Culture

Fitness trackers like Fitbit and Garmin watches make it easy for anyone to collect data about health and performance.

Now college athletic programs are moving toward implementing more data-driven trackers -- devices or apps that can monitor students' heart rates, sleep or even class attendance -- into their own programs to help keep their athletes as competitive and healthy as possible.

Researchers at the University of Washington were concerned that this shift toward more data collection might encroach on college athletes' autonomy. The team interviewed 22 athletes and staff members from three college athletics programs to see what data they collect and how they use it. The researchers highlighted potential tensions that might arise and made suggestions for increasing transparency to help implement tracking systems in a way that supports both athletes and staff. The team presented these findings Jan. 6 at the ACM Conference on Supporting Group Work in Florida.

"We're at this place where this technology is still in its early stages," said co-author Sean Munson, a UW associate professor of human centered design and engineering. "People are adopting it with a lot of good intentions but not a good understanding of the technology's limitations or how to balance the goals the technology supports with the other goals the team has or that individuals have."

While both professional and college athletic programs track their athletes' fitness, the researchers decided to focus on college athletes.

"They're still learning how to manage their bodies and their sports. And then they've got all this other stuff to do, too," said lead author Samantha Kolovson, a UW doctoral student in human centered design and engineering who rowed as an undergraduate at the University of Massachusetts Amherst. "As a computer science major, I had really tough classes. It was a lot to balance with 20 or so hours of rowing each week. I think the dual demands on student-athletes are one of the things that makes this research really interesting for us."

The researchers contacted 11 athletes and 11 staff members -- sports coaches, athletic trainers, and strength and conditioning coaches -- across three universities that were either Division I or Division III schools. The students and staff participated in multiple sports, including basketball, lacrosse, ice hockey, swimming and rowing. From the interviews, the researchers identified several types of data that coaches collected and determined potential tensions between staff and athletes.

Some of the findings include:

Students weren't always aware they were providing data. For example, coaches might acquire "wellness data" by striking up informal conversations with athletes and sharing that information with other staff members.

Coaches didn't always communicate how they were using the data they collected. The researchers found that their own perspectives mirrored this finding. "At the time, our swim team tracked three kinds of data: weight training data, heart rate data and time data," said co-author Calvin Liang, a UW doctoral student in human centered design and engineering who was on the swim team as an undergraduate student at Tufts University. "We got to see our data, but it was less clear how our coaching staff used it. During practice, if your heart rate was really low when it was supposed to be really high, a coach would probably tell you to work harder."

While athletes want to see their performance data, it might not show the whole picture of how they're physically feeling. "I didn't wear a tracker throughout college sports," said Kolovson, who found her own experiences reflected in the reports from current college athletes. "But I would have loved to see that sort of information from when I was at peak rowing fitness. How stressful was it to do a 2K or a 6K? At the same time though, I feel like I was really in tune with my body as a college athlete, and perhaps as much as I would have liked to see that information, it might have taken away from my experience or my ability to be present."

Tracker data could infringe on an athlete's personal sense of autonomy. "Right now the students are able to say, 'I feel fine and I'm ready to perform today,' even if they got three hours of sleep, which is maybe not in their best interest, but they have the choice," Kolovson said.

Athletic staff members feel a lot of pressure to use tracker data to get a competitive edge, the researchers said. But this technology is so new that there are no best practices to follow when implementing new methods. To relieve tensions for now, the researchers suggested that staff members and athletes have conversations about tracking to figure how to support athletes without taking away their autonomy.

The researchers also suggested that tracker designers could help by changing the interface of their data management software.

"Often the coaches get a portal where they can see their athletes' data, but the athletes don't have a portal on their side. Or if they do, it's to input something: They'll get a ping about a wellness survey every morning where they have to say 'I got X hours of sleep, I feel sore or don't feel sore,'" Kolovson said. "But if designers could build out that portal on the athletes' side, there is more potential for athletes to learn through self-reflection or communicate about data with the staff."

Now the research team is working on finding ways to avoid potential pitfalls and help coaches identify reasonable goals for collecting and managing their data.

"In this context, the source of the data is the athlete's body. It's not like the number of points you score or your time to run a mile. All this stuff these devices can collect is more personal," Kolovson said. "And while this process is not intending to be malicious, it's set up in a way that augments the staff members' position of power -- they are determining how the data is collected and how the system is set up. We're trying to make sure that people can use these systems in a way that works for everyone."

Proteins, the workhorse of the human cell, help digest our food, carry oxygen through the body, fight off invading microbes, and so much more -- but they only function when folded properly into specific, three dimensional structures.

Misfolded proteins contribute to a number of diseases -- including cystic fibrosis, juvenile cataracts, Alzheimer's disease and many forms of cancer.

Scientists have long ignored half of all mutations in the genetic sequences of our DNA, called synonymous or "silent" mutations, because these mutations were thought to not affect the process by which amino acid sequences lead proteins to fold properly. Now, new research from the University of Notre Dame shows these silent mutations are worth a closer look.

"Synonymous mutations were long considered to be genomic background noise, but we found they do indeed lead to altered protein folding, and in turn impair cell function," said Patricia Clark, the Rev. John Cardinal O'Hara professor of biochemistry at the University of Notre Dame, and lead author of the study. "Our results show that synonymous variations in our DNA sequences -- which account for most of our genetic variation -- can have a significant impact on shaping the fitness level of cellular proteins."

Clark and her team studied the genetic sequence of a naturally occurring antibiotic-resistant gene of the bacteria, E. coli. The bacterium presented researchers with a manageable field of study, consisting of just 4,000 genes -- compared to more than the 20,000 genes in humans. The team focused on how synonymous mutations altered the rate of protein synthesis by the ribosome, the molecular machine present within all cells, including human cells, that carries out the process of protein synthesis.

This study provides an answer to a hypothesis that has been floating around the field for more than 50 years, Clark said.

"It's been extremely challenging to test this hypothesis rigorously in live cells," she added. "The fact that we decided to work with a bacterium rather than a human cell, really helped. It enabled us to make mutations in a specific gene and determine to what extent those mutations were affecting folding."

Further study is needed to understand just how widespread protein misfolding is due to synonymous variations. "We're ignoring half of the DNA mutations that are out there, because we've decided that they're not going to cause a problem," said Clark. "Our study just showed they can cause a problem."

PHILADELPHIA (March 2, 2020) - Healthcare provider burnout is a mounting public health crisis with up to half of all physicians and one in three nurses reporting high burnout, data show. Burnout rates among nurses also correlate with lower patient satisfaction. While both factors are recognized, little is known about how effective interventions in nurse working conditions, managerial support, or resource enhancement can lessen burnout and improve patient satisfaction.

A new study from the University of Pennsylvania School of Nursing has examined how hospital organizational factors influence nurse burnout and patient satisfaction. Using data from 463 hospitals in four states, researchers learned that hospitals with the best work environments were also those with the lowest burnout and highest patient satisfaction.

"Our examination of patient satisfaction and nurse burnout is particularly timely as satisfaction is increasingly viewed as a quality indicator and directly linked to reimbursement through the Value Based Purchasing Program (VBP)," says Penn Nursing's J. Margo Brooks Carthon, PhD, APRN, FAAN, Associate Professor and lead investigator of the study. "Improving patient satisfaction scores via improved nurse work environments could also translate to increased hospital revenue by tens of thousands of dollars for those in the VBP program."

The researchers suggest that one way to improve nurse work environments and lower burnout is to attain Magnet designation or institute Magnet-like initiatives. "This includes fostering relationships between nurses, administrators, and physicians, and ensuring that nurses have decision-making authority in their practice and adequate resources and time to do their work," says Brooks Carthon.

PHILADELPHIA - Surgeons at the Sidney Kimmel Medical College at Thomas Jefferson University are pioneering the use of robotics in neuroendovascular procedures, which are performed via the blood vessels of the neck and brain.

A study by Pascal Jabbour, MD, Chief of the Division of Neurovascular Surgery and Endovascular Neurosurgery, demonstrated that the use of these robots to aid surgeons during diagnostic cerebral angiograms and transradial carotid artery stenting was both safe and effective. The research was published March 1st in the Journal of NeuroInterventional Surgery

"This technology could be groundbreaking, acting as a precursor for remote stroke interventions," Dr. Jabbour said.

When a patient suffers from a stroke, time is of the essence because the blocked vessel must be opened as quickly as possible to prevent permanent damage. Patients living in remote geographic areas have further to travel for stroke intervention, and, often, by time they arrive at a stroke center, it is too late, explains Dr. Jabbour.

"These robots would allow us to intervene remotely on those patients," he said. "The patient would still be in the community and I would be sitting here at Jefferson controlling the robot."

In the study, Dr. Jabbour and colleagues tested the use of a next-generation robotic-assisted surgical platform on 10 patients undergoing either a diagnostic cerebral angiogram or carotid artery stenting. All of the procedures were successful with no complications encountered.

Jefferson is the first center in the country to perform robotic transradial carotid stenting. Currently, robots are only approved by the FDA for use in certain general surgery procedures and in interventional cardiology procedures.

Use of robots in neuroendovascular procedures would give surgeons more precise control over the microcatheter and the microwire, two tools threaded through a patient's blood vessels during these procedures.

In addition, physicians who do these procedures regularly will have less exposure to radiation from the X-rays used during the procedure because they can operate the robot from a separate room just outside the surgical suite. Eliminating exposure to radiation would allow surgeons to forgo wearing the heavy personal protective equipment, such as lead aprons, that is typically needed during these procedures.

"The next generation of robots are ready to be launched and as soon as they are approved by the FDA we will be able to move to the next step, which is performing interventions inside the brain," says Dr. Jabbour. "Jefferson will be on the front line of this technology, training the new generation of fellows on how to use these robots before any one else in the country."

Women who chair clinical departments at public medical schools are paid an average of 88 cents for every dollar paid to their male counterparts, or about $70,000 to $80,000 less per year, researchers at the Stanford University School of Medicine and UC San Francisco report.

The disparity remains regardless of the women's academic productivity, specialization and years on the job.

"These women are at the top of their game," said Eleni Linos, MD, MPH, a professor of dermatology at Stanford. "They are skilled leaders, outstanding managers and experienced negotiators who have reached top positions in their medical schools. Gender pay gaps are often blamed on women's personal choices to reduce work hours or leave the workforce, household responsibilities, childcare or suboptimal negotiation skills. This study challenges these traditional explanations because our sample of medical department leaders have navigated these complex challenges and broken through the 'glass ceiling.' Yet they are still paid less than their male peers when controlling for many factors. Our study shows the pervasiveness of gender inequities at all levels of academic medicine."

Linos shares senior authorship of the study, which will be published March 2 in JAMA Internal Medicine, with Christina Mangurian, MD, professor of psychiatry at UCSF. Michael Mensah, MD, MPH, a former medical student at UCSF who is now a psychiatry resident at UCLA, is the lead author of the study.

The researchers surveyed publicly available salary information from 29 public medical schools in 12 states. They compared the average salaries in 2017 of 550 chairs of clinical departments. About one-sixth of the chairs were women, who, the researchers found, earned about $80,000 less per year than their male counterparts.

The researchers then controlled for the position's title to avoid comparing interim appointments with permanent positions; regional cost of living differences; length of time each person held the position; and academic specialization. But the disparity remained, with women earning about $70,000 less per year than the men.

Controlling for the number of academic publications and grants awarded by the National Institutes of Health, the researchers found that women earned about $63,600 less than men.

"When you adjust for all these factors, you still see a pay gap," Linos said. "This calls into question the common explanations for gender disparities and highlights a pervasive structural problem that needs to be addressed. Women are regularly paid less than men, even at the highest levels of academic medicine."

Bottom Line: The U.S. Preventive Services Task Force (USPSTF) now recommends that adults ages 18 to 79 be screened for hepatitis C virus (HCV) infection. The USPSTF routinely makes recommendations about the effectiveness of preventive care services and this statement updates its previous guidance that adults born between 1945 and 1965 be screened. More deaths are associated with HCV than the top 60 other reportable infectious diseases combined, including HIV. The rise in cases over the last decade is due to more injection drug use and better monitoring.

(doi:10.1001/jama.2020.1123)

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Note: More information about the U.S. Preventive Services Task Force, its process, and its recommendations can be found on the newsroom page of its website.

Boston, MA -- The body's clock keeps metabolism, blood pressure and heart rate running on schedule. But when an irregular sleep pattern disrupts this delicate ticking, what happens? A new study led by investigators from Brigham and Women's Hospital measured participants' sleep duration and timing, finding that over a five-year period, individuals who had the most irregular sleep experienced a two-fold increased risk of developing cardiovascular disease compared to those with the most regular sleep patterns. The team's findings are published in The Journal of the American College of Cardiology.

"When we talk about interventions to prevent heart attacks and stroke, we focus on diet and exercise," said lead author Tianyi Huang, ScD, of the Brigham's Channing Division of Network Medicine. "Even when we talk about sleep, we tend to focus on duration -- how many hours a person sleeps each night -- but not on sleep irregularity and the impact of going to bed at different times or sleeping different amounts from night to night. Our study indicates that healthy sleep isn't just about quantity but also about variability, and that this can have an important effect on heart health."

Huang and colleagues examined data from the Multi-Ethnic Study of Atherosclerosis (MESA), a federally funded, prospective study that included 1,992 participants who did not have cardiovascular disease at the beginning of the study. MESA consisted of a diverse study population made up of white (38 percent), African American (28 percent), Hispanic (22 percent) and Chinese American (12 percent) participants, aged 45-84 years, from six field centers across the U.S. Participants wore an activity tracker on their wrist for seven days that recorded their sleep, including bedtime, sleep duration and wake time. They were then followed for an average of 4.9 years. During that time, 111 participants experienced cardiovascular events, including heart attack, stroke and other adverse events.

The investigators divided participants into four groups ranging from those with the most irregular sleep patterns (two hours or more difference in sleep duration each night) and those with the most regular sleep patterns (less than an hour difference in sleep duration each night). They also compared those with the most consistent bedtimes (less than 30-minute difference each night) and most inconsistent bedtimes (90 minutes or more). The team found a two-fold increase in risk of cardiovascular events among those with the most irregular sleep patterns. The researchers estimate that for every 1,000 people following the most regular sleep pattern, only eight would have a cardiovascular event over one year; for every 1,000 people with the most irregular sleep patterns, 20 people would likely develop a cardiovascular event over one year.

While large for a study that uses wrist-worn activity trackers to measure sleep, the sample size for the study was modest and its follow-up time was relatively short, which meant that the researchers could not assess risk of individual adverse events such as a heart attack versus a stroke and the possibility of chance findings could not be fully excluded. If larger studies confirm these findings in the future, Huang would like to evaluate whether an intervention -- such as, sleeping longer or more regularly -- could decrease a person's risk.

"Sleep regularity is a modifiable behavior. In the future, we'd like to explore whether changing one's sleep patterns by going to bed consistently each night may reduce a person's risk of future cardiovascular events," said Huang.

Fish school by copying each other and changing directions randomly, rather than calculating and adapting to an average direction of the group, a group of scientists co-led by UNSW has shown.

In a study published today in Nature Physics, an international team from Australia, India and UK has shed light on the behavioural dynamics that govern alignment, or collective motion, of cichlid fish - offering new insights into the dynamics of schooling, and potentially the coordinated behaviour of other animals.

"In the fish that we have studied, schooling turns out to be noise-induced. It's not what anyone traditionally thought it was," says Dr Richard Morris from UNSW Science, co-leader of the study and EMBL Australia group leader in UNSW's Single Molecule Science.

"Noise, in this setting, is simply the randomness arising from interactions between individual fish."

In the study, the researchers present the first experimental evidence of noise-induced ordering, which previously only existed as a theoretical possibility. The interdisciplinary team of ecologists, physicists and mathematicians achieved this by combining the capabilities of their scientific disciplines to integrate experiments with computer simulations and analysis.

"Everyone's been aware of noise-induced phenomena, theoretically, but it's quite rare to find in practice. You can only observe it when the individuals in a study can actually make decisions. For example, you wouldn't find this type of noise-induced behaviour studying electrons or particles," says Dr Morris.

This new model proposed contradicts the standard 'moving average' theories for schooling and herding behaviour, which assume that the animals are capable of estimating the overall direction of the group.

"Every fish only interacts with one other fish at any given time. They either spontaneously change direction, or copy the direction of a different fish. Calculating an average direction of the group - which was the popular theory until now - is likely too complicated for a fish to compute," explains Dr Morris.

To study the behavioural dynamics, the researchers filmed schools of 15, 30 and 60 cichlid fish, tracking their trajectories to analyse the mechanism behind mutual alignment, or schooling.

"Smaller groups of fish schooled more coherently than large groups. This is counterintuitive, since the randomness, or noise, from individual interactions plays a bigger role in smaller groups than larger ones," Dr Morris says.

When researchers interpret data, noise is usually an unrelated factor that obscures and distracts from the information, like glare from the sun that you would try to eliminate to get a clearer photo.

In this case, Dr Morris explains that the random copying between pairs of fish gives rise to a different class of noise, and is actually what drives their highly coordinated behaviour. This new insight highlights the importance of noise, showing that noise may encode some important information about behavioural dynamics of fish and other animals.

"Here the signal is the noise. If you ignored the fluctuations completely, you couldn't explain schooling at all."

Beyond fish behaviour, the discovery has the power to reshape the understanding of collective motion in animals, and calls for a revision of how noise is treated in studies of behaviour dynamics.

Researchers report an advance in the development of a blood test that could help detect pathological Alzheimer's disease in people who are showing signs of dementia. This approach could be less invasive and less costly than current brain imaging and spinal fluid tests. The blood test detects the abnormal accumulation of a form of tau protein known as phosphorylated-tau-181 (ptau181), which is a biomarker that suggests brain changes from Alzheimer's. The study, funded by the National Institutes of Health, was published on March 2 in Nature Medicine.

Over the past 15 years, research advances in the development of biomarkers like tau protein have enabled investigators to more accurately diagnose Alzheimer's disease, select research participants, and measure response to investigational therapies. Tau and other biomarkers can be detected with PET scans of the brain and lab tests of spinal fluid. However, PET imaging is expensive and involves radioactive agents, and spinal fluid tests require spinal taps, which are invasive, complex and time-consuming. Simpler biomarker tests are still needed.

"The considerable time and resources required for screening research participants with PET scans and spinal taps slow the pace of enrollment for Alzheimer's disease treatment studies," said Richard J. Hodes, M.D., director of NIH's National Institute on Aging (NIA), which funded much of the study. "The development of a blood test would enable us to rapidly screen a much larger and more diverse group of volunteers who wish to enroll in studies."

An international team of researchers led by Adam Boxer, M.D., Ph.D., at the University of California, San Francisco, used the new test to measure the concentration of ptau181 in plasma, which is the liquid part of blood that carries the blood cells. The samples were collected from more than 400 participants from the University of California, San Francisco Memory and Aging Center, part of the NIA-funded Alzheimer's Disease Research Center; the NIH-supported Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) consortium; and a research study sponsored by Eli Lilly.

Their analysis demonstrated that the ptau181 in plasma could differentiate healthy participants from those with Alzheimer's pathology, and differentiate those with Alzheimer's pathology from a group of rare neurodegenerative diseases known collectively as frontotemporal lobar degeneration (FTLD).

"It has become clear that there are many possible biological pathways to dementia," said Roderick Corriveau, Ph.D., program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS), which also supported the study. "Finding a blood test that specifically identifies the presence of Alzheimer's pathology in the brain should greatly help researchers develop better treatments for the many who suffer from dementia."

In addition, the results with the plasma ptau181 test mirrored results with two established biomarker tests for Alzheimer's -- a spinal fluid ptau181 test and a PET brain scan biomarker known as amyloid protein. The research team, which includes the NIH's ARTFL-LEFFTDS Longitudinal Frontotemporal Lobar Degeneration (ALLFTD) research consortium that was announced last year, is now aiming to refine and improve the ptau181 blood test method.

"Because of NIH's investments, we are poised to make dramatic advances in biomarker development for Alzheimer's disease, FTLD, and related neurodegenerative disorders," said Eliezer Masliah, M.D., director of NIA's Division of Neuroscience.

In the future, improved biomarkers like ptau181 may help not just researchers but also physicians to detect and diagnose Alzheimer's and related neurodegenerative disorders earlier, when interventions are more likely to be effective.

"This research is an example of how studies on rare diseases, in this case FTLD, may provide important insights into common disorders such as Alzheimer's disease, which affects millions of people," said Tiina Urv, Ph.D., program officer in the Office of Rare Diseases Research at the NIH's National Center for Advancing Translational Sciences (NCATS), which also supported the study.

A different international team, this one led by Oskar Hansson, M.D., Ph.D., at Lund University in Sweden and supported in part by NIH, reported similar findings. Using the same plasma ptau181 test, these researchers were able to differentiate between Alzheimer’s and other neurodegenerative diseases nearly as well as they could with a spinal fluid ptau181 test and a PET brain scan for tau protein. In addition, they followed participants for several years and observed that high levels of plasma ptau181 among those who were cognitively normal or had mild cognitive impairment may be used to predict later development of Alzheimer’s dementia. These results were also published today in Nature Medicine.

A blood test that may eventually be done in a doctor's office can swiftly reveal if a patient with memory issues has Alzheimer's disease or mild cognitive impairment and can also distinguish both conditions from frontotemporal dementia. If approved, the blood test could lead to a jump in the number of Alzheimer's patients enrolling in clinical trials and be used to monitor response to those investigational treatments.

In a study led by UC San Francisco, researchers measured blood levels of phosphorylated tau 181 (pTau181), a brain protein that aggregates in tangles in patients with Alzheimer's. They found that pTau181 was 3.5-times higher in people with the disease compared to their healthy peers. In contrast, in patients with frontotemporal dementia, a condition that is often misdiagnosed as Alzheimer's, pTau181 was found to be within the same range as the control group.

The study publishes in Nature Medicine on March 2, 2020.

"This test could eventually be deployed in a primary care setting for people with memory concerns to identify who should be referred to specialized centers to participate in clinical trials or to be treated with new Alzheimer's therapies, once they are approved," said senior author Adam Boxer, MD, PhD, of the UCSF Memory and Aging Center. Being able to easily diagnose Alzheimer's disease at early stages may be especially beneficial to patients with mild cognitive impairment, some of whom may have early Alzheimer's disease. Individuals with early Alzheimer's are more likely to respond to many of the new treatments that are being developed."

Current Alzheimer's Testing Expensive, Invasive

Existing methods for diagnosing Alzheimer's include measurement of the deposits of amyloid, another protein implicated in dementia, from a PET scan; or using lumbar puncture to quantify amyloid and tau in cerebrospinal fluid. PET scans are expensive, only available in specialized centers and currently not covered by insurance, and lumbar punctures are invasive, labor intensive and not easy to perform in large populations, the authors noted.

There are 132 drugs in clinical trials for Alzheimer's, according to a 2019 study, including 28 that are being tested in 42 phase-3 trials -- the final part of a study before approval is sought from the federal Food and Drug Administration. Among those phase-3 drugs is aducanumab, which some experts believe may be the first drug approved to slow the progression of Alzheimer's.

In the study, participants underwent testing to measure pTau181 from plasma, the liquid part of blood. They were aged from 58 to 70 and included 56 who had been diagnosed with Alzheimer's, 47 with mild cognitive impairment and 69 of their healthy peers. Additionally, participants included 190 people with different types of frontotemporal dementia, a group of brain disorders caused by degeneration of the frontal and temporal lobes, areas of the brain associated with decision-making, behavioral control, emotion and language. Among adults under 65, frontotemporal dementia is as common as Alzheimer's.

Blood Test Measures Up to Established Tool

The researchers found that blood measures of pTau181 were 2.4 pg/ml among healthy controls, 3.7 pg/ml among those with mild cognitive impairment and 8.4 pg/ml for those with Alzheimer's. In people with variants of frontotemporal dementia, levels ranged from 1.9 to 2.8 pg/ml. These results gave similar information to the more established diagnostic tools of PET scan measures of amyloid or tau protein, Boxer said.

The study follows research by other investigators published last year that found high levels of plasma amyloid were a predictor of Alzheimer's. However, amyloid accumulates in the brain many years before symptoms emerge, if they emerge, said Boxer, who is affiliated with the UCSF Weill Institute for Neurosciences.

"In contrast, the amount of tau that accumulates in the brain is very strongly linked to the onset, the severity and characteristic symptoms of the disease," he said.

A companion study by Oskar Hansson, MD, PhD, of Lund University, Sweden, published in the same issue of Nature Medicine corroborated the results of the UCSF-led study. It concluded that pTau181 was a stronger predictor of developing Alzheimer's in healthy elders than amyloid.

The researchers said they hope to see the blood test available in doctor's offices within five years.

Today dairy foods sustain and support millions around the world, including in Mongolia, where dairy foods make up to 50% of calories consumed during the summer. Although dairy-based pastoralism has been an essential part of life and culture in the eastern Eurasian Steppe for millennia, the eastward spread of dairying from its origin in southwest Asia and the development of these practices is little understood. The current study, led by Shevan Wilkin and Jessica Hendy of the Max Planck Institute for the Science of Human History, presents the earliest evidence for dairy consumption in East Asia, circa 3000 BCE, and offers insights into the arrival and evolution of dairy pastoralism in prehistoric Mongolia.

Earliest dairy consumption & a possible path of entry

The highly mobile nature of pastoralist societies and the severe winds of the Eastern Steppe make detecting occupied sites with direct evidence into the lives and culture of ancient Mongolians exceedingly rare. Instead, the researchers looked for clues in ritual human burial mounds, often marked by stone monuments and occasionally featuring satellite animal graves.

In collaboration with the National University of Mongolia, researchers analyzed dental calculus from individuals ranging from the Early Bronze Age to the Mongol Period. Three-quarters of all individuals contained evidence that they had consumed dairy foods, which demonstrates the widespread importance of this food source in both prehistoric and historic Mongolia. The study's results include the earliest direct evidence for dairy consumption in East Asia, identified in an individual from the Afanasievo site of Shatar Chuluu, which dates to roughly 3000 BCE. Previous DNA analysis on this individual revealed non-local genetic markers consistent with Western Steppe Herder populations, presenting Early Bronze Age Afanasievo migrations westward via the Russian Altai as a viable candidate for the introduction of dairy and domestic livestock into eastern Eurasia.

Multiple different animal species were used for their milk

By sequencing the milk proteins extracted from the dental calculus, the scientists were able to determine which animal species were being used for dairy production, and thereby help to trace the progression of domestication, dairying, and pastoralism in the region. "Modern Mongolians use cow, sheep, goat, yak, camel, horse and reindeer for milk today, yet when each of these species were first utilized for dairy in Mongolia remains unclear," says Shevan Wilkin, lead author of the study. "What is clear is that the crucial renewable calories and hydration made available through the incorporation of dairying would have become essential across the arid and agriculturally challenging ancient Eastern Steppe."

The earliest individuals to show evidence of dairy consumption lived around 5000 years ago and consumed milk from ruminant species, such as cattle, sheep, and goats. A few thousand years later, at Bronze Age sites dated to after 1200 BCE, the researchers find the first evidence of horse milk consumption, occurring at the same time as early evidence for horse bridling and riding, as well as the use of horses at ritual burial sites. In addition, the study shows that during the Mongol Empire circa 1200-1400 CE, people also consumed the milk of camels. "We are excited that through the analysis of proteins we are able to see the consumption of multiple different animal species, even sometimes in the same individual. This gives us a whole new insight into ancient dairying practices" says Jessica Hendy, senior author of the study.

Millenia after the first evidence of horse milk consumption, horses remain vital to the daily lives of many in modern Mongolia, where mounted pastoralists rely on them to manage large herds of livestock, transport people and supplies, and provide a primary source of meat and milk. "Our findings suggest that the incorporation of horses into dairy pastoralism in Eastern Eurasia was closely linked to a broader economic transformation in the use of horses for riding, movement, and diet," says William Taylor of the University of Colorado-Boulder, one of the study's coauthors.

Although the earliest individual sampled in this study showed evidence of dairy consumption, the researchers hope future studies will examine individuals from previous time periods. "In order to form a clearer picture of the origins of dairying in this region, we need to understand the impact of western steppe herder migrations and confirm whether dairying was occurring in Mongolia prior to their arrival," Shevan Wilkin concludes.

CAMBRIDGE, MA -- Many people with autism spectrum disorders are highly sensitive to light, noise, and other sensory input. A new study in mice reveals a neural circuit that appears to underlie this hypersensitivity, offering a possible strategy for developing new treatments.

MIT and Brown University neuroscientists found that mice lacking a protein called Shank3, which has been previously linked with autism, were more sensitive to a touch on their whiskers than genetically normal mice. These Shank3-deficient mice also had overactive excitatory neurons in a region of the brain called the somatosensory cortex, which the researchers believe accounts for their over-reactivity.

There are currently no treatments for sensory hypersensitivity, but the researchers believe that uncovering the cellular basis of this sensitivity may help scientists to develop potential treatments.

"We hope our studies can point us to the right direction for the next generation of treatment development," says Guoping Feng, the James W. and Patricia Poitras Professor of Neuroscience at MIT and a member of MIT's McGovern Institute for Brain Research.

Feng and Christopher Moore, a professor of neuroscience at Brown University, are the senior authors of the paper, which appears today in Nature Neuroscience. McGovern Institute research scientist Qian Chen and Brown postdoc Christopher Deister are the lead authors of the study.

Too much excitation

The Shank3 protein is important for the function of synapses -- connections that allow neurons to communicate with each other. Feng has previously shown that mice lacking the Shank3 gene display many traits associated with autism, including avoidance of social interaction, and compulsive, repetitive behavior.

In the new study, Feng and his colleagues set out to study whether these mice also show sensory hypersensitivity. For mice, one of the most important sources of sensory input is the whiskers, which help them to navigate and to maintain their balance, among other functions.

The researchers developed a way to measure the mice's sensitivity to slight deflections of their whiskers, and then trained the mutant Shank3 mice and normal ("wild-type") mice to display behaviors that signaled when they felt a touch to their whiskers. They found that mice that were missing Shank3 accurately reported very slight deflections that were not noticed by the normal mice.

"They are very sensitive to weak sensory input, which barely can be detected by wild-type mice," Feng says. "That is a direct indication that they have sensory over-reactivity."

Once they had established that the mutant mice experienced sensory hypersensitivity, the researchers set out to analyze the underlying neural activity. To do that, they used an imaging technique that can measure calcium levels, which indicate neural activity, in specific cell types.

They found that when the mice's whiskers were touched, excitatory neurons in the somatosensory cortex were overactive. This was somewhat surprising because when Shank3 is missing, synaptic activity should drop. That led the researchers to hypothesize that the root of the problem was low levels of Shank3 in the inhibitory neurons that normally turn down the activity of excitatory neurons. Under that hypothesis, diminishing those inhibitory neurons' activity would allow excitatory neurons to go unchecked, leading to sensory hypersensitivity.

To test this idea, the researchers genetically engineered mice so that they could turn off Shank3 expression exclusively in inhibitory neurons of the somatosensory cortex. As they had suspected, they found that in these mice, excitatory neurons were overactive, even though those neurons had normal levels of Shank3.

"If you only delete Shank3 in the inhibitory neurons in the somatosensory cortex, and the rest of the brain and the body is normal, you see a similar phenomenon where you have hyperactive excitatory neurons and increased sensory sensitivity in these mice," Feng says.

Reversing hypersensitivity

The results suggest that reestablishing normal levels of neuron activity could reverse this kind of hypersensitivity, Feng says.

"That gives us a cellular target for how in the future we could potentially modulate the inhibitory neuron activity level, which might be beneficial to correct this sensory abnormality," he says.

Many other studies in mice have linked defects in inhibitory neurons to neurological disorders, including Fragile X syndrome and Rett syndrome, as well as autism.

"Our study is one of several that provide a direct and causative link between inhibitory defects and sensory abnormality, in this model at least," Feng says. "It provides further evidence to support inhibitory neuron defects as one of the key mechanisms in models of autism spectrum disorders."

He now plans to study the timing of when these impairments arise during an animal's development, which could help to guide the development of possible treatments. There are existing drugs that can turn down excitatory neurons, but these drugs have a sedative effect if used throughout the brain, so more targeted treatments could be a better option, Feng says.

"We don't have a clear target yet, but we have a clear cellular phenomenon to help guide us," he says. "We are still far away from developing a treatment, but we're happy that we have identified defects that point in which direction we should go."

What The Study Did: Researchers investigated pay differences by sex at the highest ranks of academic medicine among clinical department chairs at 29 state medical schools in 12 states.

Authors: Eleni Linos, M.D., Dr.P.H., of the Stanford University School of Medicine in California, is the corresponding author.

To access the embargoed study:  Visit our For The Media website at this link https://media.jamanetwork.com/ 

(doi:10.1001/jamainternmed.2019.7540)

Editor's Note: The article includes conflict of interest disclosures. Please see the articles for additional information, including other authors, author contributions and affiliations, conflicts of interest and financial disclosures, and funding and support.

A massive white dwarf star with a bizarre carbon-rich atmosphere could be two white dwarfs merged together according to an international team led by University of Warwick astronomers, and only narrowly avoided destruction.

They have discovered an unusual ultra-massive white dwarf around 150 light years from us with an atmospheric composition never seen before, the first time that a merged white dwarf has been identified using its atmospheric composition as a clue.

The discovery, published today (2 March) in the journal Nature Astronomy, could raise new questions about the evolution of massive white dwarf stars and on the number of supernovae in our galaxy.

This star, named WDJ0551+4135, was identified in a survey of data from the European Space Agency's Gaia telescope. The astronomers followed up with spectroscopy taken using the William Herschel Telescope, focusing on those white dwarfs identified as particularly massive - a feat made possible by the Gaia mission. By breaking down the light emitted by the star, the astronomers were able to identify the chemical composition of its atmosphere and found that it had an unusually high level of carbon present.

Lead author Dr Mark Hollands, from the University of Warwick Department of Physics, said: "This star stood out as something we had never seen before. You might expect to see an outer layer of hydrogen, sometimes mixed with helium, or just a mix of helium and carbon. You don't expect to see this combination of hydrogen and carbon at the same time as there should be a thick layer of helium in between that prohibits that. When we looked at it, it didn't make any sense."

To solve the puzzle, the astronomers turned detective to uncover the star's true origins.

White dwarfs are the remains of stars like our own Sun that have burnt out all their fuel and shed their outer layers. Most are relatively lightweight, around 0.6 times the mass of our Sun, but this one weighs in at 1.14 solar masses, nearly twice the average mass. Despite being heavier than our Sun, it is compacted into two-thirds the diameter of Earth.

The age of the white dwarf is also a clue. Older stars orbit the Milky Way faster than younger ones, and this object is moving faster than 99% of the other nearby white dwarfs with the same cooling age, suggesting that this star is older than it looks.

Dr Hollands adds: "We have a composition that we can't explain through normal stellar evolution, a mass twice the average for a white dwarf, and a kinematic age older than that inferred from cooling. We're pretty sure of how one star forms one white dwarf and it shouldn't do this. The only way you can explain it is if it was formed through a merger of two white dwarfs."

The theory is that when one star in a binary system expands at the end of its life it will envelope its partner, drawing its orbit closer as the first star shrinks. The same will happen when the other star expands. Over billions of years, gravitational wave emission will shrink the orbit further, to the point that the stars merge together.

While white dwarf mergers have been predicted to occur, this one would be particularly unusual. Most of the mergers in our galaxy will be between stars with different masses, whereas this merger appears to be between two similarly sized stars. There is also a limit to how big the resulting white dwarf can be: at more than 1.4 solar masses it is thought that it would explode in a supernova though it may be possible for that these explosions can occur at slightly lower masses, so this star is useful in demonstrating how massive a white dwarf can get and still survive.

Because the merging process restarts the cooling of the star, it is difficult to determine how old it is. The white dwarf probably merged around 1.3 billion years ago but the two original white dwarfs may have existed for many billions of years prior.

It is one of only a handful of merged white dwarfs to be identified so far, and the only one via its composition.

Dr Hollands adds: "There aren't that many white dwarfs this massive, although there are more than you would expect to see which implies that some of them were probably formed by mergers.

"In the future we may be able to use a technique called asteroseismology to learn about the white dwarf's core composition from its stellar pulsations, which would be an independent method confirming this star formed from a merger.

"Maybe the most exciting aspect of this star is that it must have just about failed to explode as a supernova - these gargantuan explosions are really important in mapping the structure of the Universe, as they can be detected out to very large distances. However, there remains much uncertainty about what kind of stellar systems make it to the supernova stage. Strange as it may sound, measuring the properties of this 'failed' supernova, and future look-alikes, is telling us a lot about the pathways to thermonuclear self-annihilation."

SPOKANE, Wash. - The average age at which teens and young adults start using drugs has been rising, according to a study published today in JAMA Pediatrics.

The study examined changes in the average age of first drug use for 18 different drugs--including alcohol and tobacco products--between 2004 and 2017 and found that average ages had increased for the majority of those drugs.

For example, the study showed that the average age at which young people first consumed alcohol or smoked cigarettes rose from 16 in 2004 to 17 in 2017. Those who reported using heroin or cocaine for the first time had an average age of just over 17 in 2004, which had risen to about 18 for heroin and close to 19 for cocaine by 2017.

"This is great news, because delaying drug use prevents early exposure, which is associated with a variety of negative health consequences, including increased risk of drug use disorder and long-term impairments such as depression, neurocognitive deficits, involvement in risky behaviors, and sexually transmitted diseases, said lead author Karl Alcover, a postdoctoral research associate in Washington State University's Elson S. Floyd College of Medicine.

In their study, the researchers used publicly available data collected as part of the National Survey on Drug Use and Health, an annual survey that looks at drug use in a representative sample of US residents aged 12 and older. They included data on 84,317 respondents between the ages of 12 and 21 who were surveyed between 2004 and 2017 and had reported first-time drug use in the previous 12 months.

The researchers analyzed the data to estimate the average age at first-time use for 18 internationally regulated drugs for each year included in the study. Looking at year-to-year trends, they found that the average age at first use had increased for 12 out of 18 drugs, including alcohol, cocaine, ecstasy, hallucinogens, heroin, inhalants, LSD, marijuana, stimulants, and tobacco products such as cigars, cigarettes and smokeless tobacco. For the other six drugs--crack cocaine, methamphetamines, opioids, PCP, sedatives, and tranquilizers--they found no statistically significant changes in the age at first use.

Increases were relatively consistent from year to year for all but two drugs: alcohol and LSD. In 2004, the average age at which young people first consumed alcohol was approximately 16 years. It increased consistently through 2014, after which it leveled off at about age 17 in 2017. The average age of first use of LSD increased significantly through 2014 and subsequently declined, but still showed an overall increase over the entire timeframe studied. These findings suggest that trends toward starting to use at a later age may have already ended for those two drugs, Alcover said.

The earliest average age of first drug use across the study timeframe was 15.4 for inhalants, whereas the latest average age was 18.0 for cocaine and crack cocaine.

"Our study shows that since 2004 fewer individuals started using drugs at age 15 and younger, which is what we would typically consider as early-onset drug use," Alcover said. "These promising trends may serve as early evidence that prevention strategies--especially those focused on teens and young adults--are working."

Alcover said the next step is to investigate what drives the trends seen in this study. The success of prevention efforts is one possible explanation, but it could also be that young people's preferences have switched to new drugs such as e-cigarettes, which were not included in the survey data. He also noted that further research should be done to understand why some drugs did not show an increase in average age, which could help improve prevention strategies for those drugs.

"Prevention of drug use is the best approach to reducing drug-related burden in the population," Alcover said.