A protein found in human sweat may protect against Lyme disease

Human sweat contains a protein that may protect against Lyme disease, according to a study from MIT and the University of Helsinki. About one-third of the population carries a genetic variant of this protein that is associated with Lyme disease in genome-wide association studies.
Photo Credit: Erik Karits

Lyme disease, a bacterial infection transmitted by ticks, affects nearly half a million people in the United States every year. In most cases, antibiotics effectively clear the infection, but for some patients, symptoms linger for months or years.

Researchers at MIT and the University of Helsinki have now discovered that human sweat contains a protein that can protect against Lyme disease. They also found that about one-third of the population carries a genetic variant of this protein that is associated with Lyme disease in genome-wide association studies.

It’s unknown exactly how the protein inhibits the growth of the bacteria that cause Lyme disease, but the researchers hope to harness the protein’s protective abilities to create skin creams that could help prevent the disease, or to treat infections that don’t respond to antibiotics.

“This protein may provide some protection from Lyme disease, and we think there are real implications here for a preventative and possibly a therapeutic based on this protein,” says Michal Caspi Tal, a principal research scientist in MIT’s Department of Biological Engineering and one of the senior authors of the new study.

Hanna Ollila, a senior researcher at the Institute for Molecular Medicine at the University of Helsinki and a researcher at the Broad Institute of MIT and Harvard, is also a senior author of the paper, which appears today in Nature Communications. The paper’s lead author is Satu Strausz, a postdoc at the Institute for Molecular Medicine at the University of Helsinki.

UC Irvine-led research team discovers role of key enzymes that drive cancer mutations

“Both APOBEC3A and APOBEC3B were known to generate mutations in many kinds of tumors, but until now we did not know how to identify the specific type caused by each,” says the study’s corresponding author, Rémi Buisson (center), UCI assistant professor of biological chemistry. He’s flanked by postdoctoral fellow Pedro Ortega (left) and graduate student Ambrocio Sanchez, UCI researchers who developed a new method to characterize the particular kind of DNA modified by the enzymes.
Photo Credit: UCI School of Medicine

A research team led by the University of California, Irvine has discovered the key role that the APOBEC3A and APOBEC3B enzymes play in driving cancer mutations by modifying the DNA in tumor genomes, offering potential new targets for intervention strategies.

The study, published today online in the journal Nature Communications, describes how the researchers identified the process by which APOBEC3A and APOBEC3B detect specific DNA structures, resulting in mutations at distinct positions within the tumor genome.

“It’s critical to understand how cancer cells accumulate mutations leading to hot spots that contribute to disease progression, drug resistance and metastasis,” said corresponding author Rémi Buisson, UCI assistant professor of biological chemistry. “Both APOBEC3A and APOBEC3B were known to generate mutations in many kinds of tumors, but until now we did not know how to identify the specific type caused by each. This finding will allow us to develop novel therapies to suppress mutation formation by directly targeting each enzyme accordingly.”

All creatures great and small: Sequencing the blue whale and Etruscan shrew genomes

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The blue whale genome was published in the journal Molecular Biology and Evolution, and the Etruscan shrew genome was published in the journal Scientific Data.

Research models using animal cell cultures can help navigate big biological questions, but these tools are only useful when following the right map.

“The genome is a blueprint of an organism,” says Yury Bukhman, first author of the published research and a computational biologist in the Ron Stewart Computational Group at the Morgridge Institute, an independent research organization that works in affiliation with the University of Wisconsin–Madison in emerging fields such as regenerative biology, metabolism, virology and biomedical imaging. “In order to manipulate cell cultures or measure things like gene expression, you need to know the genome of the species — it makes more research possible.”

The Morgridge team’s interest in the blue whale and the Etruscan shrew began with research on the biological mechanisms behind the “developmental clock” from James Thomson, emeritus director of regenerative biology at Morgridge and longtime professor of cell and regenerative bBiology in the UW School of Medicine and Public Health.  It’s generally understood that larger organisms take longer to develop from a fertilized egg to a full-grown adult than smaller creatures, but the reason why remains unknown.

“It’s important just for fundamental biological knowledge from that perspective. How do you build such a large animal? How can it function?” says Bukhman.

Alzheimer’s Drug Fermented with Help from AI and Bacteria Moves Closer to Reality

Photo-Illustration Credit: Martha Morales/The University of Texas at Austin

Galantamine is a common medication used by people with Alzheimer’s disease and other forms of dementia around the world to treat their symptoms. Unfortunately, synthesizing the active compounds in a lab at the scale needed isn’t commercially viable. The active ingredient is extracted from daffodils through a time-consuming process, and unpredictable factors, such as weather and crop yields, can affect supply and price of the drug. 

Now, researchers at The University of Texas at Austin have developed tools — including an artificial intelligence system and glowing biosensors — to harness microbes one day to do all the work instead. 

In a paper in Nature Communications, researchers outline a process using genetically modified bacteria to create a chemical precursor of galantamine as a byproduct of the microbe’s normal cellular metabolism.  Essentially, the bacteria are programmed to convert food into medicinal compounds.

“The goal is to eventually ferment medicines like this in large quantities,” said Andrew Ellington, a professor of molecular biosciences and author of the study. “This method creates a reliable supply that is much less expensive to produce. It doesn’t have a growing season, and it can’t be impacted by drought or floods.” 

The integrity of the blood-brain barrier depends on a protein that is altered in some neurodegenerative diseases

From left to right, Pilar Villacampa, Víctor Arribas and Eloi Montañez.
Photo Credit: Courtesy of University of Barcelona

Defects in the blood vessel network of the central nervous system have been linked to early symptoms of neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS). It is this complex vascular network that provides the necessary nutrients, especially glucose and oxygen to activate all neuronal functions. Now, a study led by the University of Barcelona and the Bellvitge Biomedical Research Institute (IBIDELL) reveals that the TDP-43 protein is essential for forming a stable and mature blood vessel network in the central nervous system.

According to the study the TDP-43 protein is also critical in maintaining the integrity of the blood-brain barrier, which prevents toxins and pathogens from reaching the central nervous system.

The project is led by Professor Eloi Montañez, from the Faculty of Medicine and Health Sciences of the University of Barcelona and IDIBELL, and involves teams from the Faculty of Biology and the Institute of Biomedicine of the UB (IBUB), the Josep Carreras Leukemia Research Institute, and the National Centre for Genomic Analysis (CNAG-CRG).

It's in the Blood: Donor Diets Can Trigger Allergic Reactions in Blood Recipients

Photo Credit: Aman Chaturvedi

Blood transfusions are often life-saving procedures in various medical settings. They are required not only after severe blood loss due to surgery or trauma but also as standard treatment for certain blood disorders like anemia and sickle cell disease. However, blood transfusions can have serious side effects, with allergic transfusion reactions (ATRs) being particularly prevalent among children. Although scientists believe ATRs are caused by immunoglobulin E (IgE)-mediated type 1 allergy (or “immediate hypersensitivity”), the responsible allergens are not always known.

Against this backdrop, a research team composed of Dr. Ryu Yanagisawa of Shinshu University Hospital, Japan, alongside Dr. Minoru Tozuka and Dr. Yasunori Ito from Nagano Children's Hospital, Japan, set out to find more answers. In their latest study, published online in the journal Allergy, the researchers focused their attention on what might have appeared to be an unlikely suspect. Dr. Yanagisawa, wo led the study at the University’s Division of Blood Transfusion, explains: “In our previous study, we found that pediatric patients with food allergies were characteristically more prone to ATRs. Considering that food allergies are also more prevalent in children, we decided to investigate whether the food the donor ate before giving blood could be associated with the development of ATRs in children with food allergies.”

Is life based on a seeming violation of Newton’s law in molecular interactions?

Interactions between molecules that are not equal and opposite, a seeming violation of Newton’s third law of motion, can occur naturally according to new research. A kinase enzyme adds a chemical modification to other molecules, resulting in a phosphorylated protein. Phosphatase enzymes remove the modifications, such that the kinases create products that are acted upon by phosphatases and vice versa. Researchers demonstrated that the kinase is attracted to the phosphatase, but the phosphatase is repelled by the kinase, in what is called a non-reciprocal interaction.
Illustration Credit: Niladri Sekhar Mandal / Pennsylvania State University
(CC BY-NC-ND 4.0 DEED)

It turns out that every action may not have an equal and opposite reaction, despite what Newton’s third law of motion says, according to new research conducted by a team from Penn State and the University of Maine. The finding could offer insight into how certain molecular interactions could have evolved in a pre-life world.

The work was published in the journal Chem, and the researchers said this is the first demonstration of the mechanism by which these interactions occur at the molecular level. Last year’s discovery by researchers at Kyoto University that sperm movement does not cause an opposite reaction in its environment as it moves provided an example of a seeming violation of Newton’s third law of motion, but it did not address the mechanism.

“We all have heard the phrase ‘every action has an equal and opposite reaction,’ to describe Newton’s third law of motion, but we see examples that seemingly violate this every day, especially in the behavior of complex living systems small and large where there is constant input of energy,” said Ayusman Sen, Verne M. Willaman Professor of Chemistry in the Eberly College of Science at Penn State and one of the research team leaders. “An example at the larger scale is that a predator is attracted to its prey, but the prey is repelled by the predator. This type of interaction is called non-reciprocal, and we were interested to see if it also occurred in the much simpler interactions among molecules with constant energy input.”

Scientists develop a rapid gene-editing screen to find effects of cancer mutations

Using a variant of CRISPR genome-editing known as prime editing, MIT researchers have developed a method to screen cancer-associated genetic mutations much more easily and quickly than any existing approach. This illustration, by Samuel Gould’s brother Owen Gould, is an artistic interpretation of the research and the idea of “rewriting the genome,” explains Samuel.
Illustration Credit: Owen Gould
(CC BY-NC-ND 4.0 DEED)

Tumors can carry mutations in hundreds of different genes, and each of those genes may be mutated in different ways — some mutations simply replace one DNA nucleotide with another, while others insert or delete larger sections of DNA.

Until now, there has been no way to quickly and easily screen each of those mutations in their natural setting to see what role they may play in the development, progression, and treatment response of a tumor. Using a variant of CRISPR genome-editing known as prime editing, MIT researchers have now come up with a way to screen those mutations much more easily.

The researchers demonstrated their technique by screening cells with more than 1,000 different mutations of the tumor suppressor gene p53, all of which have been seen in cancer patients. This method, which is easier and faster than any existing approach, and edits the genome rather than introducing an artificial version of the mutant gene, revealed that some p53 mutations are more harmful than previously thought.

The researchers say this technique could also be applied to many other cancer genes, and could eventually be used for precision medicine, to determine how an individual patient’s tumor will respond to a particular treatment.

“In one experiment, you can generate thousands of genotypes that are seen in cancer patients, and immediately test whether one or more of those genotypes are sensitive or resistant to any type of therapy that you’re interested in using,” says Francisco Sanchez-Rivera, an MIT assistant professor of biology, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the study.

MIT graduate student Samuel Gould is the lead author of the paper, which appears today in Nature Biotechnology.

“Molecular Rosetta Stone” Reveals How our Microbiome Talks to Us

Bacteria in the gut convert bile acids produced by the liver into a wide array of new compounds. These molecules are akin to the language of the gut microbiome, allowing them to influence distant organ systems.
Photo Credit: Lakshmiraman Oza

Researchers from Skaggs School of Pharmacy and Pharmaceutical Sciences at the University of California San Diego have uncovered thousands of previously unknown bile acids, a type of molecule used by our gut microbiome to communicate with the rest of the body.

“Bile acids are a key component of the language of the gut microbiome, and finding this many new types radically expands our vocabulary for understanding what our gut microbes do and how they do it,” said senior author Pieter Dorrestein, Ph.D., professor at Skaggs School of Pharmacy and Pharmaceutical Sciences and professor of pharmacology and pediatrics at UC San Diego School of Medicine. “It’s like going from ‘See Spot Run’ to Shakespeare.”

The results, as described by study co-author and bile acids expert Lee Hagey, Ph.D, are akin to a molecular Rosetta stone, providing previously unknown insight into the biochemical language microbes use to influence distant organ systems.

Researchers uncover protein responsible for cold sensation

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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 temperatures 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 worm that the lab studies as a model system for understanding sensory responses.

AI research gives unprecedented insight into heart genetics and structure

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A ground-breaking research study has used AI to understand the genetic underpinning of the heart’s left ventricle, using three-dimensional images of the organ. It was led by scientists at the University of Manchester, with collaborators from the University of Leeds (UK), the National Scientific and Technical Research Council (Santa Fe, Argentina), and IBM Research (Almaden, CA).

The highly interdisciplinary team used cutting-edge unsupervised deep learning to analyze over 50,000 three-dimensional Magnetic Resonance images of the heart from UK Biobank, a world-leading biomedical database and research resource.

The study, published in the leading journal Nature Machine Intelligence, focused on uncovering the intricate genetic underpinnings of cardiovascular traits. The research team conducted comprehensive genome-wide association studies (GWAS) and transcriptome-wide association studies (TWAS), resulting in the discovery of 49 novel genetic locations showing an association with morphological cardiac traits with high statistical significance, as well as 25 additional loci with suggestive evidence.  

The study's findings have significant implications for cardiology and precision medicine. By elucidating the genetic basis of cardiovascular traits, the research paves the way for the development of targeted therapies and interventions for individuals at risk of heart disease.

How Proteins Control Genes to Prevent our Cells from Maldevelopment

Ole Nørregaard Jensen is a professor and head of research at the Department of Biochemistry and Molecular Biology.
Photo Credit: Stefan Kristensen

Every time a cell in our body prepares to divide, an extremely complex process begins to ensure that the mother cell's DNA is copied into a new daughter cell along with all the correct instructions for which genes on the DNA strand should be turned off and which should be activated.

If errors occur in this process and the new cell is not identical to the mother cell, damage and disease may occur.

Researchers are therefore interested in learning more about these processes and why the copying of DNA and instructions sometimes goes wrong.

Constant DNA replication of the cell

All humans have a unique DNA strand, originating from a single cell: the fertilized egg cell, which has divided and created the billions of cells that make up the whole human being. They all contain a copy of the DNA strand created at fertilization. However, different cells decode the DNA in different ways, allowing for the formation of more than 200 different cell types. Some cell types die quickly and need to be replaced many times during life; for example, skin cells and intestinal cells are renewed every few days. Each time a new cell is created, a copy of the unique DNA strand is made for the new cell.

Shape-shifting ultrasound stickers detect post-surgical complications

Three variations of the soft, flexible ultrasound sticker device displayed on a finger.
Photo Credit: Jiaqi Liu / Northwestern University

Researchers led by Northwestern University and Washington University School of Medicine in St. Louis have developed a new, first-of-its-kind sticker that enables clinicians to monitor the health of patients’ organs and deep tissues with a simple ultrasound device.

When attached to an organ, the soft, tiny sticker changes in shape in response to the body’s changing pH levels, which can serve as an early warning sign for post-surgery complications such as anastomotic leaks. Clinicians then can view these shape changes in real time through ultrasound imaging.

Currently, no existing methods can reliably and non-invasively detect anastomotic leaks — a life-threatening condition that occurs when gastrointestinal fluids escape the digestive system. By revealing the leakage of these fluids with high sensitivity and high specificity, the non-invasive sticker can enable earlier interventions than previously possible. Then, when the patient has fully recovered, the biocompatible, bioresorbable sticker simply dissolves away — bypassing the need for surgical extraction.

The study is published in the journal Science. The paper outlines evaluations across small and large animal models to validate three different types of stickers made of hydrogel materials tailored for the ability to detect anastomotic leaks from the stomach, the small intestine and the pancreas.

Lung cancer cells protected from cigarette smoke damage, researchers find

New research shows how lung cancer cells can survive better and exhibit less cell damage when exposed to cigarette smoke in cell culture experiments compared to non-cancerous lung cells. Image shows non-cancerous lung cells (left) and lung cancer cells (right), subjected to the same concentration of cigarette smoke condensate. Non-cancerous cells have more pronounced protein aggregation granules (shown with an arrow), stained by Proteostat, a type of cell damage that can eventually lead to cell death.
Image Credit: Krasilnikova Lab / Penn State
(CC BY-NC-ND 4.0 DEED)

Lung cancer cells survive better and exhibit less cell damage when exposed to cigarette smoke in cell culture experiments compared to non-cancerous lung cells. New research by a team of undergraduate students led by a Penn State molecular biologist may have revealed how lung cancer cells can persist in smoke. The mechanism could be related to how cancer cells develop resistance to pharmaceutical treatments as well.

The team found that a protein, which is expressed at high levels in some lung cancer cells and acts as a pump to transport molecules across the cell membrane, could potentially be clearing the damaging molecules coming from cigarette smoke. These molecules, if left uncleared inside the cells, can lead to protein aggregation that can damage and eventually kill lung cells.

“Cigarette smoke contains carcinogenic compounds, such as hydrocarbons and reactive oxygen and nitrogen species, that can damage cells in various ways,” said Maria Krasilnikova, associate research professor of biochemistry and molecular biology in the Eberly College of Science at Penn State and the lead author of the paper. “One way these compounds can damage cells is by causing proteins to misfold, which can lead to the formation of protein aggregates.”

When Plants Flower: Scientists ID Genes, Mechanism in Sorghum

Brookhaven Lab biologist Meng Xie and postdoctoral fellow Dimiru Tadesse with sorghum plants like those used in this study. Note that these plants are flowering, unlike those the scientists engineered to delay flowering indefinitely to maximize their accumulation of biomass.
Photo Credit: Kevin Coughlin/Brookhaven National Laboratory

Scientists at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory and Oklahoma State University have identified key genes and the mechanism by which they control flowering in sorghum, an important bioenergy crop. The findings, just published in the journal New Phytologist, suggest strategies to delay sorghum flowering to maximize plant growth and the amount of biomass available for generating biofuels and bioproducts.

“Our studies elucidate the gene regulatory network controlling sorghum flowering and provide new insights into how these genes could be leveraged to improve sorghum for achieving bioenergy goals,” said Brookhaven Lab biologist Meng Xie, one of the leaders of the research.

Sorghum is particularly well suited for sustainable agriculture because it can grow on marginal lands in semiarid regions and can tolerate relatively high temperatures. Like many plants, its growth and flowering (reproductive) cycles are regulated by the duration of daily sunlight. And once plants start to flower, they stop growing, which has important implications for the accumulation of biomass.

For example, one natural sorghum variety can reach nearly 20 feet in height, only transitioning to the reproductive flowering phase near the end of the summer growing season when the duration of daylight diminishes. Other “day-neutral” lines flower earlier, after reaching about three feet in height, producing less vegetation but more grain.

Researchers develop artificial building blocks of life

Structural comparison of DNA and the artificial TNA, a Xeno nucleic acid with the natural base pairs AT and GC and an additional base pair (XY).
Image Credit: Courtesy of University of Cologne

For the first time, scientists from the University of Cologne (UoC) have developed artificial nucleotides, the building blocks of DNA, with several additional properties in the laboratory. They could be used as artificial nucleic acids for therapeutic applications.

DNA carries the genetic information of all living organisms and consists of only four different building blocks, the nucleotides. Nucleotides are composed of three distinctive parts: a sugar molecule, a phosphate group and one of the four nucleobases adenine, thymine, guanine and cytosine. The nucleotides are lined up millions of times and form the DNA double helix, similar to a spiral staircase. Scientists from the UoC’s Department of Chemistry have now shown that the structure of nucleotides can be modified to a great extent in the laboratory. The researchers developed so-called threofuranosyl nucleic acid (TNA) with a new, additional base pair. These are the first steps on the way to fully artificial nucleic acids with enhanced chemical functionalities. The study ‘Expanding the Horizon of the Xeno Nucleic Acid Space: Threose Nucleic Acids with Increased Information Storage’ was published in the Journal of the American Chemical Society.

How the Body Copes With Airway Closure

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There is perhaps no bodily function more essential for humans and other mammals than breathing. With each breath, we suffuse our bodies with oxygen-rich air that keeps our organs and tissues healthy and working properly — and without oxygen, we can survive mere minutes.

But sometimes, our breathing becomes restricted, whether due to infection, allergies, exercise, or some other cause, forcing us to take deep, gasping breaths to quickly draw in more air.

Now, researchers at Harvard Medical School have identified a previously unknown way in which the body counteracts restricted breathing — a new reflex of the vagus nerve that initiates deep breathing. Their work is published in Nature.

The research, conducted in mice, reveals a rare and mysterious cell type in the lungs that detects airway closure and relays the signal to the vagus nerve — the information highway that connects the brain to almost every major organ. After the signal reaches the brain, a gasping reflex is initiated that helps the animal compensate for the lack of air.

Keeping the immune system in check

Image Credit: © Julian Nüchel, Center for Biochemistry Cologne

Researchers from the UoC’s Center for Biochemistry at the Faculty of Medicine and the UoC CECAD Cluster of Excellence in Aging Research have discovered that an excessive immune response can be prevented by the intramembrane protease RHBDL4. In a study now published in Nature Communications under the title ‘RHBDL4-triggered downregulation of COPII adaptor protein TMED7 suppresses TLR4-mediated inflammatory signaling’, a previously unknown regulatory mechanism is described: The cleavage of a cargo receptor by a so-called intramembrane protease reduces the localization of a central immune receptor on the cell surface and thereby the risk of an overreaction of the immune system.

Intramembrane proteases are reactive proteins that reside in the cell membranes. They form a special group of proteases because they cut proteins within cellular membranes. Many of these unusual proteases have not yet been sufficiently characterized and only a few of the molecules they can cleave – the so-called substrates – and thus their functions are known. One of these intramembrane proteases is RHBDL4. It is located in the endoplasmic reticulum, a large intracellular membrane system that is responsible, among other things, for the correct folding of newly synthesized proteins that are fed into the secretory route.

Marine algae implants could boost crop yields

Discovery could lead to more sustainable food supply
Photo Credit: Oktavianus Mulyadi

Scientists have discovered the gene that enables marine algae to make a unique type of chlorophyll. They successfully implanted this gene in a land plant, paving the way for better crop yields on less land. 

Finding the gene solves a long-standing mystery amongst scientists about the molecular pathways that allow the algae to manufacture this chlorophyll and survive. 

“Marine algae produce half of all the oxygen we breathe, even more than plants on land. And they feed huge food webs, fish that get eaten by mammals and humans,” said UC Riverside assistant professor of bioengineering and lead study author Tingting Xiang. “Despite their global significance, we did not understand the genetic basis for the algae’s survival, until now.”

The study, published in Current Biology, also documents another first-of-its-kind achievement: demonstrating that a land plant could produce the marine chlorophyll. Tobacco plants were used for this experiment, but in theory, any land plant may be able to incorporate the marine algae gene, allowing them to absorb a fuller spectrum of light and achieve better growth. 

Unveiling Inaoside A: An Antioxidant Derived from Mushrooms

Discovering a new antioxidant compound, Inaoside A from Laetiporus cremeiporus
Image credit: Atsushi Kawamura from Shinshu University, Japan

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.