Publisher Health

University of Michigan researchers have identified the protein that enables mammals to sense cold, filling a long-standing knowledge gap in the field of sensory biology.
The findings, published in Nature Neuroscience, could help unravel how we sense and suffer from cold temperature in the winter, and why some patients experience cold differently under particular disease conditions.
“The field started uncovering these temperature sensors over 20 years ago, with the discovery of a heat-sensing protein called TRPV1,” said neuroscientist Shawn Xu, a professor at the U-M Life Sciences Institute and a senior author of the new research.
“Various studies have found the proteins that sense hot, warm, even cool temperatures — but we’ve been unable to confirm what senses temperatures below about 60 degrees Fahrenheit.”
In a 2019 study, researchers in Xu’s lab discovered the first cold-sensing receptor protein in Caenorhabditis elegans, a species of millimeter-long worms that the lab studies as a model system for understanding sensory responses.
Because the gene that encodes the C. elegans protein is evolutionarily conserved across many species, including mice and humans, that finding provided a starting point for verifying the cold sensor in mammals: a protein called GluK2 (short for Glutamate ionotropic receptor kainate type subunit 2).
For this latest study, a team of researchers from the Life Sciences Institute and the U-M College of Literature, Science, and the Arts tested their hypothesis in mice that were missing the GluK2 gene, and thus could not produce any GluK2 proteins. Through a series of experiments to test the animals’ behavioral reactions to temperature and other mechanical stimuli, the team found that the mice responded normally to hot, warm and cool temperatures, but showed no response to noxious cold.

GluK2 is primarily found on neurons in the brain, where it receives chemical signals to facilitate communication between neurons. But it is also expressed in sensory neurons in the peripheral nervous system (outside the brain and spinal cord).
“We now know that this protein serves a totally different function in the peripheral nervous system, processing temperature cues instead of chemical signals to sense cold,” said Bo Duan, U-M associate professor of molecular, cellular, and developmental biology and co-senior author of the study.
While GluK2 is best known for its role in the brain, Xu speculates that this temperature-sensing role may have been one of the protein’s original purposes. The GluK2 gene has relatives across the evolutionary tree, going all the way back to single-cell bacteria.
“A bacterium has no brain, so why would it evolve a way to receive chemical signals from other neurons? But it would have great need to sense its environment, and perhaps both temperature and chemicals,” said Xu, who is also a professor of molecular and integrative physiology at the U-M Medical School. “So I think temperature sensing may be an ancient function, at least for some of these glutamate receptors, that was eventually co-opted as organisms evolved more complex nervous systems.”
In addition to filling a gap in the temperature-sensing puzzle, Xu believes the new finding could have implications for human health and well-being. Cancer patients receiving chemotherapy, for example, often experience painful reactions to cold.
“This discovery of GluK2 as a cold sensor in mammals opens new paths to better understand why humans experience painful reactions to cold, and even perhaps offers a potential therapeutic target for treating that pain in patients whose cold sensation is overstimulated,” Xu said.
The research was supported by the National Institutes of Health. All procedures performed in mice were approved by the Institutional Animal Care and Use Committee and performed in accordance with the institutional guidelines.
Study authors are: Wei Cai, Wenwen Zhang, Chia Chun Hor, Tong Pan, Mahar Fatima, Bo Duan and X.Z. Shawn Xu of the University of Michigan; and Qin Zheng and Xinzhong Dong of the Johns Hopkins University School of Medicine

From creating images, generating text, and enabling self-driving cars, the potential uses of artificial intelligence (AI) are vast and transformative. However, all this capability comes at a very high energy cost. For instance, estimates indicate that training OPEN AI’s popular GPT-3 model consumed over 1,287 MWh, enough to supply an average U.S. household for 120 years. This energy cost poses a substantial roadblock, particularly for using AI in large-scale applications like health monitoring where large amounts of critical health information are sent to centralized data centers for processing. This not only consumes a lot of energy but also raises concerns about sustainability, bandwidth overload, and communication delays.
Achieving AI-based health monitoring and biological diagnosis requires a standalone sensor that operates independently without the need for constant connection to a central server. At the same time, the sensor must have a low power consumption for prolonged use, should be capable of handling the rapidly changing biological signals for real-time monitoring, be flexible enough to attach comfortably to the human body, and be easy to make and dispose of due to the need for frequent replacements for hygiene reasons.
Considering these criteria, researchers from Tokyo University of Science (TUS) led by Associate Professor Takashi Ikuno have developed a flexible paper-based sensor that operates like the human brain. Their findings were published online in the journal Advanced Electronic Materialson 22 February 2024.
“A paper-based optoelectronic synaptic device composed of nanocellulose and ZnO was developed for realizing physical reservoir computing. This device exhibits synaptic behavior and cognitive tasks at a suitable timescale for health monitoring,” says Dr. Ikuno.
In the human brain, information travels between networks of neurons through synapses. Each neuron can process information on its own, enabling the brain to handle multiple tasks at the same time. This ability for parallel processing makes the brain much more efficient compared to traditional computing systems. To mimic this capability, the researchers fabricated a photo-electronic artificial synapse device composed of gold electrodes on top of a 10 µm transparent film consisting of zinc oxide (ZnO) nanoparticles and cellulose nanofibers (CNFs).
The transparent film serves three main purposes. Firstly, it allows light to pass through, enabling it to handle optical input signals representing various biological information. Secondly, the cellulose nanofibers impart flexibility and can be easily disposed of by incineration. Thirdly, the ZnO nanoparticles are photoresponsive and generate a photocurrent when exposed to pulsed UV light and a constant voltage. This photocurrent mimics the responses transmitted by synapsis in the human brain, enabling the device to interpret and process biological information received from optical sensors.
Notably, the film was able to distinguish 4-bit input optical pulses and generate distinct currents in response to time-series optical input, with a rapid response time on the order of subseconds. This quick response is crucial for detecting sudden changes or abnormalities in health-related signals. Furthermore, when exposed to two successive light pulses, the electrical current response was stronger for the second pulse. This behavior termed post-potentiation facilitation contributes to short-term memory processes in the brain and enhances the ability of synapses to detect and respond to familiar patterns.
To test this, the researchers converted MNIST images, a dataset of handwritten digits, into 4-bit optical pulses. They then irradiated the film with these pulses and measured the current response. Using this data as input, a neural network was able to recognize handwritten numbers with an accuracy of 88%.
Remarkably, this handwritten-digit recognition capability remained unaffected even when the device was repeatedly bent and stretched up to 1,000 times, demonstrating its ruggedness and feasibility for repeated use. “This study highlights the potential of embedding semiconductor nanoparticles in flexible CNF films for use as flexible synaptic devices for PRC,” concludes Dr. Ikuno.
Let us hope that these advancements pave the way for wearable sensors in health monitoring applications!

Natural products have unique chemical structures and biological activities and can play a pivotal role in advancing pharmaceutical science. In a pioneering study, researchers from Shinshu University discovered Inaoside A, an antioxidant derived from Laetiporus cremeiporus mushrooms. This breakthrough sheds light on the potential of mushrooms as a source of therapeutic bioactive compounds.
The search for novel bioactive compounds from natural sources has gained considerable momentum in recent years due to the need for new therapeutic agents to combat various health challenges. Among a diverse array of natural products, mushrooms have emerged as a rich reservoir of bioactive molecules with potential pharmaceutical and nutraceutical applications. The genus Laetiporus has attracted attention for its extracts exhibiting antimicrobial, antioxidant, and antithrombin bioactivities. The species Laetiporus cremeiporus, spread across East Asia, has also been reported to show antioxidant properties. However, the identification and characterization of specific antioxidant compounds from this species have not been conducted.
In a groundbreakng study, researchers led by Assistant Professor Atsushi Kawamura from the Department of Biomolecular Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, along with Hidefumi Makabe from the Department of Agriculture, Graduate School of Science and Technology, Shinshu University, and Akiyoshi Yamada from the Department of Mountain Ecosystem, Institute for Mountain Science, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, recently discovered the antioxidant compound derived from L. cremeiporus.
The researchers collected fresh fruiting bodies of L. cremeiporus from the Ina campus of Shinshu University. The obtained extracts were concentrated and partitioned between water and ethyl acetate. After this, the extracts were subjected to advanced chromatographic techniques, which led to the successful isolation of Inaoside A, a new antioxidant phenolic compound, along with three other well-characterized bioactive compounds, i.e., 5′-S-methyl-5′-thioadenosine (MTA), nicotinamide, and adenosine. They reported their findings in an article that was made available online on 20 January 2024 and subsequently published in the journal Heliyon.
“Our study marks the pioneering discovery of Inaoside A from an extract of the edible mushroom Laetiporus cremeiporus. To date, there has been only one prior report on the biological function of an extract of L. cremeiporus. We are the first to uncover the isolation of an antioxidant compound from L. cremeiporus,” states Professor Kawamura, highlighting the breakthrough research.
Next, the researchers wanted to determine the structure of the newly found antioxidant compound. For this, they utilized one and two- dimensional NMR and other spectroscopic analyses. The structure of Inaoside A revealed a planar configuration. With a molecular formula of C17H24O7, the compound was found to feature a distinctive ribose moiety, identified as α-ribofuranoside through stereochemical analysis. Subsequent investigation into the absolute stereochemistry confirmed the D-ribose configuration, thereby reinforcing the planar structure of this compound.
The mushroom extracts were then isolated into fractions to determine the antioxidant activities of the four isolated bioactive compounds. These fractions were then examined by DPPH radical scavenging and superoxide dismutase assays. The findings were noteworthy as the DPPH radical scavenging activity exhibited by Inaoside A was significant, showing 80% inhibition at 100 μg/mL, indicative of its significant antioxidant properties. The IC50 value of Inaoside A was determined to be 79.9 μM, further highlighting its efficacy as an antioxidant agent.
What are the objectives of the researchers following the discovery of Inaoside? Professor Kawamura reveals, “We are now focusing on investigating the chemical compositions and biological properties of natural compounds obtained from mushrooms. Our goal is to uncover the potential of edible mushrooms as functional foods through this discovery.”
The identification of Inaoside A as an antioxidant from Laetiporus cremeiporus marks a significant breakthrough in natural product research, highlighting the potential of mushrooms as a source of therapeutic bioactive compounds. These findings may lead to the development of novel antioxidant-based therapies for various health conditions. Further studies should focus on synthetic research and detailed investigations into the biological activity of Inaoside A, aiming to harness its potential as a pharmaceutical lead compound.

University of Virginia School of Medicine scientists have found important answers about strokes, heart attacks and cardiovascular diseases by probing the biological glue our bodies create to protect us from those deadly dangers.
The researchers, led by Mete Civelek, PhD, wanted to better understand factors that influence our risk for cardiovascular diseases such as atherosclerosis, the hardening of the arteries. Atherosclerosis is characterized by the buildup of fatty plaques in our blood vessels. When these plaques form, our bodies build fibrous caps over them to keep them from breaking loose and causing heart attacks and strokes.
Civelek and his team thought that the scaffolding our bodies build over these plaques might contain important clues that could improve our understanding of cardiovascular diseases, the leading cause of death around the world. And by taking a clever approach, the scientists were able to obtain important new insights that could advance the development of lifesaving treatments.
“We combined two decades of human genetics findings and a unique resource of smooth muscle cells, an important component of arteries where the plaques develop,” said Civelek, of UVA’s Center for Public Health Genomics and the Department of Biomedical Engineering. “We discovered that our genetic makeup impacts the ways smooth muscle cells secrete proteins that provide strength to plaques and prevent them from rupturing and causing heart attacks and strokes.”
Vital Cellular Glue
To construct the protective scaffolding over the potentially deadly plaques, smooth muscle cells that line our blood vessels secrete what is known as “extracellular matrix” — a fibrous, glue-like material rich in proteins. Civelek and his team measured these proteins, and related proteins, in smooth muscle cells collected from 123 heart transplant donors. The scientists were then able to work backward, essentially, to identify genes that made those proteins.
Doing this let the scientists identify 20 locations on our chromosomes that house genes that influence the production of the critical proteins. It also let them pinpoint a naturally occurring gene variation that puts certain people at higher risk for hardening of the arteries, as well as identify types of proteins that contribute to our cardiovascular risk. Doctors may be able to leverage the new insights to identify patients at greatest risk of having the plaques break free and cause heart attacks or strokes, the UVA researchers say.
The findings also shed important light on why the efforts of the smooth muscle cells sometimes are beneficial and sometimes are harmful. That information will be a great asset to researchers seeking to develop new treatments for atherosclerosis and cardiovascular diseases, Civelek says.
“We identified one protein, LTBP1, that we think plays an important role in plaque stability,” he said. “We will continue to study if this protein can be a beneficial therapeutic target and hope to translate our findings to patient care soon.”

Early stages of neurodegenerative disorders are characterized by the accumulation of proteins in discrete populations of brain cells and degeneration of these cells. For most diseases, this selective vulnerability pattern is unexplained, yet it could yield major insight into pathological mechanisms. Alzheimer’s disease (AD), the world-leading cause of dementia, is defined by the appearance of two hallmark pathological lesions, amyloid plaques (extracellular aggregates of Aβ peptides) and neurofibrillary tangles (intracellular aggregates of hyperphosphorylated tau, or NFTs). While plaques are widespread in the neocortex and hippocampus, NFTs follow a well-defined regional pattern that starts in principal neurons from the entorhinal cortex.
In a new study from Boston University Chobanian & Avedisian School of Medicine, researchers have identified a gene they believe may lead to the degeneration of the neurons that are most vulnerable to AD.
“We are trying to understand why certain neurons in the brain are particularly vulnerable during the earliest stages of AD. Why they accumulate and degenerate very early is unknown. We believe elucidating this vulnerability would allow for a new therapeutic avenue for AD,” said corresponding author Jean-Pierre Roussarie, PhD, assistant professor of anatomy & neurobiology at the school.
In collaboration with leading computational genomic experts from Rice University, the BU researchers along with co-corresponding author, Patricia Rodriguez-Rodriguez, PhD, from Karolinska Institute, used cutting-edge analysis tools with machine learning to identify the gene DEK as possibly responsible for vulnerability of entorhinal cortex neurons. They injected viruses into the entorhinal cortex of experimental models and neurons grown in the lab to manipulate levels of the DEK gene. When they reduced the levels of the DEK gene, vulnerable neurons started to accumulate tau and to degenerate.
According to the researchers, preventing these neurons from degeneration by targeting DEK or proteins that collaborate with DEK, would prevent patients from developing memories loss and would curtail the disease before it spreads to larger areas of the brain. “Given that entorhinal cortex neurons are necessary for the formation of new memories and since they are so vulnerable and the first to die, this explains why the first symptom of AD is the inability to form new memories,” said Roussarie.
The researchers believe these findings are the first step in understanding how these fragile neurons die, yet they hope to uncover additional genes to fully understand what leads to the death of critical memory-forming neurons.
These findings appear online in the journal Brain.
P.R-R. was supported by the European Union’s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant agreement No 799638. P.R-R and C.T. were supported by Alzheimerfonden and Margaretha af Ugglas Stiftelse. P.R-R., M.F. and J.P.R. were supported by the Fisher Center for Alzheimer’s Disease Research. J.P.R. was supported by Cure Alzheimer’s Fund. This study was supported by the National Institute on aging of the NIH (awards RF1 AG054564 and RF1 AG047779 to J.P.R.).
Note: Angel Cedazo-Minguez is an employee at Sanofi.

Physicians treating patients with early-stage lung cancer face a conundrum: choosing potentially helpful yet toxic therapies such as chemotherapy, radiation or immunotherapy to knock out the cancer and lessen the risk of it spreading to the brain, or waiting to see if lung surgery alone proves sufficient. When up to 70% of such patients do not experience brain metastasis — the spread of cancer to the brain — the question arises: Who should receive additional aggressive treatments, and who can safely wait?
A new study led by Washington University School of Medicine in St. Louis could help physicians strike the right balance between proactive intervention and cautious monitoring for patients with early-stage lung cancer. The study, published March 4 in The Journal of Pathology, uses an artificial intelligence (AI) method to study patients’ lung biopsy images and predict whether the cancer will spread to the brain.
“There are no predictive tools available to help physicians when treating patients with lung cancer,” said Richard J. Cote, MD, the Edward Mallinckrodt Professor and head of the Department of Pathology & Immunology. “We have risk predictors that tell us which population is more likely to progress to more advanced stages, but we lack the ability to predict individual patient outcomes. Our study is an indication that AI methods may be able to make meaningful predictions that are specific and sensitive enough to impact patient management.”
Lung cancer is the leading cause of cancer death in the U.S. and worldwide. Most lung cancers are characterized as non-small cell lung cancers, which are largely, but not exclusively, caused by smoking. For early-stage cancer patients, tumors are confined to the lung, and surgery is recommended as a first line of treatment. Roughly 30% of such patients progress to advanced stages, when the cancer spreads to the lymph nodes and other organs. With the brain often affected first, such patients require additional treatments, including chemotherapy, targeted drug therapy, radiation therapy and/or immunotherapy. However, physicians have no way of knowing whose cancer will progress, so they frequently treat patients with aggressive therapies out of caution.
Cote worked with Ramaswamy Govindan, MD, the Anheuser Busch Endowed Chair in Medical Oncology and associate director of the oncology division at Washington University; Mark Watson, MD, PhD, the Margaret Gladys Smith Professor in the Department of Pathology & Immunology; and Changhuei Yang, PhD, a professor of electrical engineering, bioengineering, and medical engineering at the California Institute of Technology, to determine if AI could predict whether cancer will spread to the brain.
In diagnostic testing, a pathologist examines biopsied tissues under a microscope to identify cellular abnormalities that may hint at disease. Advanced technologies — such as AI — are being explored to replicate what a pathologist sees when making diagnoses but with greater accuracy, Cote explained.
A key question: Can AI detect abnormal features that a pathologist cannot?

The researchers trained a machine-learning algorithm to predict brain metastasis using 118 lung biopsy samples from early-stage non-small cell lung cancer patients. Some of the patients developed brain cancer during a five-year monitoring period, and some did not and were in remission. Then the researchers tested the AI method on its ability to predict brain metastasis, and to identify patients who develop no metastasis, using 40 other patients’ lung biopsy samples.
The algorithm was able to predict the eventual development of brain cancer with 87% accuracy. In comparison, four pathologists who participated in the study were an average of 57.3% accurate. Importantly, the algorithm was highly accurate in predicting which patients would not develop brain metastasis.
“Our results need to be validated in a larger study, but we think there is great potential for AI to make accurate predictions and impact care decisions,” said Govindan, who treats lung cancer patients at Siteman Cancer Center, based at Barnes-Jewish Hospital and Washington University School of Medicine. “Systemic treatments such as chemotherapy, while effective in killing cancer cells, can also harm healthy cells and are not always the preferred treatment method for all early-stage cancer patients. Identification of patients who are likely to relapse in the brain may help us develop strategies to intercept cancer early in the process of metastasis. We think AI-based predictions could, one day, inform personalized treatments.”
The AI system evaluates tumors’ and healthy cells’ features, similar to how the human brain allows us to scan facial features for quick recognition of familiar faces. However, what the algorithm sees is unknown; the scientists are working to understand the molecular and cellular features that AI uses for its predictions. This knowledge could lead to the development of novel therapeutics and influence the design of imaging instruments optimized for the collection of data for AI.
“This study started as an attempt to find predictive biomarkers,” said Yang. “But we couldn’t find any. Instead, we found that AI has the potential to make predictions about cancer progression using biopsy samples that are already being collected for diagnosis. If we can get to a prediction accuracy that will allow us to use this algorithm clinically and not have to resort to expensive biomarkers, we are talking about significant ramifications in cost-effectiveness.”

Researchers at DZNE provide evidence that traces of the widely used PFAS chemicals in human blood are associated with unfavorable lipid profiles and thus with an increased risk of cardiovascular diseases. The findings are based on data from more than 2,500 adults from Bonn and the Dutch municipality of Leiderdorp. PFAS were detectable in the blood of nearly all study participants. The study results have been published in the scientific journal Exposure and Health.
Since their invention in the 1950s, more than 10,000 different substances from the category of per- and polyfluorinated alkyl compounds (PFAS) have been developed, according to estimates. Due to their water, fat and dirt-repellent properties, they are used in thousands of products such as cosmetics, dental floss, but also in pan coatings and fire-extinguishing foam. In addition to their basic chemical structure, PFAS have another thing in common: they are nearly non-degradable. Particularly via groundwater that they enter the human food chain.
Younger people are particularly affected
The findings of the Bonn researchers are the latest contribution to the current debate on the effect of PFAS on human health. “We see clear signs of a harmful effect of PFAS on health. And we have found that at the same PFAS concentration in the blood, the negative effects are more pronounced in younger subjects than in older ones,” says Prof. Dr. Dr. Monique Breteler, Director of Population Health Sciences at DZNE. The results of the current study also suggest that even relatively low PFAS concentrations in the blood are associated with unfavorable blood lipid profiles.
“Our data shows a statistically significant correlation between PFAS in the blood and harmful blood lipids linked to cardiovascular risk. The higher the PFAS level, the higher the concentration of these lipids. Taken strictly, this is not yet a proof that PFAS chemicals cause the unfavorable blood lipid profiles. However, the close correlation supports this suspicion. It is a strong argument for stricter regulation of PFAS in order to protect health,” says the Bonn researcher. Strikingly, PFAS could be detected in the blood of almost all test subjects. Which means you cannot escape these chemicals. “Even if we don’t see an immediate health threat for the study participants we examined, the situation is still worrying. In the long term, the increased risk may very well have a negative impact on the heart and cardiovascular system,” says Breteler.
Blood samples from Bonn and the Netherlands
The current study was based on DZNE’s “Rhineland Study” — a population-based health study in the Bonn urban area — and the so-called NEO study from the Netherlands (“Netherlands Epidemiology of Obesity study”). In this framework, researchers from DZNE collaborated with experts from the Leiden University Medical Center in the Netherlands. Blood samples from a total of more than 2,500 women and men aged between 30 and 89 were included in the analyses. For this, state-of-the-art technology was used. “The technology to analyze blood samples with the accuracy required for our research has only become available in recent years,” says DZNE scientist Elvire Landstra. She is the first author of the current publication together with a colleague from Leiden.
Most detailed study so far
The blood samples were analyzed in detail using a sophisticated method known as mass spectrometry. In their analysis, the researchers focused on three of the most widespread types of PFAS — PFOA, PFOS and PFHxS — and also determined the concentration of 224 blood lipids, metabolites and amino acids. “With this ‘untargeted approach’ — an intentionally broad approach without a preconceived target — we were able to prove the connection between the PFAS concentration and a problematic profile of fatty substances, so-called lipids. These include the well-known cholesterol and various other blood lipids that are known to be risk factors for cardiovascular disease,” says Elvire Landstra. No significant differences were found between the samples from Bonn and Leiderdorp. “Our study is the most detailed on this topic to date and the one with the largest database. Previous studies had already suggested a correlation between PFAS and unhealthy blood lipids, but this link had never been as clear as in our study.”
Future studies could focus on specific areas of the body, the Bonn researchers suggest. “We looked at the blood levels. In a next step, it would make sense to investigate the occurrence of PFAS in individual organs,” Monique Breteler says.

A team of international researchers — including experts from the University of Central Florida and Emory University — has demonstrated, for the first time in a field study, that using folic acid-fortified iodized table salt can prevent multiple severe birth defects.
The importance of women having enough folic acid in their bodies before and during pregnancy to prevent permanent and life-threatening birth defects, such as spina bifida and anencephaly, has been known for decades. The World Health Organization recommends that all women should take supplement pills with 400 micrograms of folic acid daily, from the moment they begin attempting to conceive through the first three months of pregnancy.
Mandatory staple food fortification with folic acid is a cost-effective, safe, and an equitable way to address the issue. In May 2023, the World Health Assembly adopted a resolution promoting food fortification with folic acid to accelerate the slow pace of prevention of spina bifida and other birth defects associated with low maternal folate levels at the time of early pregnancy.
Yet approximately 260,000 births worldwide — about 20 per every 10,000 births — are still affected by spina bifida and anencephaly, contributing to a high number of stillbirths, elective pregnancy terminations, and deaths of infants and young children.
The problem
While folic acid has been added through mandatory staple grain food fortification in about 65 countries, including the United States, more than 100 countries have yet to implement fortification due to challenges that include limited capacity for large-scale fortification of staple grains in these regions or lack of political will.
A solution
A new study published Friday by JAMA Network Open showed that a solution is not only possible, many people already have it on their kitchen tables.

The clinical trial showed that mixing folic acid to commercially available iodized table salt, based on the existing average daily consumption of salt, increased serum folate levels among participants to levels needed for prevention of spina bifida and anencephaly. The increase was significant, a 3.7-fold improvement before and after a four-month period of using the study salt with iodine and folic acid.
“We proved that folic acid can get into the blood through salt. Hopefully countries that have not already implemented fortification programs can now look at their infrastructures and realize that salt fortification is cheap and it’s really easy to add in the amount of folic acid needed to save lives,” says Jogi Pattisapu, MD, the study’s lead author and a neurosurgeon from UCF’s College of Medicine. “It might just turn the salt a little yellow, but the participants did not mind and we know it works. What we need now is action.”
Why it matters
Pattisapu credits the study’s successful outcome to the collaborative nature of the research team, specifically the efforts and expertise of researchers from Emory University’s Rollins School of Public Health and the colleagues from multiple institutions in India, who co-led the study and recruited and monitored the 83 non-pregnant women — who were between the ages of 18-45, from four different villages in southern India — who consumed the folic acid-fortified salt as part of their regular diet during a four-month period in 2022. India has a high prevalence of spina bifida and anencephaly.
“Work was done there, by the Indian team, for their cause,” Pattisapu says. “That was very important, and it is a powerful message.”
Even though food fortification is mandatory in the United States, the researchers say the impact of this new study could be felt globally in countries with successful salt iodization programs.

“This is a global goodwill involving the health of mothers and babies. We are making sure we apply the knowledge we have,” says Vijaya Kancherla, an associate professor in the Department of Epidemiology at Rollins. “These are preventable birth defects and once it happens, you cannot cure it. Surgeries and clinical care are expensive and largely not available in low- and middle-income countries. Due to that, most babies with spina bifida die globally. So, it is a human rights issue that everyone should be worried about and should strive to find alternate solutions that prevent these conditions from occurring in the first place, no matter where one is born. We show that salt has the potential to close the prevention gap now.”
The researchers also made it clear the study does not promote salt intake, but rather adding the necessary amount of folic acid to the table salt that residents of these regions are already consuming. If the average daily salt consumption is reduced in these regions, the concentration of folic acid would simply be increased, to meet the need. This approach is already used in grain fortification program.
The researchers said at least 50 percent of the current global spina bifida cases would be prevented if the major, already existing iodized salt programs took the simple step of adding folic acid.
“We now know folic acid fortification of iodized salt can prevent folate deficiency that causes spina bifida,” says Godfrey Oakley Jr., MD, director of the Center for Spina Bifida Prevention at Rollins. “The stage is now set for a rapid acceleration of prevention of these birth defects in many countries”

Researchers have developed a photoacoustic imaging watch for high-resolution imaging of blood vessels in the skin. The wearable device could offer a non-invasive way to monitor hemodynamic indicators such as heart rate, blood pressure and oxygen saturation that can indicate how well a person’s heart is working.
“Although photoacoustic imaging is extremely sensitive to variations in hemodynamics, difficulties in miniaturizing and optimizing the imaging interface have limited the development of wearable photoacoustic devices,” said research team leader Lei Xi from the Southern University of Science and Technology in China. “To the best of our knowledge, this is the first photoacoustic wearable device that is suitable for healthcare applications.”
In the Optica Publishing Group journal Optics Letters, the researchers describe their new system, which consists of a watch with an imaging interface, a handheld computer and a backpack housing the laser and power supply. Tests with volunteers moving freely showed that the device can be used to observe blood flow variations during different activities such as walking.
“Miniaturized wearable imaging systems like the one we developed could potentially be used by community health centers for preliminary disease diagnosis or for long-term monitoring of parameters related to blood circulation within a hospital setting, offering valuable insights to inform treatments for various diseases,” said Xi. “With further development this type of system could also be helpful for the early detection of skin conditions such as psoriasis and melanoma or for analyzing burns.”
Creating a wearable imager
Photoacoustic imaging is a label-free technique that forms images by measuring light-induced sound waves created by light absorption in structures. Analyzing the photoacoustic signal intensity and distribution offers insights into the functional and structural characteristics of microvessels, which can be altered by various diseases. Although photoacoustic imaging is still primarily a research tool, it is beginning to find clinical application in areas such as cancer, vascular and dermatological imaging.
To turn what is typically a bulky instrument into something that could be worn while moving around, the researchers developed a compact optical resolution photoacoustic microscopy system based on a compact pulsed laser, tight fiber-based light path and an integrated electronic system housed in a backpack weighing 7 kilograms. They also designed a handheld device to store the images and created a miniaturized watch-type imaging interface with an adjustable focal plane and a screen display for displaying the images in real time.

The researchers designed the system so that it could be used for imaging while the wearer is freely moving around. It also features an adaptable laser focus, which is necessary for imaging multilayered structures like skin. The photoacoustic imaging system has a lateral resolution of 8.7 µm, which is sufficient to resolve most microvessels in the skin and a maximum field of view of around 3 mm in diameter, which is adequate for capturing microvascular details.
Tracking blood on the move
The researchers tested the device with volunteers to evaluate the focus shifting function of the watch and the system’s capacity to detect blood flow changes over an extended time under different conditions, such as while the wearer was walking and when a cuff was used to temporarily block blood flow to the arm. These tests showed that the system is usable and compact and stable enough to allow free movement.
The researchers are now working to create a system that employs an even smaller laser source with a higher repetition rate. This will make the system more compact and lighter while also enhancing safety and temporal resolution. “Given the rapid development of modern laser diode technology and electronic information technology, it should be entirely feasible to develop a more advanced and intelligent photoacoustic watch that doesn’t require a backpack,” said Xi.
The researchers are also working to ensure the stability of the fiber-coupled optical path over extended periods and under more intense conditions such as running and jumping. They also want to incorporate multispectral illumination, which would allow the acquisition of additional physiological parameters including oxygen saturation and blood flow velocity and the quantitative assessment of parameters such as vessel number and volume. These capabilities could help support early diagnosis of conditions such as cancer and cardiovascular diseases.

Anemonefish form mutualistic relationships with the sea anemones they live in and these associations are not random: some species such as the yellow-tail anemonefish (Amphiprion clarkii) are generalists and can live in almost any sea anemone, others like the tomato clownfish (Amphiprion frenatus) are specialists, living in only one sea anemone species, the bubble-tip sea anemone (Entacmaea quadricolor). Reasons for these preferences are unclear because we know very little about the genetic diversity of giant sea anemones.
Researchers at the Marine Eco-Evo-Devo Unit and Marine Genomics Unit at the Okinawa Institute of Science and Technology (OIST) and Academia Sinica in Taiwan have studied the evolutionary history of giant sea anemones in Japan. Rio Kashimoto, Dr. Manon Mercader, Jann Zwahlen, Dr. Saori Miura, Prof. Konstantin Khalturin and Prof. Vincent Laudet published their findings in the journal Current Biology. Their study provides a detailed analysis of the genetic diversity of the bubble-tip giant sea anemone (Entacmaea quadricolor) found in Japan.
The scientists discovered that anemonefish are better at distinguishing different populations of giant sea anemones than humans. Through one or more sensory organs, these fish identify a particular species of giant sea anemone to make their home and avoid other species. Humans, on the other hand, need to obtain samples from sea anemones and do a thorough examination of their molecular data to identify individual sea anemone species. This is precisely what the scientists at OIST did to better understand the genetic variation among these soft-bodied marine invertebrates.
Giant sea anemones have evolved into 3 very different genera: Entacmaea (bubble-tip sea anemones), Stichodactyla (carpet sea anemones), and Heteractis (magnificent sea anemones). There are currently 10 known species of giant sea anemones worldwide and 7 of these live in Okinawa. The researchers collected pieces of tentacles from all 7 species. In total, 55 samples were collected in Japan at study sites ranging from southern Okinawa to north of Tokyo.
All the genes in each sample were sequenced — a technique that enabled the researchers to determine the specific genetic information contained within RNA molecules. Using this information, they were able to construct a phylogenetic tree, a diagram showing the evolutionary relationships among species and how they evolved from a series of common ancestors.
The scientists discovered remarkable genetic variety within the bubble-tip sea anemone specimens, identifying 4 unique genetic lineages — a sequence of species considered to have evolved from its predecessor.
“Within the bubble-tip giant sea anemone species (Entacmaea) our phylogenetic tree reveals the presence of two main groups with a common ancestor in Okinawa. The first group consists of three categories of descendants, A, B, and C, which are associated with the yellow-tail anemonefish as the host species. The second group, category D, is associated with the tomato anemonefish as the host species,” Rio Kashimoto, lead author of the paper, explained.

The researchers observed this association in the wild and wanted to know if the fish can also distinguish between the two sea anemone groups in captivity. They conducted a choice experiment using a large tank at the OIST Marine Science Station, putting one sea anemone from group A at one end of the tank and one from group D at the other end. They placed either a yellow-tail or tomato juvenile anemonefish in the middle of the tank and recorded if the fish chose to stay in a sea anemone or not, and if it did, which sea anemone group the species chose.
The yellow-tail anemonefish always selected group A when they chose to stay in a sea anemone, but some fish did not select a sea anemone. Most tomato anemonefish chose the lineage D sea anemone, very few individuals chose lineage A, and some did not select a sea anemone.
“In lab experiments we observed that in most cases each anemonefish species can recognize the sea anemone lineage it is associated with in the wild, despite the fact the clades look the same. We also observed that these lineages do not express the same genes, especially genes for toxicity and color — sea anemones use venom for prey capture, digestion and defense, and they probably do not have the same odor, which may be a key part in how anemonefish recognize different lineages,” Prof. Laudet, leader of the Marine Eco-Evo-Devo Unit, stated.
“Therefore, anemonefish are able to identify distinct lineages of sea anemones that we humans can’t distinguish. We believe that these two main groups represent two cryptic species — species that we cannot identify by looking at them, but they are genetically distinct.”
This discovery means that the bubble-tip sea anemone could in fact be two different species hiding in plain sight, and that Okinawa and Japan are home to more marine biological diversity than previously thought.