Publisher Health

Published48 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Philippa RoxbyHealth reporterThere was an “alarming” 30-fold increase in measles cases in Europe last year, the World Health Organization (WHO) says.More than 30,000 people were infected in 2023, compared to 941 during the whole of 2022.The WHO believes this is a result of fewer children being vaccinated against the disease during the Covid pandemic.Health chiefs have warned that cases are still rising and “urgent measures” are needed to prevent further spread.”We have seen, in the region, not only a 30-fold increase in measles cases, but also nearly 21,000 hospitalisations and five measles-related deaths. This is concerning,” said Dr Hans Kluge, regional director for Europe at the WHO.”Vaccination is the only way to protect children from this potentially dangerous disease,” he added.Measles can be a serious illness at any age. It often starts with a high fever and a rash, which normally clears up within 10 days – but complications can include pneumonia, meningitis, blindness and seizures.Babies who are too young to have been given their first dose of vaccine, pregnant women and those who have weakened immune systems are most at risk. During pregnancy, measles can lead to stillbirth, miscarriage and a baby being born with a low birth weight.Why are measles cases rising and what is the MMR vaccine?Measles jab campaign targets unprotected millionsVaccine push urged after measles led to boy’s deathAll countries in the European region are being asked to detect and respond to measles outbreaks quickly, alongside giving vaccines to more people.The WHO said measles had affected all age groups last year – young and old alike.Overall, two in five cases were in children aged 1-4, and one in five cases were in adults aged 20 and above.Between January and October 2023, 20,918 people across Europe were admitted to hospital with measles. In two countries, five measles-related deaths were also reported.Pandemic effectVaccination rates for the first dose of the MMR vaccine, which protects against measles, slipped from 96% in 2019 to 93% in 2022.Uptake of the second dose fell from 92% to 91% over the same period.That seemingly small drop in vaccination take-up means more than 1.8 million children in Europe missed a measles vaccination during those two years.”The Covid-19 pandemic significantly impacted immunisation system performance in this period, resulting in an accumulation of un-[vaccinated] and under-vaccinated children,” the WHO reported.With international travel booming once again, and social-distancing measures removed, the risk of measles spreading across borders and within communities is much greater – especially within under-vaccinated populations, it said.Even countries that have achieved measles elimination status are at risk of large outbreaks, the WHO warned.It say that 95% of children need to be vaccinated with two doses against measles in all communities to prevent the spread of the disease.UK health officials said last week that an outbreak of highly contagious measles in the West Midlands could spread rapidly to other towns and cities with low vaccination rates.More than 3.4 million children under the age of 16 are unprotected and at risk of becoming ill from the disease, according to NHS England.Millions of parents and carers are being contacted and urged to make an appointment to ensure their children are fully vaccinated against measles.More on this storyWhy are measles cases rising and what is the MMR vaccine?Published3 hours agoChildren’s hospital isolating measles patientsPublished1 day agoMeasles jab campaign targets unprotected millionsPublished1 day agoVaccine push urged after measles led to boy’s deathPublished3 days ago

Published23 JanuaryShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesMeasles cases are likely to spread rapidly unless more people are vaccinated, the UK Health Security Agency says.More than four million parents and carers, as well as many young adults, are being contacted because they, or their children, have missed out on one, or both, doses of the measles, mumps, rubella (MMR) vaccine.What is measles and what are the symptoms?Measles is a highly contagious disease which is spread by coughs and sneezes. Common symptoms include:high feversore, red and watery eyescoughingsneezingSmall white spots may appear inside the mouth. A blotchy red or brown rash usually appears after a few days, typically on the face and behind the ears, before spreading to the rest of the body. It can be harder to see on brown and black skin.Measles normally clears up within seven to 10 days. However, complications can include pneumonia, meningitis, blindness and seizures.Babies and young children, pregnant women and those with a weakened immune system are at increased risk.Measles can be fatal, but this is rare. Over a 22 year period, between 2000-2022, 23 children and adults died in England and Wales as a result of measles or related infections.Can adults get measles?You can catch measles at any age.If you catch it while pregnant, the disease can lead to stillbirth, miscarriage or babies being born small. The NHS urges adults to ensure they have had both doses of the MMR vaccine before starting a family.Can you catch measles twice?It is possible, but highly unlikely. The body builds up immunity to the disease after catching it.Image source, Getty ImagesHow can I get the MMR vaccine?Measles vaccinations were introduced in the UK in 1968. The current two-dose MMR vaccine was introduced in 1996 and is very effective. After both MMR doses, 99% of people are protected against measles and rubella, and 88% are protected against mumps.The first MMR dose is usually given at 12 months while the second jab is administered around three years and four months.However, adults and children can have be vaccinated at any point by their GP. Pop-up clinics are being set up at schools in areas where cases have risen. Image source, Getty ImagesPeople who do not eat pork products can request an alternative jab called Priorix.If the MMR is not suitable, someone at immediate risk of catching measles can have a treatment called human normal immunoglobulin (HNIG). Measles jab campaign targets unprotected millionsGet measles vaccine, says health boss, as cases riseWhat are the side effects of the MMR jab? Most side effects are mild. The injection site can be red, sore and swollen for a few days. Babies and young children may develop a high temperature for up to 72 hours. There is no evidence linking the MMR vaccine with autism.Researcher Andrew Wakefield wrongly claimed the two were connected in 1998. His work was later dismissed, and Mr Wakefield was struck off by the General Medical Council in 2010.How common is measles, and where are the worst outbreaks?There were 1,603 suspected cases of measles in England and Wales in 2023, according to the UK Health Security Agency (UKHSA) – a sharp rise from 735 cases in 2022 and 360 in 2021.The West Midlands, particularly Birmingham, has seen the most cases in recent months – more than 200 at the latest count.There have also been smaller outbreaks in parts of London, where only 74% of five-year-olds have had two MMR doses. In a few areas, such as Hackney in east London, nearly half of children under five are not fully vaccinated.There are also small clusters of cases in other areas of England. The World Health Organization (WHO) says there was an “alarming” 30-fold increase in measles cases across Europe in 2023.More than 30,000 people were infected, compared to 941 during the whole of 2022.Warning of further measles outbreaks as cases riseWarning measles could hit tens of thousands in LondonWhy are measles cases rising?The number of young primary school children who have had both doses of the MMR vaccine is below WHO targets.Approximately 85% of children in 2022-23 had received two MMR doses by their fifth birthday, the lowest level since 2010-11. The recommended figure is 95%.In some cities, such as Liverpool, Manchester, Birmingham and Nottingham, only 75% of five-year-olds are fully vaccinated, NHS figures show.It means more than 3.4 million children in England aged under 16 are unprotected. The WHO said vaccination rates have also fallen across Europe, leaving more than 1.8 million children at risk. Child health experts say some parents underestimated the seriousness of measles because it had largely been eradicated. In addition, many routine health appointments were missed during the Covid pandemic. There are also still people who wrongly believe the MMR jab is linked to autism. Some young adults who are not vaccinated today missed out when they were children because those fears were prevalent among new parents at the time. What should you do if you get measles?The NHS advises patients to: take paracetamol or ibuprofen to relieve fever, aches and pains – aspirin should not be given to children under 16 years oldrest and drink plenty of fluidswash their hands regularly with soap, and clean their eyes with damp cotton woolput used tissues and cotton wool in the binYou should go to A&E or phone 999 if you or your child:have shortness of breathhave a high temperature that does not come down with paracetamol or ibuprofenare coughing up bloodfeel drowsy or confused have fits (convulsions)Pregnant women or those with a weakened immune system should seek urgent medical advice after contact with someone with measles.Have you been able to access the measles vaccine? Get in touch by emailing haveyoursay@bbc.co.uk.Please include a contact number if you are willing to speak to a BBC journalist. 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Published3 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Family photographA woman has said she was “horrified” after her 80-year-old father with dementia spent 36 hours on a trolley in a hospital corridor after a fall. Gail Myerscough said her dad, Brian, was taken by ambulance to Royal Blackburn Hospital’s A&E department at about 14:00 GMT on Saturday.She said he was one of dozens of patients “in pain” and in the corridor with “no privacy or dignity”. The BBC has contacted East Lancashire Hospitals NHS trust for a response. Ms Myerscough said it was “very stressful and so upsetting” to see her father who is from Blackburn in a corridor and looking “so confused” and she had been left “traumatised”.”I’ve never seen anything like it; I was horrified,” the illustrator, from Manchester, said. ‘Really shocked’She said she had to change him in the corridor. “He had no privacy or dignity and he couldn’t sleep because it was so busy and there was nowhere for us to sit,” she said. Ms Myerscough added that the patients “didn’t get fed properly” and were only offered pre-packed sandwiches. Image source, Family photographShe said “several corridors” were filled with patients on trolleys who looked “in pain”. The 52-year-old said she was “really shocked” to see a sign on her father’s trolley which read “corridor care” and felt it was “being normalised”. “Something has to be done,” she added.Patients were warned last week that wait times at the hospital’s accident and emergency department were more than 12 hours, due to a “steep rise” in people attending. The trust said it was facing one of its busiest winters.Sharon Gilligan, chief operating officer and deputy chief executive at ELHT, added: “It means the department is very crowded and many patients are having to wait over 12 hours which is not what any of us want.”Image source, Family photographMs Myerscough praised the staff who tried to help her dad, saying she could not fault them, but felt the hospital was “under-staffed and under-resourced”.”The staff did everything they could under difficult circumstances,” she said. Ms Myerscough said she was relieved when her father was finally placed in a ward in the early hours of Monday.Why not follow BBC North West on Facebook, X and Instagram? You can also send story ideas to northwest.newsonline@bbc.co.ukMore on this storyA&E wait times hit 12 hours, hospital warnsPublished5 days agoHospital trust sees record number of A&E patientsPublished14 June 2023Patients in corridors at under pressure hospitalPublished14 December 2021NHS therapy dog gets award for work during CovidPublished14 October 2021Under pressure: One hospital’s bed dilemmaPublished8 February 2017’Times are very desperate’Published6 February 2017’Special measures’ trust now rated ‘good’Published4 January 2017Related Internet LinksEast Lancashire Hospitals NHS TrustThe BBC is not responsible for the content of external sites.

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesTheresa May would tell staff: “Go and get me the Jelly Babies,” to counteract the effects of type 1 diabetes, during her time at No 10.Lady May, diagnosed in 2013, also told the Today programme the adrenaline of Prime Minister’s Questions would make her blood-sugar levels spike.Type 1 diabetes means the body produces too little of the hormone insulin, which controls blood glucose.Lady May says she copes pretty well now but “there are good days and bad days”.The condition should not stop people from doing anything – even from becoming prime minster, as she was between 2016 and 2019, Lady May said.And she pointed to Health Secretary Victoria Atkins, who was diagnosed with type 1 as a child, like most people with the condition.Artificial-pancreas technologyWhen Lady May was told she had type 1, in her 50s, she told the consultant: “I’m too old. I can’t be.”Over time, she has learned to think “very carefully” about her blood-sugar level – mainly affected by food intake and exercise – and how to control it with daily insulin injections.But when she felt her blood sugar dropping in meetings, Jelly Babies were her “go-to”.Lady May also hailed new artificial-pancreas technology, which means thousands more people will be able to manage their condition far more easily on the NHS. The system uses a glucose sensor under the skin to automatically calculate how much insulin is delivered via a pump.Image source, Getty ImagesLady May has chaired a parliamentary inquiry into the life-threatening consequences of having both type 1 diabetes and an eating disorder.Type 1 disordered eating (T1DE) – someone restricting the amount of insulin they take, to control their weight – can lead to unstable blood-sugar levels, malnutrition and a raised risk of depression and anxiety. It is also known as diabulimia. It could be affecting up to 40% of females and 15% of males with type 1 diabetes, research suggests.The parliamentary inquiry heard from Lesley and Neal Davison, whose daughter Megan had diabulimia and killed herself aged 27.Lady May told BBC News: “When I first heard about it… the idea that a young woman could actively not take her insulin because of concern about body image – because it can lead to putting on weight – I was horrified by that.”But you can understand why young people might get into that position.”Better awareness of the condition, more mental-health support and a joined-up approach by the NHS are all needed so that healthcare professionals are aware of the “conflicting pressures” on people with type 1 and an eating disorder, Lady May said.’Isolating people’Type 1 diabetes charity JDRF UK chief executive Karen Addington said T1DE was “both devastating and widespread”.”It can be a frightening and lonely experience, isolating people from their loved ones,” she said.”If you’re experiencing symptoms, you’re not alone.”Please reach out to your GP and diabetes specialist – they’re there to guide you.”More on this storyArtificial pancreas tech could be offered on NHSPublished10 January 2023Artificial pancreas to revolutionise diabetes carePublished1 April 2022Theresa May diagnosed with diabetesPublished28 July 2013’Postcode lottery’ for diabetes monitorsPublished8 November 2018Related Internet LinksAbout type 1 diabetes – NHSThe BBC is not responsible for the content of external sites.

Autosomal dominant polycystic kidney disease (ADPKD), the most common form of polycystic kidney disease, can lead to kidney enlargement and eventual loss of function. The disease affects more than 12 million people worldwide, and many patients end up needing dialysis or a kidney transplant by the time they reach their 60s.
Researchers at MIT and Yale University School of Medicine have now found that a compound originally developed as a potential cancer treatment holds promise for treating ADPKD. The drug works by exploiting kidney cyst cells’ vulnerability to oxidative stress — a state of imbalance between damaging free radicals and beneficial antioxidants.
In a study employing two mouse models of the disease, the researchers found that the drug dramatically shrank kidney cysts without harming healthy kidney cells.
“We really believe this has potential to impact the field and provide a different treatment paradigm for this important disease,” says Bogdan Fedeles, a research scientist and program manager in MIT’s Center for Environmental Health Sciences and the lead author of the study, which appears this week in the Proceedings of the National Academy of Sciences.
John Essigmann, the William R. and Betsy P. Leitch Professor of Biological Engineering and Chemistry at MIT; Sorin Fedeles, executive director of the Polycystic Kidney Disease Outcomes Consortium and assistant professor (adjunct) at Yale University School of Medicine; and Stefan Somlo, the C.N.H. Long Professor of Medicine and Genetics and chief of nephrology at Yale University School of Medicine, are the senior authors of the paper.
Cells under stress
ADPKD typically progresses slowly. Often diagnosed when patients are in their 30s, it usually doesn’t cause serious impairment of kidney function until patients reach their 60s. The only drug that is FDA-approved to treat the disease, tolvaptan, slows growth of the cysts but has side effects that include frequent urination and possible liver damage.

Essigmann’s lab did not originally set out to study PKD; the new study grew out of work on potential new drugs for cancer. Nearly 25 years ago, MIT research scientist Robert Croy, also an author of the new PNAS study, designed compounds that contain a DNA-damaging agent known as an aniline mustard, which can induce cell death in cancer cells.
In the mid 2000s, Fedeles, then a grad student in Essigmann’s lab, along with Essigmann and Croy, discovered that in addition to damaging DNA, these compounds also induce oxidative stress by interfering with mitochondria — the organelles that generate energy for cells.
Tumor cells are already under oxidative stress because of their abnormal metabolism. When they are treated with these compounds, known as 11beta compounds, the additional disruption helps to kill the cells. In a study published in 2011, Fedeles reported that treatment with 11beta compounds significantly suppressed the growth of prostate tumors implanted in mice.
A conversation with his brother, Sorin Fedeles, who studies polycystic kidney disease, led the pair to theorize that these compounds might also be good candidates for treating kidney cysts. At the time, research in ADPKD was beginning to suggest that kidney cyst cells also experience oxidative stress, due to an abnormal metabolism that resembles that of cancer cells.
“We were talking about a mechanism of what would be a good drug for polycystic kidney disease, and we had this intuition that the compounds that I was working with might actually have an impact in ADPKD,” Bogdan Fedeles says.
The 11beta compounds work by disrupting the mitochondria’s ability to generate ATP (the molecules that cells use to store energy), as well as a cofactor known as NADPH, which can act as an antioxidant to help cells neutralize damaging free radicals. Tumor cells and kidney cyst cells tend to produce increased levels of free radicals because of the oxidative stress they’re under. When these cells are treated with 11beta compounds, the extra oxidative stress, including the further depletion of NADPH, pushes the cells over the edge.

“A little bit of oxidative stress is OK, but the cystic cells have a low threshold for tolerating it. Whereas normal cells survive treatment, the cystic cells will die because they exceed the threshold,” Essigmann says.
Shrinking cysts
Using two different mouse models of ADPKD, the researchers showed that 11beta-dichloro could significantly reduce the size of kidney cysts and improve kidney function.
The researchers also synthesized a “defanged” version of the compound called 11beta-dipropyl, which does not include any direct DNA-damaging ability and could potentially be safer for use in humans. They tested this compound in the early-onset model of PKD and found that it was as effective as 11beta-dichloro.
In all of the experiments, healthy kidney cells did not appear to be affected by the treatment. That’s because healthy cells are able to withstand a small increase in oxidative stress, unlike the diseased cells, which are highly susceptible to any new disturbances, the researchers say. In addition to restoring kidney function, the treatment also ameliorated other clinical features of ADPKD; biomarkers for tissue inflammation and fibrosis were decreased in the treated mice compared to the control animals.
The results also suggest that in patients, treatment with 11beta compounds once every few months, or even once a year, could significantly delay disease progression, and thus avoid the need for continuous, burdensome antiproliferative therapies such as tolvaptan.
“Based on what we know about the cyst growth paradigm, you could in theory treat patients in a pulsatile manner — once a year, or perhaps even less often — and have a meaningful impact on total kidney volume and kidney function,” Sorin Fedeles says.
The researchers now hope to run further tests on 11beta-dipropyl, as well as develop ways to produce it on a larger scale. They also plan to explore related compounds that could be good drug candidates for PKD.
Other MIT authors who contributed to this work include Research Scientist Nina Gubina, former postdoc Sakunchai Khumsubdee, former postdoc Denise Andrade, and former undergraduates Sally S. Liu ’20 and co-op student Jake Campolo.
The research was funded by the PKD Foundation, the U.S. Department of Defense, the National Institutes of Health, and the National Institute of Environmental Health Sciences through the Center for Environmental Health Sciences at MIT.

A research team from Purdue University’s Department of Computer Science and Institute for Digital Forestry, with collaborator Sören Pirk at Kiel University in Germany, has discovered that artificial intelligence can simulate tree growth and shape.
The DNA molecule encodes both tree shape and environmental response in one tiny, subcellular package. In work inspired by DNA, Bedrich Benes, professor of computer science, and his associates developed novel AI models that compress the information required for encoding tree form into a megabyte-sized neural model.
After training, the AI models encode the local development of trees that can be used to generate complex tree models of several gigabytes of detailed geometry as an output.
In two papers published in ACM Transactions on Graphics of the Association for Computing Machinery and IEEE Transactions on Visualizations and Computer Graphics, Benes and his co-authors describe how they created their tree-simulation AI models. “The AI models learn from large data sets to mimic the intrinsic discovered behavior,” Benes said.
Non-AI-based digital tree models are quite complicated, involving simulation algorithms that consider many mutually affecting nonlinear factors. Such models are needed in endeavors such as architecture and urban planning, as well as in the gaming and entertainment industries, to make designs more realistically appealing to their potential clients and audiences.
After working with AI models for nearly 10 years, Benes expected them to be able to significantly improve the existing methods for digital tree twins. The size of the models was surprising, however. “It’s complex behavior, but it has been compressed to rather a small amount of data,” he said.
Co-authors of the ACM Transactions on Graphics paper were Jae Joong Lee and Bosheng Li, Purdue graduate students in computer science. Co-authors of the IEEE Transactions on Visualization and Computer Graphics paper were Li and Xiaochen Zhou, also a Purdue graduate student in computer science; Songlin Fei, the Dean’s Chair in Remote Sensing and director of the Institute for Digital Forestry; and Sören Pirk of Kiel University, Germany.

The researchers used deep learning, a branch of machine learning within AI, to generate growth models for maple, oak, pine, walnut and other tree species, both with and without leaves. Deep learning involves developing software that trains AI models to perform specified tasks through linked neural networks that attempt to mimic certain functionalities of the human brain.
“Although AI has become seemingly pervasive, thus far it has mostly proved highly successful in modeling 3D geometries unrelated to nature,” Benes said. These include endeavors related to computer-aided design and improving algorithms for digital manufacturing.
“Getting a 3D geometry vegetation model has been an open problem in computer graphics for decades,” stated Benes and his co-authors in their ACM Transactions paper. Although some approaches to simulating biological behaviors are improving, they noted, “simple methods that would quickly provide many 3D models of real trees are not readily available.”
Experts with biological expertise have traditionally developed tree-growth simulations. They understand how trees interact with environmental conditions. Understanding these complicated interactions depends upon characteristics bestowed upon the tree by its DNA. These include branching angles, which are much larger for pines than for oaks, for example. The environment, meanwhile, dictates other characteristics that can result in the same type of tree grown under two different conditions displaying completely different shapes.
“Decoupling the tree’s intrinsic properties and its environmental response is extremely complicated,” Benes said. “We looked at thousands of trees, and we thought, ‘Hey, let AI learn it.’ And maybe we can then learn the essence of tree form with AI.”
Scientists typically build models based on hypotheses and observations of nature. As models created by humans, they have reasoning behind them. The researchers’ models generalize behavior from several thousand trees’ worth of input data that became encoded within the AI. Then the researchers validate that the models behave the way the input data behave.
The AI tree models’ weakness is that they lack training data that describes real-world 3D tree geometry. “In our methods, we needed to generate the data. So our AI models are not simulating nature. They are simulating tree developmental algorithms,” Benes said. He aspires to reconstruct 3D geometry data from real trees inside a computer.
“You take your cellphone, take a picture of a tree, and you get a 3D geometry inside the computer. It could be rotated. Zoom in. Zoom out,” he said. “This is next. And it’s perfectly aligned with the mission of digital forestry.”

More than 11 million people in the United States take anticoagulation or antiplatelet medications, such as heparin or aspirin, to treat serious conditions like heart attack and stroke. However, these medications also put patients at risk of life-threatening bleeding in the case of injury or during surgery. To improve strategies for reducing blood loss, a team led by investigators from Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, developed a porous material that maximizes blood absorption and effectively activates clotting mechanisms, even in patients on anticoagulation or antiplatelet medication. Findings, published in PNAS, show that the bleed-stopping material, or “hemostat,” halted bleeding within an average of about five minutes in patients on anticoagulants who underwent cardiac catheterization, a dramatic reduction from traditional compression methods that can take over two hours.
“This is a next-generation hemostat that effectively stops bleeding, even in patients who take anticoagulation or antiplatelet medications,” said corresponding author Hae Lin Jang, Ph.D., of the Center for Engineered Therapeutics. “We used an exciting, interdisciplinary approach that combines engineering principles, materials science, and understandings of molecular biology to overcome the limitations of existing therapies and address a real clinical need.”
Over 5 million people globally die each year due to trauma, with over a third of these deaths attributed to uncontrolled bleeding. The researchers used what is known as a “rational engineering” approach to develop a more effective hemostat. They began by simulating blood flow through pores to determine what microscopic design would optimize absorption. They drew inspiration from the architecture of the human lungs, which contain spherical “air sacs” called alveoli that enable a high interaction rate with blood within a short time. Alveoli have a large surface area based on their tortuous porous structure, which led the researchers to engineer a highly interconnected, spherical microporous structure in their material to rapidly absorb blood and accumulate clotting components like platelets in a highly concentrated manner, which facilitate blood clotting.
The researchers developed the alveoli-like structure using chitosan, which can be extracted from shellfish. Chitosan is already used in some hemostats: its positively charged surface is known to strongly attract negatively charged platelets and fibrinogen, the two major components of a blood clot. However, contrary to previous assumptions, the researchers discovered that chitosan also directly stimulates blood clotting by activating the TLR-2 clotting pathway, making it a viable mechanism for increasing blood clotting even in patients on anticoagulants.
The researchers demonstrated the efficacy of the material in 70 patients who underwent cardiovascular catheterization procedures while on the anticoagulant heparin, with bleeding observed to stop after a mean time of about five minutes for patients on low-dose heparin and in under about nine minutes in patients on heparin doses of up to 12,500 IU.
Other advantages of the hemostatic material included its easy application and removal. The chitosan pad eliminated the need for strong and prolonged compression, which can take several hours and requires extensive nursing. Furthermore, gauze removal can cause severe pain to patients and is frequently associated with a reoccurrence of bleeding; in contrast, the more absorptive chitosan hemostat was removed relatively cleanly from wounds and received high patient comfort scores.
The researchers are continuing to study the wound-healing process after application of the chitosan hemostat. Moreover, they are investigating other next-generation wound dressings, which may be able to deliver drugs or improve the cleanliness of the wound environment, thus reducing the need for frequent changes.
“This hemostat can save valuable time in emergency situations,” said first author Vivian K. Lee, Ph.D., of the Center for Engineered Therapeutics. “In emergencies, it can be extremely challenging to screen the prescription information of a patient to provide appropriate anticoagulation reversal therapy to patients on anticoagulants. If a hemostat can bypass a medication’s anticoagulating mechanisms, it can be used in a wide range of patients, saving time, and potentially saving lives.”

Cleft lip and palate are the most common craniofacial birth defects in humans, affecting more than 175,000 newborns around the world each year. Yet despite decades of research, it’s still not known what causes most cases or what can be done to prevent them. But a recent study from the University of Wisconsin School of Veterinary Medicine (SVM) has uncovered new information about orofacial development in mice that researchers believe could one day help reduce the risk of these birth defects in humans.
Published this week in the Proceedings of the National Academy of Sciences (PNAS) the study provides the first direct evidence of a mechanism called DNA methylation being required for craniofacial development. DNA methylation is a process where a group of molecules are added to DNA that change the expression of genes without actually altering the DNA sequence. It’s also affected by various environmental factors. The researchers discovered that disruption to DNA methylation interferes with development of the lip and palate and causes these birth defects in mice.
Led by Robert Lipinski, associate professor of comparative biosciences at the UW School of Veterinary Medicine, the research is an important step toward developing preventive strategies that could one day lessen the risk of cleft lip and palate, known collectively as orofacial clefts (OFCs), in both animals and humans.
“We knew from past research that genetics and the environment interact to cause these types of birth defects, but our understanding of the environmental component lagged far behind that of genetics.” says Lipinski. “Unlike genetics, we don’t have a permanent record of the prenatal environment that can be examined retrospectively, but connecting OFCs to DNA methylation helps narrow our focus on the particular environmental influences that modify the risk for these types of birth defects.”
His team’s work confirmed the essential role of DNA methylation in regulating orofacial development during embryonic development and demonstrates how disruptions to that process alter the ability of stem cells to form the connective tissue of craniofacial bone and cartilage, resulting in OFCs.
Lipinski and his team arrived at these results by first genetically manipulating DNA methylation in two separate groups of mouse embryos. The experiments resulted in seemingly contradictory results, with OFCs developing in one group of mice, but not the other. To understand why there was a difference between the groups, the team conducted another round of experiments in which they inhibited DNA methylation in mouse embryos at different stages of development. The timing of when DNA methylation occurs, was critical to the development of orofacial clefts.
They found that exposure on the 10th gestational day resulted in OFCs but administering the same inhibitor just 48 hours later resulted in normal orofacial development.

Identifying this narrow window of gestational sensitivity is important, Lipinski says, because it not only helps narrow the focus of the next stage of his team’s research but it will also help design future public education initiatives once more is known about the modifiable environmental and behavioral risk factors that impact OFC risk in humans. The 10th gestational day in mouse embryos corresponds with the beginning of the 5th week of embryonic development in humans-a stage at which many pregnancies may not yet be recognized.
“We know DNA methylation can be influenced by a variety of environmental factors, including maternal stress, diet, and exposure to drugs, toxins and environmental pollutants, and having a better understanding how orofacial development is regulated by environmentally sensitive mechanisms could directly inform birth defect prevention strategies,” he says. “This next phase of our team’s research is focused on identifying specific factors that influence DNA methylation during orofacial development and which could therefore alter OFC risk.”
Lipinski and his team are uniquely positioned to pursue this next stage of research because of another important outcome of the study: a new in vitro model the team developed. The model will allow them to rapidly screen thousands of dietary and environmental factors in a laboratory dish before testing the impact of specific factors on cleft susceptibility in mouse models.
The results in cell and animal models will help the researchers more quickly and accurately identify factors likely to be of consequence to human development[ETM1] .
Orofacial clefts of the upper lip and palate affect approximately 1 in 700 newborns, and individuals with OFCs navigate feeding difficulties as infants that require multiple surgeries, dental procedures, and speech therapy during childhood and adolescence. Studies have shown higher mortality rates at all stages of life for individuals with OFCs.
This study was supported by funding from the National Institutes of Health under award numbers R03DE027162, R56DE030917, RO1DE032710, U01 DK11807, and R01DK099328, and T32ES007015. Additional support was also provided by the University of Wisconsin Hilldale Undergraduate Research Award.

Low back pain is a major cause of disability around the globe, with more than 570 million people affected. In the United States alone, health care spending on low back pain was $134.5 billion between 1996 and 2016, and costs are increasing.
“The good news is that most episodes of back pain recover, and this is the case even if you have already had back pain for a couple of months,” University of South Australia Professor Lorimer Moseley says.
“The bad news is that once you have had back pain for more than a few months, the chance of recovery is much lower. This reminds us that although nearly everyone experiences back pain, some people do better than others, but we don’t completely understand why.”
The systematic review and meta-analysis, conducted by an international team of researchers, included 95 studies with the goal of understanding the clinical course of acute (< 6 weeks), subacute (6 to less than 12 weeks) and persistent (12 to less than 52 weeks) low back pain. For people with new back pain, pain and mobility problems lessened significantly in the first 6 weeks, but then recovery slowed. This study filled a gap in a 2012 paper from the same research team, with new findings showing that many people with persistent low back pain (more than 12 weeks) continue to have moderate-to-high levels of pain and disability. "These findings make it clear that back pain can persist even when the initial injury has healed," Prof Moseley says. "In these situations, back pain is associated with pain system hypersensitivity, not ongoing back injury. This means that if you have chronic back pain -- back pain on most days for more than a few months -- then it's time to take a new approach to getting better." He notes that there are new treatments based on training both the brain and body that "focus on first understanding that chronic back pain is not a simple problem, which is why it does not have a simple solution, and then on slowly reducing pain system sensitivity while increasing your function and participation in meaningful activities." The authors state that identifying slowed recovery in people with subacute low back pain is important so that care can be escalated and the likelihood of persistent pain reduced. Further research into treatments is needed to help address this common and debilitating condition, and to better understand it in people younger than 18 and older than 60 years.

During the past decade, there has been significant development of new sulfur containing compounds that are used in various industries, including pharmaceuticals and agricultural products. Sulfoximines, sulfonimidoyl fluorides and sulfonimidamides are types of sulfur-containing chemical compounds that have wide-ranging potential as therapeutic drugs. However, the synthesis process for these compounds is complex and has several limitations. In a new article published in Nature Chemistry, Moffitt Cancer Center researchers describe their development of a new reagent that allows a more efficient approach to make sulfoximines, sulfonimidoyl fluorides and sulfonimidamides that may be used in medicines.
There are four main chemical approaches that are commonly used to create sulfoximines, sulfonimidoyl fluorides and sulfonimidamides. Recently an additional approach called sulfur fluorine exchange (SuFEx) chemistry has gained attention. But the approach has several limitations to its widespread use, such as the requirement for the use of high pressures.
The Moffitt research team wanted to develop a more efficient process to create sulfoximines, sulfonimidoyl fluorides and sulfonimidamides. Through a variety of chemical experiments and processes, they developed a reagent called t-BuSF that serves as a hub in the SuFEx chemical process to synthesize these sulfur-containing compounds. The use of t-BuSF decreased the number of steps required to make these compounds and improved the reaction times and stability of their chemical precursors. The researchers further demonstrated the potential utility of t-BuSF in medicinal chemistry in over 70 examples and by preparing five therapeutical targets and intermediates. They showed that t-BuSF was able to create these products in high yields with fewer synthesis steps.
“Given the cost-effectiveness and the chemical space accessible from this reagent platform, it is expected to have positive impacts on the discovery sciences from the development of new medicines and agrochemicals to the discovery of new ligands, organocatalysts and materials,” said Justin Lopchuk, Ph.D., associate member of the Department of Drug Discovery at Moffitt.
This study was supported by the National Institutes of Health (R35-GM142577, P30-CA076292) and the University of South Florida’s Chemical Purification, Analysis, and Screening Core Facility.