Publisher Health

A new biocompatible polymer-based composite material could soon replace metal plates in treating difficult and unstable fractures. Developed at KTH Royal Institute of Technology in Stockholm, the newly-developed material is as strong as dental composites yet non-toxic.
The material and a surgical method, which were published in Advanced Functional Materials, will be used in clinical studies in 2023 and 2024, with a focus on hand fractures.
Michael Malkoch, professor of fibre and polymer technology at KTH, says that the material and method, AdhFix, will enable customized plating for fixation of fractures with a more comfortable, less complicated recovery. Collarbone and rib fractures in particular are ideally suited for the proposed treatment, since such injuries are not easy to stabilize.
Metal plates cannot be easily customized in shape, and they tend to adhere to soft tissue, resulting in debilitating complications, says Malkoch. For example, researchers in the U.S. have found that nearly 64 percent of finger fractures treated with metal plates result in mobility complications.
The alternative surgical method, AdhFix, combines screws with a build-up of the polymer/hydroxyapatite composite instead. The composite is shaped in situ before being rapidly cured on demand via high-energy visible-light-induced thiol-ene coupling chemistry.
Evaluations on human cadaver hands with proximal phalanx fractures show that AdhFix withstands the forces from finger flexing exercises. In models of in vivo femur fractures in rats, the methodology supported bone healing without degradation, adverse effects or soft-tissue adhesions.
“No fracture is the same as the other, this is one of the absolute advantages of the material,” says Malkoch. “A surgeon can tailor the fixation plate according to the patient’s bone shape and the structure of the fracture. The hospital also does not have to store metal plates.”
Malkoch says the material and method also may be applied to veterinary care as well. Animals with metal plates are known to avoid going outdoors in cool temperatures because the metal conducts the cold differently than the KTH researchers’ composite.
The work was carried out with RISE in Gothenburg and hand surgeons working at Karolinska Institutet and Södersjukhuset. Daniel Hutchinson, researcher in polymer and fibre technology at KTH, led the study.
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Materials provided by KTH, Royal Institute of Technology. Note: Content may be edited for style and length.

A rare genetic defect that affects the so-called ALG2 gene can cause serious metabolic diseases in humans. It does so through the defective formation of proteins and sugar molecules. Until now, its rareness and complexity made it difficult to study this congenital glycosylation disorder. A research team led by Prof. Dr Joachim Wittbrodt and Dr Thomas Thumberger from the Centre for Organismal Studies (COS) of Heidelberg University has finally succeeded in introducing the underlying mutation in the ALG2 gene in a fish model, thus allowing the causes of these complex diseases to be studied at the molecular level.
Human cells are kept alive by the activity of millions of proteins. As they mature, these proteins must be modified in a myriad of ways, such as through the addition of sugar molecules — a crucial change for proper function. Defects in this sugar-adding process, also known as sugar decoration, are often lethal at the very early stages of development. As Prof. Wittbrodt explains, in rare cases a genetic defect causes sugar-addition deficiencies, which then manifest as congenital disorders of glycosylation. “Correct protein glycosylation requires a number of enzymes functioning together like clockwork,” states the researcher. The ALG2 gene has an especially important task in this process. It codes an enzyme needed for the correct branching of the sugar chain. If this process is disturbed, patients appear unaffected at birth but develop problems in different organs, such as the eyes, brain, and muscles, during early childhood.
The team led by Prof. Wittbrodt and Dr Thumberger used the CRISPR/Cas9 gene editing scissors to introduce an ALG2 mutation in a fish model, the Japanese rice fish or medaka. “Fish are particularly good models for these disorders because they develop outside the mother, making them very suitable for studying early embryonic defects,” explains Dr Thumberger. In addition, the genome of the Japanese rice fish can be edited efficiently and precisely. “Our fish are genetic twins, so to speak, so the effect of individual changes can be directly identified as compared to non-genetically altered fish.”
Although the evolutionary distance between humans and fish is vast, the researchers report many of the same symptoms in the fish model that appear in ALG2 patients, including specific neuronal defects. They were surprised by the results yielded by the analysis of the total medaka organism, which took into account the full spectrum of different cell types. “Although all cells of the fish showed the same reduced ALG2 activity, some cell types were more affected than others,” states Prof. Wittbrodt. In the retina of the fish eye, cone cells needed for colour-sensing were unaffected, but there was a progressive loss of rod cells needed for vision in low light, thus rendering the fish night-blind. Now the researchers hope to identify the proteins that cause the rod cells to die off because of diminished sugar binding.
“Our studies on the medaka fish model showed that all symptoms could be prevented by supplying fully functional ALG2 mRNA — the blueprint for producing the correct ALG2 enzyme. We were able to effectively reverse the genetic defect in the fish model. That means that we can now systematically analyse the individual function areas of the ALG2 enzyme. We are particularly interested in the cell type-specific response in the context of the whole organism,” stresses Joachim Wittbrodt. Building on this research, the Heidelberg research team plans to study the molecular mechanisms and causes for the development of such complex metabolic diseases in humans.
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Materials provided by University of Heidelberg. Note: Content may be edited for style and length.

Children who were exposed to higher levels of trace minerals manganese and selenium during their mothers’ pregnancy had a lower risk of high blood pressure in childhood, according to a study led by researchers at the Johns Hopkins Bloomberg School of Public Health.
The researchers analyzed the levels of toxic metals and trace minerals in blood samples drawn from nearly 1,200 women in the Boston area who gave birth between 2002 and 2013. They found that higher levels of selenium or manganese in the mothers’ blood were associated with lower blood pressure readings in their children at clinic visits 3 to 15 years later.
The researchers also observed that manganese had a stronger inverse relationship with childhood blood pressure when maternal blood levels of cadmium, a toxic heavy metal, were higher — hinting that manganese lowers blood pressure in part by countering a blood pressure-raising effect of cadmium.
The results appear online June 23 in Environmental Health Perspectives.
“These results suggest that healthy levels of selenium and manganese in mothers’ diets during pregnancy may protect their children against developing high blood pressure,” says study senior author Noel Mueller, PhD, assistant professor in the Bloomberg School’s Department of Epidemiology. “This work highlights the importance of nutrition and environmental exposures in the womb for a child’s cardiovascular health and, as we continue research this further, could eventually lead to updated nutritional guidance and environmental regulations aimed at preventing disease.”
Hypertension is one of the major modifiable risk factors for other debilitating and deadly diseases including heart disease, stroke, kidney failure, and Alzheimer’s disease. It is also very common; the U.S. Centers for Disease Control and Prevention estimates that about half of Americans over the age of 20 have hypertension — defined as systolic blood pressure above 130 mm Hg or diastolic blood pressure above 80 mm Hg — or have been prescribed antihypertensive drugs.

Vaccines minister Nadhim Zahawi says the UK’s vaccination programme has passed another key milestone, with more than 60% of the adult population now fully vaccinated.Speaking at a Downing Street briefing he said: “The vaccination programme has been delivered in the community, by the community and for the community”.

A paper published in the journal Nature Medicine on long-COVID, describes persistent symptoms six months after acute COVID-19, even in young home isolated people.
The study from the Bergen COVID-19 Research Group followed infected patients during the first pandemic wave in Bergen Norway.
“The main novel finding is that more than fifty per cent of young adults up to 30 years old, isolated at home, still have persistent symptoms six months after mild to moderate disease,” the leader of the group, Professor Nina Langeland explains.
The most common symptoms were loss of smell and/or taste, fatigue, shortness of breath, impaired concentration, and memory problems.
“There was a significant correlation between high antibody levels and symptoms in home isolated patients, other risk factors for symptoms were asthma or other chronic lung disease,” says Professor Rebecca Cox, Head of the Influenza Centre at University of Bergen and Haukeland University Hospital and co-leader of the research group.
Impaired memory and concentration difficulties
In non-hospitalized COVID-19-patients, thirty per cent experienced fatigue which was the most common symptom. Children under the age of 16 years had fewer long-term symptoms than adults, but Associate Professor Bjørn Blomberg, and first author of the article, underlines:
“The cognitive symptoms of impaired memory and concentration difficulties are particularly worrying for young people at school or university and highlights the importance of vaccination to prevent the long-term health implications of COVID-19.”
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Materials provided by The University of Bergen. Original written by Ingrid Ovidie Lydersen Hagerup. Note: Content may be edited for style and length.

A new study by Penn State researchers, who looked at emergency room admissions across the U.S. over a recent five-year period in a novel way, suggests that the agriculture industry is even more dangerous than previously believed.
The research revealed that from Jan. 1, 2015, to Dec. 31, 2019, more than 60,000 people were treated in emergency departments for nonfatal, agricultural-related injuries. Significantly, nearly a third of those injured were youths, according to study author Judd Michael, Nationwide Insurance Professor of Agricultural Safety and Health and professor of agricultural and biological engineering, College of Agricultural Sciences.
“This study revealed the true magnitude of the agricultural-related injury problem,” he said. “We were slightly surprised at the sheer number of farm-related injuries and concerned by the high number of youths who were injured.”
Before this research, knowledge of nonfatal agricultural injuries was somewhat limited by the available sources of information, Michael noted. Existing data are based mostly on regional or national periodic surveys, he added. The Bureau of Labor Statistics captures only nonfatal occupational injuries through its Survey of Occupational Injuries and Illnesses, often called the SOII.
That survey collects data on work-related nonfatal injuries and illnesses among employees in all industries in the U.S. But its data exclude self-employed farmers and family members as well as workers on farms with fewer than 11 employees.
“It has been estimated that the SOII was undercounting occupational injuries and illnesses in agriculture by about 78%,” Michael said.

Stem cell therapy is at the cutting edge of regenerative medicine, but until now researchers and clinicians have had to painstakingly evaluate stem cell quality by looking at each cell individually under a microscope. Now, researchers from Japan have found a way to speed up this process, using the power of artificial intelligence (AI).
In a study published in February in Stem Cells, researchers from Tokyo Medical and Dental University (TMDU) reported that their AI system, called DeepACT, can identify healthy, productive skin stem cells with the same accuracy that a human can.
Stem cells are able to develop into several different kinds of mature cells, which means they can be used to grow new tissues in cases of injury or disease. Keratinocyte (skin) stem cells are used to treat inherited skin diseases and to grow sheets of skin that is used to repair large burns.
“Keratinocyte stem cells are one of the few types of adult stem cells that grow well in the lab. The healthiest keratinocytes move more quickly than less healthy cells, so they can be identified by the eye using a microscope,” explains Takuya Hirose, one of the lead authors of the study. “However, this method is time-consuming, labor-intensive, and error-prone.”
To address this, the researchers aimed to develop a system that would identify and track the movement of these stem cells automatically.
“We trained this system through a process called ‘deep learning’ using a library of sample images,” says the co-lead author, Jun’ichi Kotoku. “Then we tested it on a new group of images and found that the results were very accurate compared with manual analysis.”
In addition to detecting individual stem cells, the DeepACT system also calculates the ‘motion index’ of each colony, which indicates how fast thecells at the central region of the colony move compared with those at the marginal region. The colonies with the highest motion index were much more likely than the colonies with lower motion index to grow well, making them good candidates for generating sheets of new skin for transplantation to burn patients.
“DeepACT is a powerful new way to perform accurate quality control of human keratinocyte stem cells and will make this process both more reliable and more efficient,” states Daisuke Nanba, senior author.
Given that skin transplants can fail if they contain too many unhealthy or unproductive stem cells, being able to quickly and easily identify the most suitable cells would be a considerable clinical advantage. Automated quality control could also be valuable for industrial stem cell manufacturing, to help ensure a stable cell supply and lower production costs.
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Materials provided by Tokyo Medical and Dental University. Note: Content may be edited for style and length.

An accurate, non-invasive, and low-cost method of testing for COVID-19 using samples taken from the screens of mobile phones has been developed by a team led by UCL researchers at Diagnosis Biotech.
The study, published in eLife and led by Dr Rodrigo Young (UCL Institute of Ophthalmology), analysed swabs from smartphone screens rather than directly from people, and found that people who tested positive by the regular nasal swabbing PCRs were also positive when samples were taken from phone screens.
The new method — known as Phone Screen Testing (PoST) — detected the COVID-19 virus on the phones of 81 to 100% of contagious people with a high viral load, suggesting it is as accurate as antigen lateral flow tests.
Globally active screening for COVID-19 is still a priority as new variants keep emerging and the vaccination rollout is not guaranteed in many countries. However, testing is expensive and can be physically unpleasant, both of which are significant hurdles on the road to an effective test and trace system.
As PoST is an environmental test, rather than a clinical test, it is both non-invasive and less expensive that a traditional nasal swabbing PCR. This means not only is it suitable for rollout in lower-income countries, but it also removes the discomfort of current COVID-19 testing options, potentially increasing take-up of regular testing among the general population. In addition, PoST sampling takes less than a minute and does not require medical personnel, which eases mass adoption in big facilities and large-scale applications.
Dr Rodrigo Young said: “Like many, I was very worried about the economic and social impact that the pandemic would leave behind, particularly in lower-income countries. We knew that the only effective way to stop the spreading is to regularly test as many people as possible, but this was not happening because it’s too expensive and uncomfortable.
“We immediately knew this was something special, as PoST is a method that would not only make COVID-19 mass testing much easier but could also be used to contain outbreaks of new naturally occurring and man-made viruses, to avoid future pandemics.”
Diagnosis Biotech, a Chilean startup founded by UCL’s Dr Young, has been performing COVID-19 screenings in companies and schools in Chile to avoid outbreaks and maintain operational continuity, as frequent measurement of all workers or students allows the early identification of asymptomatic people and helps to control the spread of the virus.
A machine is currently under development by Diagnosis Biotech which will build on this research, safely taking a phone for PoST sampling and deliver the results directly via SMS to minimise contact.
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Materials provided by University College London. Note: Content may be edited for style and length.

Advisers to the Centers for Disease Control and Prevention are scheduled to meet on Wednesday to address reports of rare heart problems in young people immunized with the coronavirus vaccines made by Pfizer-BioNTech and Moderna.The reports involve conditions called myocarditis, inflammation of the heart muscle; and pericarditis, inflammation of the membrane surrounding the heart. Most cases have been mild, with symptoms like fatigue, chest pain and disturbances in heart rhythm that quickly clear up. The agency is tracking nearly 800 reports, although not all have definitively been linked to the vaccines.The C.D.C. advisers’ meeting comes as the Biden administration publicly acknowledges that it expects to fall short of its goal of getting 70 percent of Americans partly vaccinated by July 4. The shortfall, officials said on Tuesday, results in part from reluctance among younger Americans to be immunized.Experts have said that the benefits of immunization far outweigh the risk of the possible problems, but they are expected to revisit that debate, particularly for adolescents and young adults.More than half of the heart problems were reported in Americans ages 12 to 24, while that age group accounted for only 9 percent of the millions of doses administered. The numbers are higher than would be expected for those ages.As of May 31, 216 people had experienced myocarditis or pericarditis after one dose of either vaccine, and 573 after the second dose. While most cases were mild, 15 patients remained in hospitals at that time. The second dose of the Pfizer-BioNTech vaccine was linked to about twice as many cases as the second dose of the vaccine made by Moderna.“We look forward to more clarity regarding the potential risk of myocarditis after mRNA vaccines to increase vaccine confidence and vaccination rates,” said Dr. Yvonne Maldonado, chair of the Committee on Infectious Diseases at the American Academy of Pediatrics.Recommendations from the C.D.C. advisers after Wednesday’s meeting may also influence decisions to immunize children younger than 12 when vaccines become available for that age group. Some experts have questioned whether the benefits to children outweigh the potential risks, given the low odds of serious illness in young children.The C.D.C. strongly recommends Covid-19 vaccines for Americans ages 12 and older. The agency reported this month that the number of hospitalizations related to Covid-19 among adolescents in the United States was about three times higher than hospitalizations linked to influenza over three recent flu seasons.As of June 10, nearly 17,000 children in 24 states had been hospitalized for Covid-19 and 330 children had died, according to data collected by the American Academy of Pediatrics.

By the time people with Alzheimer’s disease start exhibiting difficulty remembering and thinking, the disease has been developing in their brains for two decades or more, and their brain tissue already has sustained damage. As the disease progresses, the damage accumulates, and their symptoms worsen.
Researchers at Washington University School of Medicine in St. Louis have found that high levels of a normal protein associated with reduced heart disease also protect against Alzheimer’s-like brain damage — at least in mice. The findings, published June 21 in Neuron, suggest that raising levels of the protein — known as low-density lipoprotein receptor (LDL receptor) — could potentially be a way to slow or stop cognitive decline.
The discovery of LDL receptor as a potential therapeutic target for dementia is surprising since the protein is much better known for its role in cholesterol metabolism. Statins and PCSK9 inhibitors, two groups of drugs widely prescribed for cardiovascular disease, work in part by increasing levels of LDL receptor in the liver and some other tissues. It is not known whether they affect LDL receptor levels in the brain.
“There are not yet clearly effective therapies to preserve cognitive function in people with Alzheimer’s disease,” said senior author David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. “We found that increasing LDL receptor in the brain strongly decreases neurodegeneration and protects against brain injury in mice. If you could increase LDL receptor in the brain with a small molecule or other approach, it could be a very attractive treatment strategy.”
The key to the importance of LDL receptor lies in a different protein, APOE, that also is linked to both cholesterol metabolism and Alzheimer’s disease. High cholesterol in the blood is associated with increased risk of Alzheimer’s disease, although the exact nature of the association is unclear.
During the long, slow development of Alzheimer’s disease, plaques of a protein called amyloid gradually accumulate in the brain. After many years, another brain protein called tau starts forming tangles that become detectable just before Alzheimer’s symptoms arise. The tangles are thought to be toxic to neurons, and their spread through the brain foretells the death of brain tissue and cognitive decline. First author Yang Shi, PhD, a postdoctoral researcher, and Holtzman previously showed that APOE drives tau-mediated degeneration in the brain by activating microglia, the brain’s cellular janitorial crew. Once activated, microglia can injure neural tissue in their zeal to clean up molecular debris.
Higher levels of LDL receptor limit the damage APOE can do in part by binding to APOE and degrading it. Higher levels of LDL receptor in the brain, therefore, should pull more APOE out of the fluid surrounding brain cells and mitigate damage even further, the researchers reasoned.
As part of this study, Shi, Holtzman and colleagues including co-senior author Jason Ulrich, PhD, an associate professor of neurology, studied mice predisposed to develop Alzheimer’s-like neurodegeneration because they had been genetically modified to develop tau buildup in the brain, much like people with Alzheimer’s disease and other forms of dementia. The researchers bred the tau mice with mice genetically modified to express high levels of LDL receptor in their brains. The resulting offspring had high levels of LDL receptor and a propensity to develop Alzheimer’s-like brain damage by the time they were 9 months old, which is similar to middle age in a person.
Then, the researchers compared the four groups: normal mice, tau mice, mice with high levels of LDL receptor, and tau mice with high levels of LDL receptor. At 9 months, the normal mice and the mice with high levels of LDL receptor had healthy looking brains. The tau mice had severe brain atrophy and neurological damage. In comparison, the tau mice with high levels of LDL receptor were in much better shape. They had significantly less brain shrinkage and damage, their levels of certain forms of tau and APOE were significantly lower, and their microglia were shifted toward a less damaging pattern of activation.
“Alzheimer’s develops slowly through multiple phases, and the degeneration phase when tau is building up is when the symptoms arise and worsen,” Holtzman said. “In terms of quality of life for people with Alzheimer’s, this is a phase in which it would be great if we could intervene. I think this LDL receptor pathway is a good candidate because it has a strong effect, and we know it can be targeted in other parts of the body. This has motivated us over the last few years to try to develop programs to modulate the receptor in other ways.”
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Materials provided by Washington University School of Medicine. Original written by Tamara Bhandari. Note: Content may be edited for style and length.