Ultrasounds can help predict the risk of preterm births

Researchers have developed a way to use ultrasound to predict whether a pregnant person is at risk of delivering a baby prematurely, which occurs in upward of 10% of pregnancies in the U.S.
The new method — the result of more than 20 years of collaboration between researchers in nursing and engineering at University of Illinois Chicago and University of Illinois Urbana-Champaign — measures microstructural changes in a woman’s cervix using quantitative ultrasound. The ultrasound method works as early as 23 weeks into a pregnancy, according to the research, which is published in the American Journal of Obstetrics & Gynecology Maternal Fetal Medicine.
The current method for assessing a woman’s risk of preterm birth is based solely on whether she has previously given birth prematurely. This means there has been no way to assess risk in a first-time pregnancy.
“Today, clinicians wait for signs and symptoms of a preterm birth,” such as a ruptured membrane, explained lead author Barbara McFarlin, a professor emeritus of nursing at UIC. “Our technique would be helpful in making decisions based on the tissue and not just on symptoms.”
In a study of 429 women who gave birth without induction at the University of Illinois Hospital, the new method was effective at predicting the risk of preterm births during first-time pregnancies. And for women who were having a subsequent pregnancy, combing the data from quantitative ultrasound with the woman’s delivery history was more effective at assessing risk than just using her history.
The new approach differs from a traditional ultrasound where a picture is produced from the data received. In quantitative ultrasound, a traditional ultrasound is performed but the radio frequency data itself is read and analyzed to determine tissue characteristics.
The study is the culmination of a research partnership that began in 2001 when McFarlin was a nursing PhD student at UIC. Having previously worked as a nurse midwife and sonographer, she had noticed that there were differences in the appearance of the cervix in women who went on to deliver preterm. She was interested in quantifying this and discovered that “no one was looking at it.”
She was put in touch with Bill O’Brien, a UIUC professor of electrical and computer engineering, who was studying ways to use quantitative ultrasound data in health research. Together, over the past 22 years, they established that quantitative ultrasound could detect changes in the cervix and, as McFarlin had suspected long ago, that those changes help predict the risk of preterm delivery.

The preterm birth rate hovers around 10-15% of pregnancies, O’Brien said. “That’s a very, very high percentage to not know what is happening,” he said.
If a clinician could know at 23 weeks that there was a risk of preterm birth, they would likely conduct extra appointments to keep an eye on the fetus, the researchers said. But since there had previously been no routine way to assess preterm birth risk this early, there have been no studies to show what sort of interventions would be helpful in delaying labor. This study, O’Brien explains, will allow other researchers to “start studying processes by which you might be able to prevent or delay preterm birth.”
The research was funded by the National Institutes of Health’s National Institute of Child Health and Human Development. Additional coauthors are UIC nursing PhD student Michelle Villegas-Downs; UIUC statistics PhD student Mehrdad Mohammadi and statistics professor Douglas Simpson; and engineering professor Aiguo Han at Virginia Tech.

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Exposure to flame retardants linked to premature birth, higher birth weight

In the largest study of its kind, researchers at UC Davis Health found that exposure to organophosphate ester flame retardants during pregnancy was associated with preterm birth, especially among females. The chemicals were also linked to higher birth weight, a concern for increased obesity risk. The major new research study was published in Environmental Health Perspectives.
“The importance of this study lies in unraveling the potential impact of exposure to environmental chemicals during pregnancy on fetal development. Our findings guide our understanding of how these chemicals may be silently seeding lasting challenges for the health of the next generation,” said Jiwon Oh, first author of the study and a postdoctoral scholar in the Department of Public Health Sciences, Division of Environmental and Occupational Health.
OPEs phased in as polybrominated flame retardants phased out
In the mid-2000s, one class of chemicals, polybrominated diphenyl ether flame retardants, were gradually phased out of use due to concerns about their potential toxicity.
Organophosphate esters, or OPEs, gradually took their place. They are now widely used in foams found in furniture, baby products, electronics, textiles and building materials to prevent fires and make plastics more flexible.
Because of their chemical structure, OPEs slowly degrade and become part of dust. Individuals are exposed to OPEs through their skin or when they ingest or inhale indoor dust.
The chemicals are frequently detected in urine samples from the U.S. general population, including samples from pregnant people. For this study, the researchers wanted to determine what impact OPEs might have on fetal development during pregnancy.

Research conducted across U.S.
Researchers at multiple institutions, including UC Davis, conducted the study. It included 6,646 mother-child pairs from 16 cohorts across the U.S. from the Environmental Influences on Child Health Outcome (ECHO) study. The participants came from various regions and had diverse backgrounds.
Researchers measured nine OPE biomarkers in urine samples of pregnant people collected between 2007 and 2020, with most samples obtained during the second and third trimesters.
They assessed birth outcomes, including gestational age at birth and birth weight, primarily using medical records or parent reports.
Preterm births and greater birth weight
The researchers found three of the nine OPEs were associated with increased risks of preterm birth (before 37 weeks of pregnancy), especially among female newborns. These included: dibutyl phosphate di-isobutyl phosphate bis(butoxyethyl) phosphatePreterm births can put infants at risk of health issues, including breathing and feeding problems, developmental delays, cerebral palsy, and vision and hearing problems.

Three other OPEs — bis(1-chloro-2-propyl) phosphate, bis(2-methylphenyl) phosphate, and dipropyl phosphate — were linked to greater birth weight-for-gestational-age.
High birth weight is associated with childhood obesity, which increases the risk of health conditions like diabetes and cardiovascular disease.
“There were over 6,000 pregnancies included in this study, and with such a large study, we are very confident of our findings,” said Deborah Bennett, senior author of the study and a professor of environmental health in the Department of Public Health Sciences. “Policy options to reduce exposure to organophosphate ester flame retardants should be considered.”
OPEs are metabolic and endocrine-disrupting chemicals
The researchers noted that OPEs may affect thyroid hormone levels and cause inflammation and oxidative stress, which could play a role in the preterm births. OPEs are also endocrine disruptors, so they may contribute to abnormal placental development, and the impact may vary based on the sex of the fetus.
“Because OPEs are from building materials, textiles, electronics and other products, consumers cannot choose products that do not contain OPEs,” Oh said. “Only policy changes and regulations can mitigate their exposure.”
Resources Read the study How much is the dust in your home affecting your child?

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mRNA therapeutic successfully combats ovarian cancer in mice

Each year, several thousand women in Germany die from ovarian cancer. In many cases, the disease is only detected when it is very advanced and metastases have already formed — usually in the intestines, abdomen or lymph nodes. At such a late stage, only 20 to 30 percent of all those affected survive the next five years. “Unfortunately, this situation has hardly changed at all over the past two decades,” says Professor Klaus Strebhardt, Director of the Department of Molecular Gynecology and Obstetrics at University Hospital Frankfurt.
96 percent of all ovarian cancer (high-grade) patients share the same clinical picture: The tumor suppressor gene p53 has mutated and is now non-functional. The gene contains the building instructions for an important protein that normally recognizes damage in the genetic material (DNA) of each cell. It then prevents these abnormal cells from proliferating and activates repair mechanisms that rectify the damage. If this fails, it induces cell death. “In this way, p53 is very effective in preventing carcinogenesis,” explains Strebhardt. “But when it is mutated, this protective mechanism is eradicated.”
If a cell wants to produce a certain protein, it first makes a transcript of the gene containing the building instructions for it. Such transcripts are called mRNAs. In women with ovarian cancer, the p53 mRNAs are just as defective as the gene from which they were copied. “We produced an mRNA in the laboratory that contained the blueprint for a normal, non-mutated p53 protein,” says Dr. Monika Raab from the Department of Molecular Gynecology and Obstetrics, who conducted many of the key experiments in the study. “We packed it into small lipid vesicles, known as liposomes, and then tested them first in cultures of various human cancer cell lines. The cells used the artificial mRNA to produce functional p53 protein.”
In the next step, the scientists cultivated ovarian tumors — organoids — from patient cells sourced by the team led by Professor Sven Becker, Director of the Women’s Clinic at University Hospital Frankfurt. After treatment with the artificial mRNA, the organoids shrank and began to die.
To test whether the artificial mRNA is also effective in organisms and can combat metastases in the abdomen, the researchers implanted human ovarian tumor cells into the ovaries of mice and injected the mRNA liposomes into the animals some time later. The result was very convincing, says Strebhardt: “With the help of the artificial mRNA, cells in the animals treated produced large quantities of the functional p53 protein, and as a result both the tumors in the ovaries and the metastases disappeared almost completely.”
That the method was so successful is partly due to recent advances in mRNA technology: Normally, mRNA transcripts are very sensitive and degraded by cells within minutes. However, it is meanwhile possible to prevent this by specifically modifying the molecules. This extends their lifespan substantially, in this study to up to two weeks.
In addition, the chemical composition of the artificial mRNA is slightly different to that of its natural counterpart. This prevents the immune system from intervening after the molecule has been injected and from triggering inflammatory responses. In 2023, the Hungarian scientist Katalin Karikó and her American colleague Drew Weissman were awarded the Nobel Prize in Physiology or Medicine for this discovery. “Thanks to the development of mRNA vaccines such as those of BioNTech and Moderna, which went into action during the SARS-CoV-2 pandemic, we now also know how to make the molecules even more effective,” explains Strebhardt.
Strebhardt, Raab and Becker are now looking for partners to join the next step of the translational project: testing on patients with ovarian cancer. “What is crucial now is the question of whether we can implement the concept and the results in clinical reality and use our method to help cancer patients,” says Strebhardt. The latest results make him very optimistic that the tide could finally turn in the treatment of ovarian carcinomas. “p53 mRNA is not a normal therapeutic that targets a specific weak point in cancer cells. Instead, we are repairing a natural mechanism that the body normally uses very effectively to suppress carcinogenesis. This is a completely different quality of cancer therapy.”

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New model predicts how shoe properties affect a runner's performance

A good shoe can make a huge difference for runners, from career marathoners to couch-to-5K first-timers. But every runner is unique, and a shoe that works for one might trip up another. Outside of trying on a rack of different designs, there’s no quick and easy way to know which shoe best suits a person’s particular running style.
MIT engineers are hoping to change that with a new model that predicts how certain shoe properties will affect a runner’s performance.
The simple model incorporates a person’s height, weight, and other general dimensions, along with shoe properties such as stiffness and springiness along the midsole. With this input, the model then simulates a person’s running gait, or how they would run, in a particular shoe.
Using the model, the researchers can simulate how a runner’s gait changes with different shoe types. They can then pick out the shoe that produces the best performance, which they define as the degree to which a runner’s expended energy is minimized
While the model can accurately simulate changes in a runner’s gait when comparing two very different shoe types, it is less discerning when comparing relatively similar designs, including most commercially available running shoes. For this reason, the researchers envision the current model would be best used as a tool for shoe designers looking to push the boundaries of sneaker design.
“Shoe designers are starting to 3D print shoes, meaning they can now make them with a much wider range of properties than with just a regular slab of foam,” says Sarah Fay, a postdoc in MIT’s Sports Lab and the Institute for Data, Systems, and Society (IDSS). “Our model could help them design really novel shoes that are also high-performing.”
The team is planning to improve the model, in hopes that consumers can one day use a similar version to pick shoes that fit their personal running style.

“We’ve allowed for enough flexibility in the model that it can be used to design custom shoes and understand different individual behaviors,” Fay says. “Way down the road, we imagine that if you send us a video of yourself running, we could 3D print the shoe that’s right for you. That would be the moonshot.”
The new model is reported in a study appearing this month in the Journal of Biomechanical Engineering. The study is authored by Fay and Anette “Peko” Hosoi, professor of mechanical engineering at MIT.
Running, revamped
The team’s new model grew out of talks with collaborators in the sneaker industry, where designers have started to 3D print shoes at commercial scale. These designs incorporate 3D-printed midsoles that resemble intricate scaffolds, the geometry of which can be tailored to give a certain bounce or stiffness in specific locations across the sole.
“With 3D printing, designers can tune everything about the material response locally,” Hosoi says. “And they came to us and essentially said, ‘We can do all these things. What should we do?'”
“Part of the design problem is to predict what a runner will do when you put an entirely new shoe on them,” Fay adds. “You have to couple the dynamics of the runner with the properties of the shoe.”
Fay and Hosoi looked first to represent a runner’s dynamics using a simple model. They drew inspiration from Thomas McMahon, a leader in the study of biomechanics at Harvard University, who in the 1970s used a very simple “spring and damper” model to model a runner’s essential gait mechanics. Using this gait model, he predicted how fast a person could run on various track types, from traditional concrete surfaces to more rubbery material. The model showed that runners should run faster on softer, bouncier tracks that supported a runner’s natural gait.

Though this may be unsurprising today, the insight was a revelation at the time, prompting Harvard to revamp its indoor track — a move that quickly accumulated track records, as runners found they could run much faster on the softier, springier surface.
“McMahon’s work showed that, even if we don’t model every single limb and muscle and component of the human body, we’re still able to create meaningful insights in terms of how we design for athletic performance,” Fay says.
Gait cost
Following McMahon’s lead, Fay and Hosoi developed a similar, simplified model of a runner’s dynamics. The model represents a runner as a center of mass, with a hip that can rotate and a leg that can stretch. The leg is connected to a box-like shoe, with springiness and shock absorption that can be tuned, both vertically and horizontally.
They reasoned that they should be able to input into the model a person’s basic dimensions, such as their height, weight, and leg length, along with a shoe’s material properties, such as the stiffness of the front and back midsole, and use the model to simulate what a person’s gait is likely to be when running in that shoe.
But they also realized that a person’s gait can depend on a less definable property, which they call the “biological cost function” — a quality that a runner might not consciously be aware of but nevertheless may try to minimize whenever they run. The team reasoned that if they can identify a biological cost function that is general to most runners, then they might predict not only a person’s gait for a given shoe but also which shoe produces the gait corresponding to the best running performance.
With this in mind, the team looked to a previous treadmill study, which recorded detailed measurements of runners, such as the force of their impacts, the angle and motion of their joints, the spring in their steps, and the work of their muscles as they ran, each in the same type of running shoe.
Fay and Hosoi hypothesized that each runner’s actual gait arose not only from their personal dimensions and shoe properties, but also a subconscious goal to minimize one or more biological measures, yet unknown. To reveal these measures, the team used their model to simulate each runner’s gait multiple times. Each time, they programmed the model to assume the runner minimized a different biological cost, such as the degree to which they swing their leg or the impact that they make with the treadmill. They then compared the modeled gait with the runner’s actual gait to see which modeled gait — and assumed cost — matched the actual gait.
In the end, the team found that most runners tend to minimize two costs: the impact their feet make with the treadmill and the amount of energy their legs expend.
“If we tell our model, ‘Optimize your gait on these two things,’ it gives us really realistic-looking gaits that best match the data we have,” Fay explains. “This gives us confidence that the model can predict how people will actually run, even if we change their shoe.”
As a final step, the researchers simulated a wide range of shoe styles and used the model to predict a runner’s gait and how efficient each gait would be for a given type of shoe.
“In some ways, this gives you a quantitative way to design a shoe for a 10K versus a marathon shoe,” Hosoi says. “Designers have an intuitive sense for that. But now we have a mathematical understanding that we hope designers can use as a tool to kickstart new ideas.”
This research is supported, in part, by Adidas.

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Bullying 'normal occurrence' at Newcastle NHS trust, say CQC

Published2 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, GoogleA “significant deterioration” in leadership at an NHS trust probably had a “knock-on effect” on its standard of services, a watchdog has found. Inspectors found staff felt encouraged to “turn a blind eye” to bullying in hospitals run by the Newcastle Hospitals NHS Foundation Trust. The Care Quality Commission (CQC) downgraded the trust’s overall rating to “requires improvement”. The trust said it “fully accepts” the report.Bosses at Newcastle Hospitals NHS Foundation Trust said recommendations were being worked on “as a matter of urgency”.’Inadequate’ leadershipInspections were carried out between June and September in surgery, services for children and young people, and medical care at the Freeman Hospital and the Royal Victoria Infirmary (RVI), as well as maternity services and urgent and emergency care at the RVI. The trust’s patient transport service (known as NECTAR) was also inspected. A report released on Wednesday saw its overall rating decline from “outstanding”, which it was awarded in 2019, to “requires improvement”. How “well-led” the trust was declined from “outstanding” to “inadequate”. “Safety” dropped from “good” to “requires improvement”, “effective and responsive” declined from “outstanding” to requires “improvement”, while “caring” dropped from “outstanding” to “good”.’Unacceptable’Ann Ford, CQC’s director of operations in the north, said: “We found a significant deterioration in how well the trust was being led.”Our experience tells us that when a trust isn’t well led, this has a knock-on effect on the standard of services being provided to people. “Some staff told us that bullying was a normal occurrence, and they were encouraged to ‘turn a blind eye’ and not report this behaviour. “This is completely unacceptable.” Since the inspection, a new chief executive and other senior leaders have joined the trust. The CQC said they will continue to monitor the trust and will return to carry out another inspection.Analysis by Sharon Barbour, BBC Look North Health CorrespondentFor years Newcastle Hospitals proudly displayed its “outstanding” rating. The Freeman is world-renowned for its cardiac work, and the RVI was the first to treat Covid patients in the UK. Behind the scenes, however, serious problems were brewing – particularly in the cardiac surgery unit, which is where the CQC began to focus its attention.Whistleblowers reported bullying, some around safety concerns, and there were claims and counter claims. It is the leadership which has come in for the harshest criticism, and not only because of failings in managing the cardiothoracic unit. Now there is new boss, Sir Jim Mackey. His priority is changing the culture.He’s also planning to sort IT issues, which meant thousands of clinical letters to GPs were not sent out.Newcastle Hospitals is not the only trust struggling to keep hold of fine ratings. Covid, strike action, A&E delays, staffing, funding and social care shortages are all leaving trust bosses with a lot to fix. The report is very bad news for staff – but the rating for caring, well that was “good”. ‘Working together’Newcastle Hospitals’ new chief executive, Sir James Mackey, said: “We fully accept the CQC’s reports. “Their clear recommendations for attention and improvement are being worked on as a matter of urgency and I am confident we can fix this by working together across the organisation and focussing on what matters to patients and staff.”The trust said they have put in an improvement programme, which included having an “open and honest” incident reporting system.Image source, BBC A further targeted inspection took place in the cardiothoracic surgery department at the Freeman Hospital in September, in response to concerns raised by whistleblowers regarding the culture, specifically about bullying and harassment and safety concerns.The watchdog said trainees felt the atmosphere in theatres was “toxic” and “disrespectful of them, and others”. No new rating came from that inspection, but the trust has since updated their action plan to include specific actions in relation to culture, the CQC said.Follow BBC Newcastle on Facebook, X (formerly Twitter), and Instagram. Send your story ideas to northeastandcumbria@bbc.co.uk.More on this storyHospital trust’s ‘outstanding’ status suspendedPublished2 November 202324,000 hospital letters lost in computer errorPublished26 September 2023Junior doctors removed from ‘bullying’ heart unitPublished28 September 2021Related Internet LinksNewcastle Hospitals NHS Foundation TrustCare Quality CommissionThe BBC is not responsible for the content of external sites.

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Footballer Michael Owen on sight loss: 'I'd swap eyes with my son if I could'

Published3 hours agoShareclose panelShare pageCopy linkAbout sharingBy Beth RoseBBC Access AllFormer England striker, Michael Owen, says he would “swap eyes” with his son if it was possible to help the teenager see again.James Owen, 17, who hoped to follow in his father’s footsteps, was diagnosed with Stargardt disease, a degenerative eye condition, when he was eight. Speaking on the BBC Access All podcast, Michael said: “If I could give him my eyes and we could do a swap, I would.”I would pay every cent I’ve got to make James see again.”James is from a legendary footballing family. Michael, played as striker for clubs including Liverpool, Real Madrid and, somewhat controversially went on to play at Liverpool’s north-west rival, Manchester United. His father Terry Owen started his own footballing career at Everton in 1966. The beautiful game was very much in James’s blood, but it slowly dawned on the Owens that something unusual was going on with their young son. James was a nifty player when he was on the ball, but he often failed to track passes or notice player movements further down the field.It became more concerning when he struggled to compete on bigger pitches and it was all getting too fast paced, James admits.At home or on holiday Michael says he often got frustrated when trying to take family photographs as his young son always seemed to look to the side of the camera rather than at it.Even so, Michael says it came as a “hammer-blow” when he and wife Louise were referred to an eye specialist and they were informed of James’s diagnosis.Listen to the Access All podcast with Michael and James Owen, and spot the moment when the tables turn and Michael starts to interview Access All’s blind presenter , Emma Tracey, about her experiences…According to the RNIB, Stargardt disease is an inherited eye condition that affects the macula, the central part of the retina, and causes a reduction in vision there. Understandably, Michael says it left him with parental guilt. “As a parent you just want everything to be perfect – and he is – but of course it was a sad time.”Thinking about the future – will he be able to drive? Will he be able to work? All these things run through your mind.”He says the procedures and tests which followed over the years while medical staff monitored James’s condition were also hard to watch. “You’re pushing your son forward to get something you know is going to be painful. It’s just horrible to see. You want to take all the pain away.”James told Access All presenter Emma Tracey, who is blind herself, that his “central vision is blurry” and that “I struggle with seeing different colours and different lights” although he has “good peripheral vision”.He has learned to adapt to the world around him, by using tricks that other visually impaired people will know well.”I’ll notice what colour my dad’s jumper is. So if I ever go out, then I would be able to recognise him from the colour, not from his face because I struggle with detail.”Michael, who now focuses on training racehorses, says “time is a great healer” and while James had found it difficult to comprehend the diagnosis when he was younger, he has since become very positive about it. “He’s just mentally very, very strong. He’s got a great mindset,” Michael says. “I’ve got four children and I’m probably the least worried about James’s future.”The father and son are about to release their first documentary – Football is for Everyone – exploring James’s sight loss and an adapted version of football called futsal. The duo follow the visually impaired futsal England squad as they compete in the 2023 visually impaired world cup hosted in Birmingham. The game is played on a smaller, indoor, pitch with a heavier ball that doesn’t bounce so much. Players are classified by their visual impairments and only so many players of the same classification can play at once. The goalkeepers are fully sighted but are confined to the goal.When he joined a training session, James quickly got to grips with the game. “I did actually score at some point while training with the England team which I’m quite happy about.” Then he pauses, and confesses. “I actually got megged and then scored an own goal. It was not a great moment.”Michael can’t help but jokingly stick the knife in: “It’s one of the most embarrassing things in football, if you get nutmegged.”Nutmegging, for the uninitiated, is when one player kicks the ball through another player’s legs. Adding an own goal into the mix, just increases the humiliation. “It’s just been a surreal experience,” James says of making the documentary which started before the pandemic. “I used to be quite shy as a kid, but it’s definitely brought me out my shell.”Although he has sidelined football, James says “I’ve got a lot of dreams”. He has found a passion for business, which he is studying at college and hopes to own his own business in the future, although he says he is keeping his options open about what that might be.Michael has a hunch. “When I retire from work in 30 years or something, he’ll probably take over the ‘family empire’,” he laughs. James and Michael’s documentary, Football Is For Everyone is available from the 30th of January on TNT Sports and Discovery Plus. You can listen to the podcast and find information and support on the BBC Access All page.

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Millions lose access to free NHS earwax removal

Published23 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Jim ReedHealth reporterAlmost 10 million people in England can no longer access free NHS earwax removal services, the RNID has warned.The hearing loss charity said there was “no medical reason” for the withdrawal of NHS services across parts of England since 2019.And some people unable to afford private treatment were turning to “dangerous self-removal methods”.The government said GPs can still refer patients on to a specialist service if the problem is linked to hearing loss.Each year, about 2.3 million people in the UK need earwax treatment, according to the NHS.It is more common among older people, hearing-aid users and those with a learning disability. Wax build-up in the ear canal can cause painful symptoms including tinnitus, earache and hearing loss.It often requires removal before a hearing test and can interfere with certain hearing aids, causing a distracting whistling sound.Image source, Helen KendallHelen Kendall, 76, from Bath, Somerset, says she now has to pay £240 a year for private treatment, because the GPs in her area no longer offer a free service.”When the wax builds up, I find it very difficult,” she says. “I lost some of my confidence and became unable to follow conversations.”It led to increased isolation and I found I was withdrawing.”I’m a sociable person – I volunteer at a food bank, I’m part of an art group and cook for a lunch club and I love the cinema.”All of these rely on me being able to hear properly.”National Institute of Health and Care Excellence guidelines say wax removal should be provided in GP surgeries or other local ear-care services. There are two main methods:microsuction – a small vacuum sucks out waxelectronic irrigation – a machine gently pumps pressurised water into the earThe RNID sent Freedom of Information requests to all 42 integrated health boards across England.Of the 40 that responded:. 18 funded a full service15 restricted eligibility or did not offer the service across all their GP surgeriesseven commissioned no treatment at all The charity’s director of health, Crystal Rolfe, said: “For the 10 million people who live in areas where there is no provision, the only option is to pay for it, which we know can cost up to £100 for just one procedure.”Previous research shows that 26% of people say they wouldn’t be able to afford that, partly because some people need to have earwax removed several times a year.”GettyNo NHS ear wax services7 areasBirmingham & Solihull, Cornwall & Scilly Isles, Dorset, Mid & South Essex, NW London, SW London, Suffolk & NE EssexSource: RNIDThe charity is concerned that a lack of provision in some areas means more patients may be trying to remove wax themselves. The strong advice is “never put anything in your ear smaller than your elbow”. Other objects – from cotton buds to paper clips and hairpins or even fingers – should never be used in the ear canal itself. “For most people, it’s a self-cleansing mechanism and the wax just comes out on its own,” Ms Rolfe says. “If it’s got stuck in your ear, then you should go and see a GP, who might sometimes suggest olive oil drops in the first instance.”Some commercial drops are available over the counter – but there is “little evidence” drops or sprays will resolve the issue in more than one out of every five people, the RNID says.Drops would not be recommended for those who have had a recent infection or operation – and the patient should speak to a pharmacist first.The government said local health boards are responsible for commissioning services in their area based on the needs of the population, and GPs can still refer patients to a specialist audiology service if the problem is linked to hearing loss.An NHS England spokeswoman said information about treating earwax safely at home was also available on the NHS website.The Scottish and Welsh governments remained “committed to ensure the availability of NHS earwax-removal services”, the RNID said.And it would “lobby for the same commitment” in Northern Ireland, once devolved government was restored.More on this storyPatients go private over ear wax removal wait timePublished17 March 2022Why ear wax syringing is no longer free – ministerPublished25 September 2020Related Internet LinksEarwax build-up – NHSThe BBC is not responsible for the content of external sites.

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Walking fitness can predict fracture risk in older adults

The ability to walk one kilometre comfortably can help predict fracture risk, according to researchers at the Garvan Institute of Medical Research. The findings, published today in JAMA Network Open, suggest that simply asking a patient about walking limitation could allow clinicians to identify those in need of further bone health screening and prescribe interventions that could prevent fractures from occurring.
“We’ve discovered that trouble walking even short distances appears closely tied to higher fracture risk over the following five years,” says lead author of the study, Professor Jacqueline Center, Head of Garvan’s Clinical Studies and Epidemiology Lab. “Just a few simple questions about how far someone can walk could give doctors an early warning sign to check bone health.”
The researchers examined data on nearly 267,000 adults aged 45 and older from the Sax Institute’s 45 and Up Study, a major ongoing research initiative that has been tracking health outcomes in adults in NSW for more than 15 years. Participants were asked if health issues limited their ability to walk various distances, with answer options of ‘not at all,’ ‘a little,’ or ‘a lot’. The group was then followed for five years to track fracture outcomes.
The researchers found that one in five adults reported some walking limitation at the beginning of the study. Those with more difficulty walking were significantly more likely to experience a fracture during follow-up. For example, women who said they were limited ‘a lot’ in walking one kilometre had a 60% higher fracture risk than women with no limitation. For men, the increased risk was over 100%.
“We saw a clear ‘dose-response’ pattern, where greater walking limitation meant higher fracture risk. This suggests a direct relationship between low walking ability and weaker bones,” says first author of the study Dr Dana Bliuc, Senior Research Officer at Garvan.
Approximately 60% of all fractures in the study were attributable to some level of walking limitation. The link remained strong even after accounting for other factors like age, falls, prior fractures, and weight, and the findings were consistent across different fracture sites like hips, vertebrae, arms, and legs.
“In this generally healthy community-based population, we still found one in five people had trouble walking a kilometre,” says Professor Center. “We think this simple assessment could help identify many more at-risk individuals who may benefit from bone density screening or preventative treatment.”
Osteoporosis medications, lifestyle changes, and other interventions are available to improve bone strength and avoid first or repeat fractures. However, screening rates currently remain low, meaning many miss out on fracture risk assessments. Finding easy but accurate ways to detect at-risk people is an important target for research.

“Fracture risk assessment generally relies on a bone density test, which many people have not had when seeing their doctor,” says Professor Center. “Asking about walking ability takes just seconds and could be a free, non-invasive way to tell if someone needs their bones checked.”
The researchers stress that walking limitation may have many causes beyond weak bones, from heart disease to arthritis. However, a difficulty in walking even short distances appears closely tied to fracture risk independently.
“We hope these findings will encourage clinicians to consider walking ability as a red flag for possible bone health issues. For patients, if you can’t walk a full kilometre comfortably, it may be wise to ask your doctor about getting your bones checked,” says Dr Bliuc.

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Bioengineers on the brink of breaching blood-brain barrier

Imagine the brain as an air traffic control tower, overseeing the crucial and complex operations of the body’s ‘airport.’ This tower, essential for coordinating the ceaseless flow of neurological signals, is guarded by a formidable layer that functions like the airport’s security team, diligently screening everything and everyone, ensuring no unwanted intruders disrupt the vital workings inside.
However, this security, while vital, comes with a significant drawback: sometimes, a ‘mechanic’ — in the form of critical medication needed for treating neurological disorders — is needed inside the control tower to fix arising issues. But if the security is too stringent, denying even these essential agents entry, the very operations they’re meant to protect could be jeopardized.
Now, researchers led by Michael Mitchell of the University of Pennsylvania are broaching this long-standing boundary in biology, known as the blood-brain barrier, by developing a method akin to providing this mechanic with a special keycard to bypass security. Their findings, published in the journal Nano Letters, present a model that uses lipid nanoparticles (LNPs) to deliver mRNA, offering new hope for treating conditions like Alzheimer’s disease and seizures — not unlike fixing the control tower’s glitches without compromising its security.
“Our model performed better at crossing the blood-brain barrier than others and helped us identify organ-specific particles that we later validated in future models,” says Mitchell, associate professor of bioengineering at Penn’s School of Engineering and Applied Science, and senior author on the study. “It’s an exciting proof of concept that will no doubt inform novel approaches to treating conditions like traumatic brain injury, stroke, and Alzheimer’s.”
Search for the key
To develop the model, Emily Han, a Ph.D. candidate and NSF Graduate Research Fellow in the Mitchell Lab and first author of the paper, explains that it started with a search for the right in vitro screening platform, saying, “I was combing through the literature, most of the platforms I found were limited to a regular 96-well plate, a two-dimensional array that can’t represent both the upper and lower parts of the blood-brain barrier, which correspond to the blood and brain, respectively.”
Han then explored high-throughput transwell systems with both compartments but found they didn’t account for mRNA transfection of the cells, revealing a gap in the development process. This led her to create a platform capable of measuring mRNA transport from the blood compartment to the brain, as well as transfection of various brain cell types including endothelial cells and neurons.

“I spent months figuring out the optimal conditions for this new in vitro system, including which cell growth conditions and fluorescent reporters to use,” Han explains. “Once robust, we screened our library of LNPs and tested them on animal models. Seeing the brains express protein as a result of the mRNA we delivered was thrilling and confirmed we were on the right track.”
The team’s platform is poised to significantly advance treatments for neurological disorders. It’s currently tailored for testing a range of LNPs with brain-targeted peptides, antibodies, and various lipid compositions. However, it could also deliver other therapeutic agents like siRNA, DNA, proteins, or small molecule drugs directly to the brain after intravenous administration.
What’s more, this approach isn’t limited to the blood-brain barrier as it shows promise for exploring treatments for pregnancy-related diseases by targeting the blood-placental barrier, and for retinal diseases focusing on the blood-retinal barrier.
Next Steps
The team is eager to use this platform to screen new designs and test their effectiveness in different animal models. They are particularly interested in working with collaborators with advanced animal models of neurological disorders.
“We’re collaborating with researchers at Penn to establish brain disease models,” Han says. “We’re examining how these LNPs impact mice with various brain conditions, ranging from glioblastoma to traumatic brain injuries. We hope to make inroads towards repairing the blood-brain barrier or target neurons damaged post-injury.”
This research was supported by the National Institute of Health (Award DP2 TR002776, Grant No. T90DE030854 and F30HL162465−01A1); a Burroughs Wellcome Fund Career Award at the Scientific Interface; and the National Science Foundation (Award CBET-2145491 and 1845298).

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A new 3D bioprinted model offers a novel tool to study common liver disease, and perhaps find an effective treatment

Metabolic dysfunction- associated steatohepatitis, or MASH, is an inflammatory, liver-scarring disease that has reached epidemic proportions, with an estimated 1.5% to 6.5% of U.S. adults afflicted by the condition, and roughly 24% of adults having nonalcoholic fatty liver disease (NAFLD).
MASH, previously known as nonalcoholic steatohepatitis, or NASH, is a more serious complication of NAFLD, now called metabolic dysfunction-associated steatotic liver disease, or MASLD. The nomenclature changed recently to reduce the stigma attached to the older terms. Neither disease is associated with alcohol consumption.
What hasn’t changed is the lack of effective treatments. There are no approved pharmacological therapies for MASH, in part due to a lack of adequate preclinical models for study and testing. In a new paper published on December 27, 2023, in The American Journal of Pathology, researchers at Sanford Burnham Prebys, with colleagues at Viscient Biosciences — a San Diego-based biotech — and UC San Diego and Salk Institute, described a three-dimensonal bioprinted liver tissue model employing liver cells from healthy or MASH-diseased donors.
“These tissues display all of the characteristics of MASH, including fibrosis, without any additional disease-inducing agents,” said senior and corresponding study author David A. Brenner, M.D., president and CEO of Sanford Burnham Prebys and a longtime leader in liver disease research.
Co-author Jeffrey Miner, Ph.D., co-founder and chief scientific officer of Viscient Biosciences, underscored the importance of being able to produce a high-fidelity in vitro human primary cell model of MASH. “This approach utilizes the patient’s own diseased cells, allowing them to generate the disease within the bioprinted tissue. We specifically exclude agents that artificially induce disease. We believe this advance enhances the translation of our results to human clinical trials and drug discovery.”
Researchers were able to create their model by layering a mix of primary liver cells and supporting non-parenchymal liver cells (hepatic stellate, liver sinusoidal endothelial and Kupffer) to create bioprinted 3D tissues derived from patient cells.
Notably, the resulting diseased tissues displayed fibrosis, an abnormal accumulation of collagen, which in the liver results in progressive scarring and dysfunction, leading to cirrhosis and liver cancer. With no way to stop or reverse fibrosis, the only recourse is an organ transplant.

The new models offered a peek at the underlying pathology, illuminating the roles of hepatic stellate and liver sinusoidal endothelial cells in the disease process.
“This model represents a fully human system with the potential to detect clinically active targets and therapies,” said Miner. “That’s important given that current discovery and animal models have not translated into any approved drugs.”
More about MASLD and MASH
MASLD is a spectrum of diseases characterized by excess fat (steatosis) in the liver. It affects approximately 30% of adults worldwide, with 20% of those patients developing inflammatory MASH that can progress to increasing levels of fibrosis, cirrhosis, liver failure and hepatocellular carcinoma.
In the coming years, MASH is expected to surpass hepatitis C as the main cause of liver transplantation in the United States. The mortality rate of patients with MASH is 7.9%, twice as high as that of the general population. The prevalence of MASH in the United States is estimated to double every 10 years, with approximately 43 million Americans expected to be affected by the disease by 2025.
Additional authors on the study include Philip K. Tan, Traci Ostertag, Haylee Aidnik and Keith Murphy, Viscient Biosciences; Sara B. Rosenthal and Daisy Chilin-Fuentes, UC San Diego; and Sara Linker, the Salk Institute.
The study was supported by funding from Viscient Biosciences, San Diego, California.
Disclosure: Miner and Murphy are co-founders of Viscient Biosciences. Brenner is a scientific advisor. Tan and Aidnik are employees of Viscient; Ostertag is a former employee, and Linker is a former consultant.

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