Although dengue outbreaks cannot be prevented, it is possible to anticipate them. An international research team including scientists from the Institut Pasteur and Beijing Normal University in China has recently identified a global climate indicator that may help improve predictions about the magnitude of dengue outbreaks several months in advance. This indicator, which can be used for any world region, is based on temperature fluctuations at the surface of the Indian Ocean. Obtaining reliable long-term predictions could facilitate efforts to tackle this infection, which has been on the rise for several decades and threatens half of the world’s population. The research results were published in the journal Science on May 10, 2024.
The ability to anticipate dengue outbreaks is crucial in planning control measures against the mosquitoes that transmit the disease and mobilizing hospital staff and equipment. And this is vitally important, because although vaccines have been developed, there is no specific treatment for the symptoms of this “tropical influenza,” and the severity of outbreaks can vary hugely from one year to the next. “The dynamics of dengue are complex because the virus responsible for infection exists in four different forms, or serotypes, which can change from one year to the next and one country to the next,” explains Simon Cauchemez, joint last author of the study and Head of the Mathematical Modeling of Infectious Diseases Unit at the Institut Pasteur. “So the magnitude of dengue outbreaks can vary considerably from one season to the next.”
We now know that the reproduction and infectivity of Aedes genus mosquitoes that transmit dengue viruses, and by extension the transmission rate and scale of outbreaks, are closely correlated with local temperature and rainfall. But these parameters can only be predicted between two weeks and three months in advance, and the quality of forecasts decreases rapidly for longer-term predictions. Global climate indicators like El Niño-Southern Oscillation (ENSO) can generally be predicted over a longer period, beyond six months. An international team therefore decided to study 30 global climate indicators to determine whether monitoring such indicators could help predict dengue outbreaks further in advance.
The team compiled two large datasets: the total number of annual dengue cases reported in 46 countries in South-East Asia and America over 30 years (1990-2019), and also the monthly number of dengue cases in 24 countries over six years (2014-2019). They found that of all the indicators under consideration, the Indian Ocean basin-wide (IOBW) index, which measures temperature fluctuations at the surface of the Indian Ocean, was the global indicator that was most closely correlated to annual dengue incidence in both the northern and southern hemispheres.
“Our results revealed that incorporating the IOBW index into our mathematical model resulted in predictions that closely matched real-world data, compared to the model excluding the IOBW index,” notes Huaiyu Tian, co-last author of the study and Director of the Center for Global Change and Public Health, Beijing Normal University. “The extended lead time and improved predictive ability underscore the significance of the IOBW index in dengue forecasting and early warning systems.”
These interesting theoretical findings will need to be validated in real conditions. “Our aim is to develop predictive models for dengue outbreaks in Guadeloupe, French Guiana and Martinique, and we will now explore whether the IOBW index can effectively improve these predictions,” explains Simon Cauchemez. “Climate is not the only factor that influences dengue outbreaks. For these predictive models we will also need to take into account other factors like immunity levels in the population, strains previously in circulation, etc.”
If the findings are borne out, the new indicator could help improve the prediction of dengue outbreaks, thereby also improving efforts to tackle this infectious disease, which affects 50,000 million people each year. The incidence of dengue has risen dramatically in recent years, especially in mainland France. Between January 1 and April 19, 2024, 1,679 imported dengue cases were reported to Santé publique France, compared with 131 over the same period in 2023.

A new study led by investigators from Mass General Cancer Center, a founding member of the Mass General Brigham healthcare system, reveals that statins — commonly used cholesterol-lowering drugs — may block a particular pathway involved in the development of cancer that results from chronic inflammation. The findings are published in Nature Communications.
“Chronic inflammation is a major cause of cancer worldwide,” said senior author Shawn Demehri, MD, PhD, a principal investigator at the Center for Cancer Immunology and Cutaneous Biology Research Center of Massachusetts General Hospital and an associate professor of Dermatology at Harvard Medical School. “We investigated the mechanism by which environmental toxins drive the initiation of cancer-prone chronic inflammation in the skin and pancreas,” says Demehri, who is also theBob and Rita Davis Family MGH Research Scholar 2023-2028. “Furthermore, we examined safe and effective therapies to block this pathway in order to suppress chronic inflammation and its cancer aftermath.”
Demehri and his colleagues’ study relied on cell lines, animal models, human tissue samples and epidemiological data. The group’s cell-based experiments demonstrated that environmental toxins (such as exposure to allergens and chemical irritants) activate two connected signaling pathways called the TLR3/4 and TBK1-IRF3 pathways. This activation leads to the production of the interleukin-33 (IL-33) protein, which stimulates inflammation in the skin and pancreas that can contribute to the development of cancer.
When they screened a library of U.S. Food and Drug Administration-approved drugs, the researchers found that a statin, pitavastatin, effectively suppresses IL-33 expression by blocking the activation of the TBK1-IRF3 signaling pathway. In mice, pitavastatin suppressed environmentally-induced inflammation in the skin and the pancreas and prevented the development of inflammation-related pancreatic cancers.
In human pancreas tissue samples, IL-33 was over-expressed in samples from patients with chronic pancreatitis (inflammation) and pancreatic cancer compared with normal pancreatic tissue. Also, in analyses of electronic health records data on more than 200 million people across North America and Europe, use of pitavastatin was linked to a significantly reduced risk of chronic pancreatitis and pancreatic cancer.
The findings demonstrate that blocking IL-33 production with pitavastatin may be a safe and effective preventive strategy to suppress chronic inflammation and the subsequent development of certain cancers.
“Next, we aim to further examine the impact of statins in preventing cancer development in chronic inflammation in liver and gastrointestinal tract and to identify other novel, therapeutic approaches to suppress cancer-prone chronic inflammation” said Demehri.

The research group of Professor Riitta Lahesmaa have discovered a novel modulator for human regulatory T cells. This novel regulator can strengthen or dampen immune response and provides a new basis for therapeutic approaches for immune mediated diseases. The Lahesmaa group is based at Turku Bioscience Centre of the University of Turku and Åbo Akademi University in Finland and is part of the InFLAMES Research Flagship.
The T cells in our blood fight against cancer, viruses and bacteria. Specific regulatory T cells are required to control faulty immune responses, and disruption in their function may lead to autoimmune diseases or cancer.
The scientists at Turku Bioscience Centre have now discovered a novel RNA that controls the development and function of regulatory T cells. This long intergenic noncoding RNA (lincRNA) modulates the levels of transcription factor FOXP3 and the suppressive function of human regulatory T cells by controlling the interleukin-2 receptor. The finding potentially enables the development of new therapeutic approaches to control the human immune response.
“Our discovery provides a basis for developing precision medicine treatments for autoimmune diseases and cancer. Regulatory T cells are already being studied in patients to treat type 1 diabetes, and our novel lincRNA molecule could, for example, be used to boost the production of these cells for therapeutic use,” says Professor Riitta Lahesmaa from the University of Turku in Finland.
The discovery is particularly interesting because cancer cells are able to hide from the immune system by specifically manipulating regulatory T cells. Recently introduced immune activator therapeutic monoclonal antibodies for cancer are attempting to break this hiding process. Lahesmaa suggests that by targeting the novel lincRNA molecule, it may be possible to release immune activation in cancer without using expensive antibodies.
Expression of lincRNAs is highly tissue and cell specific so targeting these molecules will enable precision therapy against desired targets.

Osteoporosis, a condition characterized by porous and fragile bones, poses a significant threat to skeletal health. As the very framework of the human body, bones provide crucial structural support. When bone mass diminishes, it not only compromises this support but also impairs overall function, leading to a diminished quality of life. With the aging population experiencing a surge in osteoporosis cases, the strain on healthcare resources for long-term care is evident. Hence, there is a need to understand the mechanisms that contribute to osteoporosis and develop effective targeted therapies to minimize its long-term impact.
Osteoblasts and osteoclasts are two types of cells crucial for the maintenance and remodeling of bone tissue. While osteoblasts are the bone-forming cells responsible for synthesizing and depositing new bone tissue, osteoclasts are the bone-resorbing cells involved in the breakdown and removal of old or damaged bone tissue. An increase in the proportion of osteoclasts leads to loss of bone mass in conditions like osteoporosis, rheumatoid arthritis (joint inflammation), and bone metastases (cancer that has spread to the bones). Osteoclasts arise from the differentiation of macrophages or monocytes, which are types of immune cells. Suppressing osteoclast differentiation can, therefore, serve as a therapeutic strategy to prevent bone loss. However, the precise molecular mechanisms governing the complex process of bone remodeling remain unclear.
In a new groundbreaking study, Professor Tadayoshi Hayata, Mr. Takuto Konno, and Ms. Hitomi Murachi from Tokyo University of Science, along with their co-workers, delved deeper into the molecular regulation of osteoclast differentiation. Receptor activator of nuclear factor kappa B ligand (RANKL) stimulation induces the differentiation of macrophages into osteoclasts. Further, bone morphogenetic protein (BMP) and transforming growth factor (TGF)-β signaling pathways have been implicated in the regulation of RANKL-mediated osteoclast differentiation. In the current study, the researchers sought to investigate the role of Ctdnep1 — a phosphatase (an enzyme that removes phosphate groups) that has been reported to suppress BMP and TGF-β signaling.
Giving further insight into their work set to be published on July 30, 2024, in Volume 719 of Biochemical and Biophysical Research Communications, Prof. Hayata states, “RANKL functions as an ‘accelerator’ for osteoclast cell differentiation. Driving a car requires not only the accelerator but also the brakes. Here, we find that Ctdnep1 functions as a ‘brake’ on osteoclast cell differentiation.”
First, the researchers examined the expression of Ctdnep1 in mouse-derived macrophages treated with RANKL and untreated control cells. They noted that Ctdnep1 expressionremained unchanged in response to RANKL stimulation. However, it localized in the cytoplasm in granular form in the macrophages and differentiated into osteoclasts, distinct from its normal peri-nuclear localization in other cell types, indicating its cytoplasmic function in osteoclast differentiation.
Further, Ctdnep1 knockdown (downregulation of gene expression) resulted in an increase in tartrate-resistant acid phosphatase-positive (TRAP) osteoclasts; wherein TRAP is a marker for differentiated osteoclasts. Additionally, Ctdnep1 knockdown led to an increase in the expression of crucial differentiation markers including ‘Nfatc1’, a RANKL-induced master transcription factor for osteoclast differentiation. These results support the ‘brake function’ of Ctdnep1, whereby, it negatively regulates osteoclast differentiation.
Moreover, Ctdnep1 knockdown also led to increased absorption of calcium phosphate, suggestive of the suppressive role of Ctdnep1 in bone resorption. Lastly, while, Ctdnep1 knockdown did not alter BMP and TGF-β signaling, cells deficient in Ctdnep1 showed elevated levels of phosphorylated (activated) proteins downstream of the RANKL signaling pathway. These findings suggest that the suppressive effect of Ctdnep1 in osteoclast differentiation may not be mediated by BMP and TGF-β signaling, but, through the negative regulation of RANKL signaling and Nfatc1 protein levels.
Overall, these findings provide novel insights into the process of osteoclast differentiation and reveal potential therapeutic targets which can be pursued to develop treatments that address bone loss due to excessive osteoclast activity. In addition to diseases characterized by bone loss, Ctdnep1 has also been reported as a causative factor in medulloblastoma — a childhood brain tumor. The authors are, therefore, optimistic that their research can be extended to other human diseases beyond bone metabolism.
Prof. Hayata concludes by saying, “Our findings suggest that Ctdnep1 is necessary to prevent excessive osteoclastogenesis. These results can further expand the knowledge on how the phosphorylation-dephosphorylation network controls osteoclast differentiation, and may provide new therapeutic strategies for bone diseases related to excessive osteoclast cell activity.”

Researchers from the Institute of Oncology of the University of Oviedo (IUOPA), the Josep Carreras Leukaemia Research Institute, the University of Barcelona and the Centre for Biomedical Research in Cancer Network (CIBERONC) have demonstrated that some childhood leukaemia originate during embryonic development, although they do not manifest after a few months after birth.
Acute myeloid leukaemia is the second most common type of acute leukaemia in childhood and can be diagnosed within a few months of life. The early onset of the disease had led to the suspicion that the tumour could have a prenatal origin. However, proving this theory has been challenging due to the lack of prenatal or birth samples.
‘The opportunity to study the origin of this leukaemia arose from the case of a five-month-old baby diagnosed with acute myeloid leukaemia at the Hospital Niño Jesús in Madrid,’ explains Pablo Menéndez, ICREA professor at the University of Barcelona and the Josep Carreras Institute. ‘The parents, who had preserved the umbilical cord blood, opened a line of research that until now had not been possible to address,’ adds the researcher.
Using precision medicine techniques, researchers analysed the complete genome of the tumour. Unlike tumours in adults, where thousands of mutations are detected, only two chromosomal alterations were identified in this leukaemia. ‘Genome analysis allowed us to design a personalised diagnostic method to monitor the disease,’ says Xose S. Puente, Professor of Biochemistry at the University of Barcelona. Puente, Professor of Biochemistry and Molecular Biology at the University of Oviedo. ‘But these data raise new questions, such as when the tumour arose and in what order these mutations have appeared,’ he highlights. These questions are difficult to answer, since such research requires blood samples from the baby before the diagnosis, something that is impossible in the vast majority of cases. However, in this particular case, the existence of a frozen umbilical cord sample allowed researchers to separate different populations of blood cells at birth and to study whether any of the chromosomal alterations detected in the tumour were already present during foetal development.
The study revealed that a translocation between chromosome 7 and 12 was already present in some haematopoietic stem cells in the umbilical cord. In contrast, the other chromosomal alteration, a trisomy of chromosome 19, was not present in the foetus, but was found in all tumour cells, suggesting that it contributes to increasing the malignancy of the leukemic cells. ‘These data are highly relevant for understanding the development of a devastating disease, and the existence of this umbilical cord sample was crucial to be able for conducting a study that had been impossible until now in acute myeloid leukaemia’, adds Talía Velasco, researcher at the Josep Carreras Institute and the University of Barcelona and co-leader of the study.
In addition to reconstructing the genomic alterations that the cells undergo to generate this leukaemia, the study has also identified a molecular mechanism that had not been observed before in this type of leukaemia and which causes the activation of a gene, called MNX1, which is frequently altered in this type of tumour. Knowledge of these alterations is essential for developing cell and animal models that allow us to understand the disease’s evolution and develop new therapies for treating these pathologies.
The study has been led by Xose S. Puente, Professor of Biochemistry and Molecular Biology at the University of Oviedo-IUOPA, Talía Velasco and Pablo Menéndez, from the Josep Carreras Institute and the University of Barcelona, with participation from researchers from four other institutions, including the Hospital Infantil Universitario Niño Jesús, the Hospital Universitario Central de Asturias, the Instituto de Biomedicina y Biotecnología de Cantabria and the Instituto de Investigación Sanitaria La Princesa de Madrid.
This research has been made possible thanks to the collaboration of the parents and funding from the Ministry of Science, Innovation and Universities, the European Research Council, the AECC Scientific Foundation, the Foundation Unoentrecienmil, the “La Caixa” Foundation, the Government of Catalonia, CIBERONC and the III Health Institute.

Using a combination of cutting-edge immunologic technologies, researchers have successfully stimulated animals’ immune systems to induce rare precursor B cells of a class of HIV broadly neutralizing antibodies (bNAbs). The findings, published in Nature Immunology, are an encouraging, incremental step in developing a preventive HIV vaccine.
HIV is genetically diverse making the virus difficult to target with a vaccine, but bNAbs may overcome that hurdle because they bind to parts of the virus that remain constant even when it mutates. Germline targeting is an immune system-stimulating approach that guides naïve (precursor) B cells to develop into mature B cells that can produce bNAbs. A class of bNAbs called 10E8 is a priority for HIV vaccine development because it neutralizes a particularly broad range of HIV variants. The 10E8 bNAb binds to a conserved region of the glycoprotein gp41 on HIV’s surface involved in its entry into human immune cells. Designing an immunogen — a molecule used in a vaccine that elicits a specific immune system response — to stimulate production of 10E8 bNAbs has been challenging because that key region of gp41 is hidden in a recessed crevice on HIV’s surface. Prior vaccine immunogens have not generated bNAbs with the physical structure to reach and bind to gp41.
To address this challenge, the researchers engineered immunogens on nanoparticles that mimic the appearance of a specific part of gp41. They vaccinated rhesus macaque monkeys and mice with those immunogens and elicited specific responses from the 10E8 B cell precursors and induced antibodies that showed signs of maturing into bNAbs that could reach the hidden gp41 region. They observed similar responses when they used mRNA-encoded nanoparticles in mice. The researchers also found that the same immunogens produced B cells that could mature to produce an additional type of gp41-directed bNAb called LN01. Finally, their laboratory analysis of human blood samples found that 10E8-class bNAb precursors occurred naturally in people without HIV, and that their immunogens bound to and isolated naïve human B cells with 10E8-like features. Together these observations suggest that the promising immunization data from mice and macaques has the potential for translation to humans.
The research was conducted by the Scripps Consortium for HIV/AIDS Vaccine Development, one of two consortia supported by the National Institutes of Health’s (NIH) National Institute of Allergy and Infectious Diseases (NIAID). The research also was supported by collaborating partners including the Bill & Melinda Gates Foundation and other NIH Institutes and Offices. According to the authors, these findings support the development of the immunogens as the first part of a multi-step vaccine regimen for humans. Their work further supports research in developing a germline-targeting strategy for priming the immune system to elicit a bNAb called VRC01. This bNAb was discovered by NIAID researchers almost 15 years ago. The goal of this line of research is to develop an HIV vaccine that generates multiple classes of bNAbs to prevent HIV.

A drug approved to treat certain autoimmune diseases and cancers successfully alleviated symptoms of a rare genetic syndrome called autoimmune polyendocrine syndrome type 1 (APS-1). Researchers identified the treatment based on their discovery that the syndrome is linked to elevated levels of interferon-gamma (IFN-gamma), a protein involved in immune system responses, providing new insights into the role of IFN-gamma in autoimmunity. The study, led by researchers at the National Institutes of Health’s National Institute of Allergy and Infectious Diseases, was published today in the New England Journal of Medicine.
In a three-stage study, conducted in mice and people, the researchers examined how APS-1 causes autoimmune disease. The syndrome is marked by dysfunction of multiple organs, usually beginning in childhood, and is fatal in more than 30% of cases. This inherited syndrome is caused by a deficiency in a gene that keeps the immune system’s T cells from attacking cells of the body, leading to autoimmunity; chronic yeast infections in the skin, nails, and mucous membranes; and insufficient production of hormones from endocrine organs, such as the adrenal glands. Symptoms include stomach irritation, liver inflammation, lung irritation, hair loss, loss of skin coloring, tissue damage, and organ failure.
In the first stage of this study, researchers led by scientists in NIAID’s Laboratory of Clinical Immunology and Microbiology examined the natural history of APS-1 in 110 adults and children. Blood and tissues were analyzed to compare gene and protein expression in people with and without APS-1. They found elevated IFN-gamma responses in the blood and tissues of people with APS-1, indicating that IFN-gamma may play an important role in the disease and providing a pathway to target for treatment.
In the second stage of the study, the scientists examined mice with the same gene deficiency that causes APS-1 in people, finding that the animals also experienced autoimmune tissue damage and elevated IFN-gamma levels. Mice also deficient in the gene for IFN-gamma did not have autoimmune tissue damage, which showed a direct link between IFN-gamma and APS-1 symptoms. With this understanding, the researchers looked for a drug that could be used to lower IFN-gamma activity in people. They selected ruxolitinib, a Janus kinase inhibitor, because it acts by shutting down the pathway driven by IFN-gamma. When ruxolitinib was administered to the mice with the gene deficiency that causes APS-1, IFN-gamma responses were normalized and T cells were prevented from infiltrating tissues and damaging organs. These results showed that ruxolitinib could alleviate effects of the gene deficiency, suggesting that it could be effective for treatment of APS-1 in people.
The researchers administered ruxolitinib, which was supplied by the NIH Clinical Center, to five people — two adults and three children — with APS-1 in the third stage of the study. The dosing and regimens were tailored to the individuals, and the treatments were continued for over a year. The drug was safe and tolerated well, and improvement in symptoms was seen in all study participants. Blood and tissue analyses revealed decreased production of IFN-gamma from T cells, as well as normalized levels of IFN-gamma in the blood. Many APS-1-related symptoms were reduced, including hair loss, oral yeast infections, stomach and bowel irritation, hives, and thyroid inflammation.
The results revealed that normalizing IFN-gamma levels using ruxolitinib could reduce the damaging effects of APS-1 in people. The scientists note that a study with a larger and more diverse group of patients is needed to determine whether ruxolitinib and similar drugs are suitable treatments for individuals with APS-1. They write that understanding the role of IFN-gamma in autoimmunity may lead to the development of treatments for related diseases. This research highlights the importance of finding the causes of and treatments for rare diseases.

Brain cancer is difficult to treat when it starts growing, and a prevalent type, known as a glioma, has a poor five-year survival rate. In a new study published in Proceedings of the National Academy of Sciences, Mayo Clinic researchers report on a new surgical platform used during surgery that informs critical decision-making about tumor treatment within minutes. Time is of the utmost importance when dealing with aggressive malignant tumors.
The platform uses mass spectrometry to identify a key gene mutation in brain cancer, known as isocitrate dehydrogenase (IDH) mutations, in real time. Mass spectrometry is a sensitive technique used to analyze substances in tissue samples, including those altered in cancer.
The study involved more than 240 small tissue biopsies from patients undergoing asleep and awake brain surgery for suspected glioma at Mayo Clinic between 2021 and 2023, and an additional 137 biopsies from an international collaborator. Neurosurgeons collected biopsy samples from the core of the tumor to identify the mutations, as well as from areas around it, to assess if the tumor had spread.
Each tissue sample was placed on a glass slide steps away from the patients during ongoing surgery. The samples were analyzed through the mass spectrometer, which allowed researchers to rapidly assess — within two minutes — whether an IDH mutation was present.
The researchers say that, in addition to enabling real-time diagnosis, the platform allows surgeons to determine a patient’s prognosis and perform tumor resection to improve patient outcomes. In the future, the new platform will help surgeons take advantage of the window of opportunity in the operating room to tailor treatment to the molecular features of a tumor, a more personalized approach to medicine.
Researchers hope new therapies developed to target IDH mutations can be delivered in the operating room at the time of surgery.
“The ability to identify this mutation during brain surgery means that we can treat patients locally before they leave the operating room,” says the study’s senior author, Alfredo Quiñones-Hinojosa, M.D., dean of research and chair of the Department of Neurosurgery at Mayo Clinic in Florida.
“Therefore, we will be able to bring the fight against cancer to the operating room, before chemotherapy and radiation treatments begin, and before the disease has progressed and invaded further.” Dr. Quiñones-Hinojosa is also director of the Brain Tumor Stem Cell Research Laboratory.
In the study, researchers were able to diagnose IDH gene mutations with 100% accuracy. They are conducting more research to find other signatures in tumors where the mutation is absent. In addition, they plan to broaden their discoveries to include other types of brain cancers.

Skin can send certain health-related signals, such as dry skin feeling tighter to indicate the need for moisture. But what if skin could be smarter, capable of monitoring and sharing specific health information, such as the concentration of glucose in sweat or heart rate? That was the question driving a team led by Penn State researchers that recently developed an adhesive sensing device that seamlessly attaches to human skin to detect and monitor the wearer’s health.
The details of the smart skin, including how it can be efficiently reprogrammed to detect various signals and even recycled, were published in Advanced Materials. The paper was included in the “Rising Stars” series, which is coordinated by multiple journals to highlight work by early career researchers around the world. The researchers also filed a provisional patent application on the work.
“Despite significant efforts on wearable sensors for health monitoring, there haven’t been multifunctional skin-interfaced electronics with intrinsic adhesion on a single material platform prepared by low-cost, efficient fabrication methods,” said co-corresponding author Huanyu “Larry” Cheng, the James L. Henderson, Jr. Memorial Associate Professor of Engineering Science and Mechanics in the Penn State College of Engineering. “This work, however, introduces a skin-attachable, reprogrammable, multifunctional, adhesive device patch fabricated by simple and low-cost laser scribing.”
Cheng explained that conventional fabrication techniques for flexible electronics can be complicated and costly, especially as sensors built on flexible substrates, or foundational layers, are not necessarily flexible themselves. The sensor’s rigidity can limit the flexibility of the entire device. Cheng’s team previously developed biomarker sensors using laser-induced graphene (LIG), which involves using a laser to pattern 3D networks on a porous, flexible substrate. The interactions between the laser and the materials contained in the substrate produce conductive graphene.
“However, the LIG-based sensors and devices on flexible substrates are not intrinsically stretchable and can’t conform to interface with human skin for bio-sensing,” Cheng said, noting that human skin is changeable in shape, temperature and moisture levels, especially during physical exertion when monitoring heart rate, nerve performance or sweat glucose levels might be necessary. “Although LIG can be transferred to stretchable elastomers, the process can greatly reduce its quality.”
As a result, Cheng said, it’s more difficult to program a sensor device to monitor specific biological or electrophysical signals. Even when the device can be appropriately programmed, its sensing performance is often degraded.
“To address these challenges, it is highly desirable to prepare porous 3D LIG directly on the stretchable substrate,” said co-author Jia Zhu, who graduated with a doctorate in engineering science and mechanics from Penn State in 2020 and is now an associate professor at the University of Electronic Science and Technology of China.

The researchers achieved this goal by making an adhesive composite with molecules called polyimide powders that add strength and heat resistance and amine-based ethoxylated polyethylenimine — a type of polymer that can modify conductive materials — dispersed in a silicone elastomer, or rubber. The stretchable composite not only accommodates direct 3D LIG preparation, but also its adhesive nature means it can conform and stick to non-uniform, changeable shapes — like humans.
The researchers experimentally confirmed that the device can monitor the pH value, glucose and lactate concentrations in sweat as well as can be detected via finger prick blood draws. It can also be reprogrammed to monitor heart rate, nerve performance and sweat glucose concentrations in real time. Reprogramming is as simple as applying clear tape over the LIG networks and peeling them off. The substrate can then be re-lasered to new specifications, up to four times before it becomes too thin. Once it becomes too thin, the entire device can be recycled.
Critically, according to Cheng, the device remains adhesive and capable of monitoring even when the skin is made slick with sweat or water. Currently powered by batteries or near-field communication nodules, like a wireless charger, the device could potentially harvest energy and communicate over radio frequencies, which researchers said would result in a standalone, stretchable adhesive platform capable of sensing desired biomarkers and monitoring electrophysical signals. The team said they plan to work toward this goal, in collaboration with physicians, to eventually apply the platform to manage various diseases such as diabetes and monitor acute issues like infections or wounds.
“We would like to create the next generation of smart skin with integrated sensors for health monitoring — along with evaluating how various treatments impact health — and drug delivery modules for in-time treatment,” Cheng said.

Many adults with diabetes and the associated complication of peripheral neuropathy, which can be painful as well as harmful, are often prescribed drugs at doses and for durations that could impose an increased risk of cognitive impairment.
A new study, led by Regenstrief Institute and Purdue University College of Pharmacy Research Scientist Noll Campbell, PharmD, M.S., is one of the first explorations of prescribing patterns of tricyclic antidepressants for treatment of diabetic peripheral neuropathy at healthcare facilities predominantly serving diverse populations of low socioeconomic status.
With a study population of adults 18 years and older that was 44 percent White and 42 percent Black, the researchers found that almost two-thirds of the prescribed tricyclic antidepressants were above the dosage threshold that has been associated with an increased risk of dementia in older adults. Black patients were more likely to be prescribed these drugs at higher doses, disproportionately increasing their risk for dementia compared with White patients.
The current body of evidence, much of it established and confirmed in studies by Regenstrief Institute research scientists, supports the existence of a relationship between long-term use of anticholinergic medications, such as tricyclic antidepressants, and cognitive impairment, including dementia. Research suggests use of anticholinergics in older adult populations increases risk of dementia 30 to 50 percent.
Diabetic peripheral neuropathy, a syndrome which occurs when neurons are damaged and impairs neurological function in the extremities causing pain, numbness, susceptibility to infection and other complications, is relatively common among adults living with long-term or uncontrolled Type I or Type II diabetes. Current diabetes care guidelines include use of tricyclic antidepressants to manage pain and co-existing depression; however, these guidelines don’t describe the risks of long-term use of these drugs, which are intended to work in the nerves and brain.
“Using data from electronic health records, we found tricyclic antidepressants being prescribed to people with diabetes for periods of five years, sometimes up to eight or nine years, at a rate that puts about two thirds of tricyclic antidepressants users at higher risk of dementia,” said Dr. Campbell, an aging brain and pharmacy services researcher. “Deprescribing may modify risk for dementia and there are other options of medications not associated with cognitive impairment that may be as effective, but we found very, very little evidence of routine evaluation of drug efficacy occurring in the clinical care environment.
“Older Black adults in the U.S. are disproportionately diagnosed with dementia as compared to older White adults. Is it disease or is it medication they are taking? It’s difficult to modify disease but it’s within our control to modify the types of medicines that we are using to manage disease states.”