodents, and body size explained most of it."

"Native rodents just scale from being a small 'mouse' shape to being a bigger 'rat' shape!" Dr Marcy said.

"And this relationship between skull shape and size is at least ten million years old, because invasive rodents - like the house mouse and Norway rat - share this pattern, too."

To understand the patterns of adaptation they expected to see, the team scanned hundreds of rodent skulls of 38 species from museums using 3D surface scanners, and analysed their shape using a statistical procedure called geometric morphometrics.

The researchers think this astonishing conservatism of shape may have to do with the very successful specialization of rodent jaws, allowing their skulls to be a true multi-purpose tool.

"Rodent skulls and jaws have a complicated yet highly versatile arrangement that seems to work well in a multitude of conditions. We think that this discourages evolutionary change. We saw unusual skull shapes only in extreme cases of ecological adaptation, for example in the water mouse or rakali which is a very unusual meat-eating predatory rodent."

Dr Weisbecker notes that the results make an important point in one of the biggest questions in evolutionary biology - why some groups of animals are more diverse than others.

An Australian-led study has provided new insight into the behaviour of rotating superfluids.

A defining feature of superfluids is that they exhibit quantised vortices – they can only rotate with one, or two, or another integer amount of rotation.

Despite this key difference from classical fluids, where vortices can spin with any strength, many features of the collective dynamics of vortices in both classical and quantum fluids are similar.

However, in this study the FLEET team at the University of Queensland demonstrate one stark difference in the behaviour between classical and quantum fluids. The authors consider the expansion of vortex clusters to show that for any initial arrangement of quantised vortices, a ‘Rankine’ super-vortex will form.

“The behaviour of many vortices in a superfluid is often chaotic and difficult to describe theoretically,” explains lead author Oliver Stockdale. “Our study overcomes this challenge by providing an exact solution to the vortex dynamics.”

The solution shows that a cluster of chiral vortices (vortices which all spin in the same direction) expands to form a constant density distribution that has a shape similar to a top hat. Such a distribution of vortices, known as a Rankine vortex, is forbidden in classical fluids due to their viscosity.

Why all superfluids ultimately become Rankine distributions

“Superfluids have zero viscosity and can support a Rankine vortex”, explains Oliver. “The striking result of this finding is that all initial distributions of vortices, regardless of how they are arranged, expands to form a Rankine vortex. This long-time equivalent behaviour is known as the universal dynamics and demonstrates the mechanism for how a superfluid dissipates its energy via quantised vortices.”

The authors employ a recently developed theory that describes the vortices themselves as a fluid.

“Just as hydrodynamics describes the behaviour of many fluid particles, it can be used to describe the motion of many vortices, which form a ‘vortex fluid’ within the ordinary fluid,” says co-author Matt Reeves.

“However, the vortex fluid exhibits additional ‘anomalous’ stresses; these extra forces arise due to the nature of the vortices that restrict their rotation to be quantised.

The anomalous terms give unusual fluid behaviours, including a viscosity which is negative. Essentially, the negative viscosity causes the exact opposite behaviour to a normal, classical fluid – it steepens the vortex density gradients, until the distribution becomes a Rankine vortex.”  nbsp;An example expansion within vortex fluid theory can be seen in Fig. 1, where an initially non-uniform vortex fluid expands to form a Rankine vortex.

To support their theoretical findings, the authors simulate the dynamics of thousands of vortices computationally. As opposed to describing the vortices as a fluid, these simulations consider each vortex as an individual entity. As with the vortex fluid theory, the authors find that any initial vortex distribution expands to form a Rankine vortex. An example of the numerical result can be seen in Fig. 2, where a Gaussian initial distribution expands to form a Rankine vortex.

Finally, the authors analysed data from an experiment that observed the expansion of a vortex cluster in a real superfluid, which was created using ultracold rubidium atoms.

“Whilst the vortex fluid theory assumes there are many vortices present, the experiment could only create approximately eleven vortices. Despite the low vortex number, there was evidence that the Rankine vortex emerged after the cluster expanded,” explains project leader Prof Matthew Davis. The experimental vortices can be seen in Fig. 3, as highlighted by the white circles.

Not only did this study demonstrate the first solution to the complicated vortex fluid theory, it provided the theory’s first experimental test. The experiment quantitatively predicted key features of the theory and demonstrated a platform to further test properties of the Rankine vortex, such as predictions that it supports an analogue fraction quantum Hall effect.

Vortices are a ubiquitous phenomenon in superfluid systems. To work towards FLEET’s goal of producing an ultra-efficient superfluid transistor, a more complete understanding of how vortices behave in flowing superfluids is needed. This study by the FLEET team is a step towards such a transistor.

The study

The paper Universal dynamics in the expansion of vortex clusters in a dissipative two-dimensional superfluid was published in Physical Review Research in July 2020 (DOI 10.1103/PhysRevResearch.2.033138).

This study was carried out in collaboration with the ARC Centre of Excellence for Engineered Quantum Systems (EQUS), the Graduate School of China Academy of Engineering Physics, and the Dodd-Walls Centre for Photonic and Quantum Technologies (NZ).

Journal

Physical Review Research

DOI

10.1103/PhysRevResearch.2.033138