Publisher Health

Like DNA, RNA molecules contain information through unique combinations of four different nucleotides. However, through a molecular process called RNA editing, chemical changes can be made to adenosine nucleotides that convert them to a nucleotide called inosine by enzymes known as adenosine deaminases (ADARs). ADAR-mediated RNA modification is essential for survival and two ADARs, ADAR1 and ADAR2, have been identified in mammals. In a recently published article in Immunity, a group at Osaka University studied mice containing specific mutations in ADAR1 and found that defects in the mutant enzyme RNA binding led to abnormal growth and development in the mice.
Two versions of ADAR1 protein exist in mouse cells: p110 and p150. Previous research suggested that ADAR1 edits double-stranded RNA (dsRNA) so that a cellular sensor called MDA5 recognizes it correctly as “self” RNA and does not mistake it for viral RNA (which would lead MDA5 to induce an immune response). Interestingly, the ADAR1 p150 enzyme contains a specific binding domain for a special type of RNA called Z-RNA. Double-stranded RNA typically forms a right-handed helical structure but Z-RNA is dsRNA that forms a left-handed structure.
“Mutations in ADAR1 p150, including within the domain that recognizes Z-RNA, have been associated with a genetic inflammatory disorder known as Aicardi-Goutières syndrome (AGS),” says lead author of the study Taisuke Nakahama. “We wanted to examine how this biological function affects AGS pathogenesis.”
To investigate this, the team generated genetically altered lab mice that had a point mutation in both alleles of the gene encoding ADAR1 p150. This mutation abolished the Z-RNA binding ability of the mutant ADAR1. Mutant mice showed severely inhibited growth relative to wild-type (non-mutant) mice.
“Mutant mice had abnormally developed organs, including critical ones like the brain, spleen, and colon,” explains senior author Yukio Kawahara. “Fascinatingly, their malformed brains showed characteristics similar to those of encephalopathy observed in human AGS patients.”
Mutant mice also displayed high expression levels of interferon-stimulated genes, resulting in a chronic inflammatory state. Through additional mechanistic experiments, the team demonstrated that the ADAR1 p150 Z-binding domain is essential for proper RNA editing catalyzed by this enzyme.
“Our work suggests that this domain’s interaction with Z-RNA is a critical initial step for preventing the immune system from believing this molecule is a foreign invader,” explains Nakahama.
This study pinpoints improper Z-RNA recognition as a contributor to AGS pathogenesis. These findings will assist in the development of novel therapeutic methods for treating this disorder and may also help us further understand responses to infections of RNA viruses like SARS-CoV-2.
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New testing methods, developed by Newcastle University scientists, provide a simple and more precise way to quantify the transmission and spread of antimicrobial resistance (AMR).
Researchers from Newcastle University, and colleagues from Spain, Canada and Egypt, have successfully trialled two new qPCR assays to help detect the presence of transmissible AMR using water and wastewater samples. Publishing their results in the journal Water Research, the scientists present a DNA-based testing method that provides a surrogate for monitoring AMR, which will make AMR screening cheaper and more accessible around the world.
The study presents a method, which is similar to methods used on wastewater samples to detect SARS-CoV-2, that differentiates between bacteria who are carrying AMR genes versus no AMR genes. There is currently no simple “silver bullet” assay for triaging AMR based on DNA from wastewater — this new assay may provide this role. It can be used for rapid screening of transmissible AMR to identify locations where more expensive analysis can be justified.
Study co-author, Professor David Graham, of Newcastle University’s School of Engineering, said: “The use of wastewater is becoming an increasingly vital tool for guiding healthcare decisions during the pandemic. We have shown that the same principle can be used to address other problems, including reducing the spread of superbugs. The method provides a more exact way of determining AMR by measuring DNA in wastewater samples.”
AMR is major global public health issue that has implications on the effective treatment of a growing number of infections caused by bacteria, parasites, viruses and fungi. Antibiotic use selects for resistance strains in human and animal wastes, which can be released to the environment via wastewater, spreading antibiotic resistance genes (ARGs) and bacteria across nature.
The findings are especially important in light of a recent report by the World Economic Forum on the economic cost of AMR, in which Professor Graham was a co-contributor. The report showed that the cost of AMR is closely related to the capacity of local healthcare systems, with areas without robust healthcare surveillance seeing the greatest levels of AMR and healthcare costs. The report showed AMR costs to the wider economy due to reduced labour supply result in worktime and productivity losses, with waterborne AMR leading to 3.5 million additional sick days yearly, at a cost of $300 million globally.
Study co-author Dr Marcos Baluja, of Newcastle University’s School of Engineering added: “We are now aware of the environmental dimension of AMR and its implication in public health. At Newcastle University, we work to understand this complex ecological and evolutionary problem and design feasible methods to identify the hotspot of AMR selection and maintenance in the environment. These tools are crucial to efficiently interrogate the environment and design comprehensive strategies to mitigate dissemination of environmental sources of AMR.”
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A non-toxic, bacteria-based system developed at the University of Massachusetts Amherst can detect when it is inside a cancer cell and then release its payload of therapeutic drugs directly into the cell. The work, published in Nature Communications today, could lead to effective, targeted therapies for currently untreatable cancers, such as liver or metastatic breast cancer.
The inability to penetrate solid tumor cell membranes has, until now, prevented researchers from being able to effectively target critical cancer pathways. Current delivery methods, such as nanoparticles, cell-penetrating peptides and antibody drug conjugates, have limited efficacy because of their poor ability to enter cells, their inability to specifically target cancer cells, and their susceptibility to degradation from the cell’s natural protection against foreign invaders.
The groundbreaking UMass Amherst work has demonstrated in the lab that not only can it easily enter cells, but it can specifically target cancer cells to deliver proteins (drugs) directly while leaving healthy cells alone. And once its protein payload is delivered, the bacteria dissipate and clear.
“We can actually detect [the protein] in the tumors, but we can’t detect it in the livers and spleens” of mouse models, says Neil Forbes, chemical engineering and Institute for Applied Life Science, whose lab conducted the research. “It delivers it just to the tumors. When we looked at the immune response and the liver damage, we didn’t see any difference to saline.”
The delivery system was developed by Nele Van Dessel, bioengineer and co-first author on the paper, as a post-doc in Forbes’s lab. It uses a highly modified type of salmonella that is injected into the bloodstream.
Salmonella are known to accumulate in tumors, but it was not known that they invade cancer cells. Van Dessel’s system can accurately measure this cell penetration because the engineered salmonella turn green once they breach the cell membrane.

The skin bacterium Staphylococcus aureus often develops antibiotic resistance. It can then cause infections that are difficult to treat. Researchers at the University of Bonn have uncovered an ingenious way in which a certain strain of Staphylococcus aureus protects itself against the important antibiotic vancomycin. The results have now been published in the journal Microbiology Spectrum.
In the study, the researchers investigated the development of resistance in a Staphylococcus aureus strain that is innocuous to humans. For this purpose, they grew the strain in the laboratory in nutrient media to which they added successively increasing amounts of vancomycin. Staphylococci are rapidly mutating bacteria. The strain studied also lacks a mechanism that normally repairs these genetic changes. This means it acquires new properties particularly quickly, including those associated with greater tolerance to vancomycin. In the presence of the antibiotic, only these mutants survive.
“This gave us a strain within eight weeks that was able to cope with more than a 100-fold increase in the concentration of the antibiotic,” explains Prof. Dr. Gabriele Bierbaum from the Institute of Medical Microbiology, Immunology and Parasitology at the University Hospital Bonn. The researchers now wanted to find out how the strain, with the designation VC40 manages this.
Molecular protective suit
Bacteria are single-celled organisms that are enclosed in a thin membrane of lipids. This is almost as delicate as a soap bubble and the internal pressure of the staphylococcal cell would burst the membrane. The membrane is therefore surrounded by a cell wall, which encloses the bacterium like an extremely robust protective garment. This wall consists of several layers of carbohydrate chains that are cross-linked by peptides, the peptidoglycan. This creates a stable fabric.
Staphylococci and other bacteria produce the basic building blocks of this fabric within the cell and then transport them out through the membrane. The antibiotic vancomycin traps them there and prevents them from being incorporated into the wall. As a result, the cells die.

Collagen, the main component of the skin’s extracellular matrix, can cause a pathological condition if it is in excess. Applying an electric field to the skin affects collagen pathways, temporarily reducing collagen production and increasing its degradation. This is what researchers from the CNRS, Université Toulouse III — Paul Sabatier and Toulouse INP have just demonstrated, along with an Israeli researcher1. Published on 21 October 2021 in the Journal of Investigative Dermatology, these results open new therapeutic perspectives for the topical treatment of skin fibrosis characterized by excessive collagen deposition.
When an electric field is applied around a tumour, it “permeabilizes” the cells locally and temporarily. This permeabilization ensures, for example, the massive entry of anticancer molecules into cells and tissues, which reduces the amount of doses injected into patients and limits side effects: this is the hospital-based approach of electrochemotherapy that has been used to treat skin tumours since the 1980s.
Interestingly, physicians using this method, and for that matter the patients themselves, have observed an aesthetic and functional healing of the sites treated in this way. However, the mechanisms behind this observation had never been elucidated.
A research team, involving researchers from the CNRS, the Université Toulouse III — Paul Sabatier and Toulouse INP, used a highly sophisticated synthetic skin model, especially used to treat large burns. This artificial skin model has the advantage of being rich in extracellular matrix, comparable to human skin in terms of composition and organization. This matrix is mainly composed of collagen, well known in cosmetics for its role in the skin’s mechanical properties. Collagen, like the whole extracellular matrix, is finely regulated, in particular by its degradation by specialized enzymes which prevent it from being in excess. If this balance is disturbed, the matrix reaches a pathological or disease state, as is the case with fibrotic or hypertrophic scars, characterized by excessive collagen deposition.
Using this artificial skin model, scientists have shown that applying an electric field to the skin affects many genes that influence collagen production and maturation. As soon as four hours after applying the electric field, less collagen is produced. This lasts for several days. In addition, enzymes that degrade collagen have increased activity for at least 48 hours.
The application of an electric field to the skin therefore presents a great potential for future therapeutic use in the treatment of skin fibrosis.
Notes
1 — Participating scientists were from the laboratory Interactions moléculaires et réactivité chimique et photochimique (CNRS/Université Toulouse III — Paul Sabatier), the Centre interuniversitaire de recherche et d’ingénierie des matériaux (CNRS/Université Toulouse III — Paul Sabatier/Toulouse INP) and the Centre de microscopie électronique appliquée à la biologie (Université Toulouse III — Paul Sabatier). A researcher from Tel Aviv University in Israel also participated in the study.
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New findings from the international The Environmental Determinants of Diabetes in the Young (TEDDY) study add to a growing body of evidence indicating that type 1 diabetes is not a single disease. The presentation and, perhaps, cause of autoimmune diabetes differs among genetically high-risk children, the research suggests.
In a cohort study published July 22 in Diabetologia, lead author Jeffrey Krischer, PhD, director of the Health Informatics Institute at the USF Health Morsani College of Medicine, and TEDDY colleagues compared the characteristics of type 1 diabetes diagnosed in children before vs. after age 6. The paper’s senior author was Beena Akolkar, PhD, of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
“Our results underscore the importance of taking into account the age at development of multiple autoantibodies when evaluating risk factors for progression to a diabetes diagnosis,” said lead author Dr. Krischer, a Distinguished University Health Professor and co-chair for the National Institutes of Health-funded TEDDY consortium. “When the changing picture of autoantibody presentation is considered, it appears type 1 diabetes at an early age is a more aggressive form of the disease.”
In type 1 diabetes, a misdirected immune response attacks and destroys insulin-producing beta cells in the healthy person’s pancreas — a process occurring over months or many years. Four autoantibodies directed against the pancreatic β-cells  — glutamic acid decarboxylase autoantibody (GADA), insulin autoantibody (IA), insulinoma-associated-protein-2 autoantibody (IA2-2A), and zinc transporter 8 autoantibody (ZnT8A) — are thus far the most reliable biological indicators of early type 1 diabetes, before symptoms appear. Not all children who test positive for one or more autoantibodies progress to a diagnosis of type 1 diabetes, which requires lifelong administration of insulin to control blood sugar levels and reduce health complications.
Over the last decade, TEDDY researchers have learned more about how the order, timing and type of autoantibodies can help predict which genetically susceptible children are most likely to get type 1 diabetes as they age.
For this multisite study in the U.S. and Europe, the researchers analyzed data from 8,502 children, all at genetically high risk for developing autoimmunity and type 1 diabetes. The children were followed from birth to a median of 9 years. Over this period, 328 study participants (3.9%) progressed from a presymptomatic stage in which autoantibodies first appeared in their circulating blood (signaling initial autoimmunity) to the onset of symptomatic type 1 diabetes.
Half of the 328 participants (2.0%) were diagnosed before age 6, while the other half (1.9%) developed diabetes between ages 6 and 12. The aim was to determine whether the younger group diagnosed with type 1 diabetes differed from the older group, which would suggest that a different form of type 1 diabetes emerges in children as they grow older.
Among the findings: As expected, TEDDY participants who progressed to diabetes between ages 6 and 12 were more likely to have first-appearing autoantibodies to the pancreatic enzyme glutamic acid decarboxylase (GAD autoantibodies), while first-appearing insulin autoantibodies (IA antibodies) were much more common in younger children developing the disease. The rate of progression to type 1 diabetes was slower if multiple (two or more) autoantibodies appeared after age 6 than if they were present before age 6. The significant association of country of origin with diabetes risk found in the younger group declined in the older group. Conversely, the link between certain genotypes and a higher likelihood of developing diabetes significantly increased in the older children. Among children 6 and older with multiple autoantibodies, family history did not appear to play a role in whether the child progressed to type 1 diabetes.”Much of the observed differences in the relationship between genes and environmental exposures can be explained by the age at appearance of autoantibodies,” Dr. Krischer said. “That is important, because it means factors linked with diabetes risk need to be conditioned on age to be properly understood. There may be different environmental exposures occurring at different ages that trigger autoimmunity, or the same environmental trigger may act differently at different ages.”
The research was funded by grants from the NIDDK and several other NIH institutes, JDRF, and the Centers for Disease Control and Prevention (CDC); and supported in part by NIH/NCATS Clinical and Translational Science Awards.
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Materials provided by University of South Florida (USF Health). Original written by Anne DeLotto Baier. Note: Content may be edited for style and length.

With age, the human heart gradually loses its ability to repair itself following injury. Damage wrought by injuries such as cardiac ischemia and heart attack, which are associated with decreased oxygen levels in the heart, can cause the heart to function below normal capacity, making it difficult for patients to carry out day-to-day activities.
To augment heart repair after ischemic injury, researchers have turned to stem cell-based therapies, which replace dead heart tissue with new, functional tissue. In most cases, however, fewer than 1 percent of stem cells survive transplantation into the heart, due primarily to the cells’ inability to cope with the metabolic demands of the ischemic environment.
Now, in new research, scientists at the Lewis Katz School of Medicine at Temple University show that, at least in mice, this obstacle can be overcome through the reintroduction of LIN28 — a protein normally expressed in the developing heart — into stem cells derived from adult heart tissue. LIN28 renders adult cardiac stem cells more metabolically flexible, greatly improving their chances of survival.
“LIN28 is very active in the developing heart, but not in the adult heart,” explained Mohsin Khan, PhD, Assistant Professor of Cardiovascular Sciences at the Cardiovascular Research Center at the Lewis Katz School of Medicine and senior investigator on the new study. “We found that when we expressed LIN28 in cardiac stem cells from adult heart tissue, the adult cells were reprogrammed to have metabolic characteristics of young, developing heart cells. The process was essentially like reverse aging.”
The new findings were published online in the journal Redox Biology.
The fetal heart is specially adapted to function under low-oxygen conditions. Post-natally, this low-oxygen tolerance is lost, however, and by adulthood, the heart is extremely sensitive to decreases in oxygen availability. Changes in cellular metabolism are the underlying reason for this shift, and recent studies suggest that these metabolic differences in the heart help determine the fate of stem cells following transplantation.
In the new study, Dr. Khan and colleagues were interested in finding out whether metabolic regulators that are expressed in the developing heart could impart a sort of metabolic flexibility to cardiac tissue-derived stem-like cells (CTSCs). CTSCs are present in both neonatal and adult heart tissue but only express LIN28 in the developing heart. In adult heart tissue, CTSCs possess regenerative potential and generally are dormant.
The team began by reintroducing LIN28 expression in adult mouse CTSCs in vitro and analyzing the effects on signaling pathways involved in cellular metabolism, growth, and regeneration. They found that LIN28 expression produced a robust regenerative response, modifying CTSCs to promote growth and survival in response to oxidative stress. The researchers linked the modifications to the Let7/PDK1 signaling pathway, which is known to regulate aerobic metabolism in cells. Transplantation of LIN28-expressing CTSCs into the heart in mice that had suffered heart attack resulted in significant improvements in cardiac structure and function. These effects were mediated via the same pathways identified in the in vitro assessments.
“LIN28 modified energy production in CTSCs, leading to the secretion of many factors that are beneficial for heart cell survival,” Dr. Khan explained. “Overall, the cells took on a more youthful phenotype.”
Dr. Khan plans next to translate the new findings into a larger animal model and to determine whether human-derived cardiac stem cells can be reprogrammed by LIN28. “These studies could have important implications for how we approach stem cell therapy for heart disease in humans,” he said.
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Brain tumors are difficult to contain and often resistant to conventional treatment methods. Predicting tumor cell behavior requires a better understanding of their invasion mechanism. Now, researchers from University of Fukui, Japan, have used high-density nanofibers that mimic the microenvironment of the brain to capture these tumor cells, opening doors to novel therapeutic solutions for aggressive brain cancer.
Our body heals its injuries by essentially replacing damaged cells with new cells. The new cells often migrate to the site of injury, a process known as “cell migration.” However, abnormal cell migration can also facilitate the transport and spread of cancer cells within the body. Glioblastoma multiforme (GBM) is one such example of a highly invasive brain tumor that spreads via migration of the tumor cells. The frequency at which such tumor cells spread and grow make conventional tumor removal methods ineffective. Furthermore, options such as radiotherapy and chemotherapy are harmful to healthy cells and cause adverse effects. In order to develop improved therapeutic strategies, a precise understanding of the invasion mechanism of GBM cells is necessary.
An alternative treatment strategy in consideration involves capturing the migrating tumor cells. It turns out that cell migration is dictated by the structure and the orientation of the “extracellular matrix” (ECM) — fibrous structures surrounding the cells. By engineering similar structures of desired geometries, it is, therefore, possible to exert control over the migration process.
Now in a study published in ACS Applied Bio Materials, researchers from University of Fukui, Japan, have designed a platform based on nanofibers that resemble the ECM to examine their effect on GBM cells. “We fabricated a nanofibrous sheet in which the fiber density changes from end to end gradually using a technique called ‘electrospinning’ and carried out a culture experiment of brain tumor cells,” says Dr. Satoshi Fujita, who headed the study.
The researchers observed clear distinctions in cell movement in nanofibers of different densities. They found that the denser fibers promoted the formation of “focal adhesions” clusters in the cells that resulted in a slower cell migration.
Taking advantage of this negative correlation between cell movement and fiber density, the researchers were able to control and direct the migration of cells by designing a nanofibrous sheet with stepwise varying densities. By arranging the fibers in a high-to-low density configuration, they were able to restrict the movement of cells as most of them were captured in the high-density zones. On the other hand, a low-to-high density configuration had the opposite effect and encouraged migration.
In addition, they noticed that the gaps between the zones hindered cell migration, leading to cells being trapped in the high-density zones. This one-way migration was observed for the first time and the researchers named it “cell trapping” after fish and insect traps that cause their prey to travel along a single direction before trapping it.
“The study demonstrates the feasibility of capturing migrating cells using electrospun nanofibers that mimic the microenvironment of the brain,” comments Dr. Fujita.
With such remarkable findings, the team is excited about the future prospects of their nanofiber-based platform. “It is available for the design of scaffolding materials, which are the basis of regenerative medicine, in combination with various fiber processing technologies and material surface treatment technologies. This could lead to the development of practical applications of regenerative medicines,” speculates Dr. Fujita, “In addition, it can be used as a processing technology for culture carriers for efficient production of biological drugs including proteins, antibodies, and vaccines.”
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An antidepressant best known as Prozac could offer the first treatment for the leading cause of blindness among people over 50, new research from the University of Virginia School of Medicine suggests.
UVA’s Bradley D. Gelfand, PhD, and collaborators have found early evidence that the drug fluoxetine may be effective against atrophic (or “dry”) age-related macular degeneration, a condition that affects nearly 200 million people worldwide. The drug has shown promise in the scientists’ lab tests and animal models, and the researchers bolstered by their results by examining two huge insurance databases encompassing more than 100 million Americans. That analysis concluded that patients taking fluoxetine were less likely to develop atrophic macular degeneration (AMD).
Based on their findings, the researchers are urging clinical trials to test the drug in patients with AMD. If successful, they believe the drug could be administered either orally or via a long-lasting implant in the eye.
“These findings are an exciting example of the promise of drug repurposing, using existing medicines in new and unexpected ways,” said Gelfand, of UVA’s Center for Advanced Vision Science. “Ultimately, the best way to test whether fluoxetine benefits macular degeneration is to run a prospective clinical trial.”
Fluoxetine and AMD
The researchers believe fluoxetine works against AMD by binding with a particular agent of the immune system known as an inflammasome. This inflammasome, NLRP3-ASC, triggers the breakdown of the pigmented layer of the eye’s retina.

Scientists at the University of Groningen have created wearable, stitchable, and sensitive sensors from flexible polymers and bundles of carbon fibre. Like our skin, these sensors respond to pressure and can measure body position and movement. They could be used to measure disease progress in Parkinson’s disease, or sense joint movement in athletes, for example. A description of these applications was presented in the Nature Partnership journal (npj) Flexible Electronics on 14 October.
Sensors can be useful to monitor our health. However, this requires flexible sensors that will not cause discomfort to the user. Wearable sensors, stitched into clothing, would be useful as well. Ajay Kottapalli, assistant professor at the Engineering and Technology institute Groningen (ENTEG, part of the University of Groningen), together with his PhD student Debarun Sengupta, has already developed different types of sensors, often inspired by nature. He has now created sensors that can mimic the sensory capabilities of our skin.
Applications
Kottapalli used electrospun carbon fibres for his sensors. These fibres are piezoresistive, which means that their conductivity changes when they are stretched. Sensors are made by embedding the fibres in a flexible elastomer in a perpendicular pattern, creating ‘pixels’ where two fibres cross. ‘Electrospinning is similar to the way in which fabric is made, and the material can be stitched, whereby it is possible to use conductive yarn that can act as an electrode,’ says Kottapalli. The sensors can therefore be integrated into everyday clothing or gloves, or applied as patches on joints. They will measure bending movements, but they are also sensitive to pressure.
A detailed description of the sensors was published recently in npj Flexible Electronics. In the latest paper, published in the same journal on 14 October, Kottapalli and his research team focus on applications. For instance, the authors integrated the sensors into a glove. This allowed measurements of finger movement and fingertip pressure, or touch. ‘The glove can tell you the hardness of an object, like a normal hand can.’ Application on a hand prosthesis would be one option. In that case, the sensor output would have to be fed into the patient’s nervous system. A special quality of these sensors is that they can measure touch, gestures, and proprioception. ‘This is a unique combination,’ says Kottapalli. ‘Our sensors have a skin-like function.’
Washable
The sensors could also be used by athletes. Many elite athletes already wear shirts with electrodes that measure muscle activity. ‘Our sensors would add body movement to this, which is an entirely different approach. Apart from joint movement, we could also register breathing movements.’ Sensors could be placed in tight-fitting shirts, socks, gloves, or the soles of shoes. A final advantage is that the sensors are expected to be washable, although this was not yet described in the article. Kottapalli: ‘My PhD student Debarun Sengupta is actively working on that.’
Assisted walking
Kottapalli also won an NWA (Dutch Science Agenda) Idea Generator grant last year, with which he is trying to use these sensors for biomedical applications that leverage the functionality of such sensors. Together with Amar Kamat (a former postdoctoral researcher in Kottapalli’s team, currently at CTO Sencilia B.V.) and Natanael Gomes (a research engineer in the team), Kottapalli is testing the sensors in a rehabilitation centre for Parkinson’s disease patients at the Paramedisch Centrum voor Reumatologie en Revalidatie (PCRR, Paramedical Centre for Rheumatology and Rehabilitation) Hilberdink, Groningen. ‘They are being used to monitor the deterioration of their gait over time.’ This is achieved by placing sensors in shoe soles and on knee or foot joints. In the near future, this might lead to assisted walking for these patients. Kottapalli: ‘Some patients already use a system that gives them instructions on walking speed and step length through earphones. We know that just before a fall, patients take shorter steps. Our sensor system could alert them to this.’
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