Human astroviruses are a leading viral cause of the stomach bug—think vomiting, diarrhea, and fever. It often impacts young children and older adults, leading to vicious cycles of sickness and malnutrition, particularly for those in low and middle income countries. It’s very commonly found in wastewater studies, meaning it’s frequently circulating in communities. As of now, there are no vaccines for this virus.

New research from the lab of Rebecca DuBois, a professor of biomolecular engineering at the University of California, Santa Cruz, reveals the strategy that the human astrovirus uses to enter the body. A study detailing these results was published in the journal Nature Communications.

“We uncovered a really important part of the virus lifecycle, and now we know exactly where on the virus this important interaction with the human receptor occurs,” DuBois said. “Now we can develop vaccines that will target it and block that interaction—it really guides future vaccine development.”

The team’s discovery also illuminates the possibility of repurposing existing, FDA-approved treatments to target astrovirus. DuBois and her team will continue to pursue both vaccines and treatments for astrovirus, with the support of around $416,000 via a new R21 award from National Institutes of Health.

Assessing astrovirus

The DuBois lab at the Baskin School of Engineering studies the molecular structure of viruses—mostly those that primarily affect children—to understand how they enter human cells and reveal new targets for vaccines and treatments.

Within the last two years, scientists discovered that astrovirus enters the body by binding to a protein in human cells called the neonatal Fc receptor. This receptor plays a key role in supplying antibodies to babies via breastmilk, and continues to support overall health later in life by moving antibodies and other proteins through the bloodstream.

However, it’s not enough to know what the virus binds to—it’s crucial to discover exactly how the binding works to allow the virus to enter the body. DuBois’ lab sought to understand how the virus engages this receptor at the molecular level.

“Viruses have to use host machinery to replicate, and the very first step is that the virus has to enter our cells,” said Adam Lentz, a Ph.D. student in DuBois’ lab who spearheaded this study. “That step of cell entry is where we’re really interested, and we want to fully understand how this happens—what proteins, what receptors, what other human factors it’s using to get inside. Ultimately, once we understand how it enters our cells, we can take the next step of figuring out how to stop it.”

To do so, the engineers created replicas of both the astrovirus and the receptor in the lab, mixing them together to observe exactly how and where the two bind. Using X-ray crystallography, a technique that reveals the structure of a protein at the atomic level, they discovered that the virus attaches to the same exact site on the receptor that antibodies do.

“The virus is hijacking the pathway that humans use for beneficial purposes to get inside the cell,” DuBois said. “I think that’s one of the most exciting findings—we discovered exactly how the virus is using this receptor to sneak into our cells.”

FDA-approved treatments already exist to target this antibody pathway for other disease contexts, such as for some types of auto-immunity. The research from the DuBois lab reveals a path to repurpose these treatments and test for their ability to protect against astrovirus disease —shortening the timeline for development of new therapies.

DuBois is particularly interested in developing vaccines for astrovirus, and the close study of astrovirus revealed that the pathogen frequently mutates near the location where it binds to the receptor. This means that the virus evolves often to evade the human immune system—much like influenza—and suggests that a multi-strain approach may be needed for an effective vaccine.

“If we can make a vaccine that is multivalent, we can protect against many strains of the virus,” DuBois said.

Original Publication
Authors: Adam Lentz, Sarah Lanning, Khurshid R. Iranpur, Lena Ricemeyer, Carlos F. Arias and Rebecca M. DuBois.
Journal: Nature Communications
DOI: 10.1038/s41467-025-65203-2
Article Title: Structure of the human astrovirus capsid spike in complex with the neonatal Fc receptor
Article Publication Date: 3-Nov-2025

Original Source: https://news.ucsc.edu/2025/11/target-for-astroviruses/

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Scientists at UC San Diego have moved one step closer to unlocking a superpower held by some of nature’s greatest “masters of disguise.”

Octopuses, squids, cuttlefish and other animals in the cephalopod family are well known for their ability to camouflage, changing the color of their skin to blend in with the environment. This remarkable display of mimicry is made possible by complex biological processes involving xanthommatin, a natural pigment.

Because of its color-shifting capabilities, xanthommatin has long intrigued scientists and even the military, but has proven difficult to produce and research in the lab — until now.

In a new study, a team led by UC San Diego’s Scripps Institution of Oceanography describes a major breakthrough in understanding nature’s ability to camouflage, as they successfully developed a new way to produce large amounts of xanthommatin pigment.

Their nature-inspired method massively over-produced the pigmented material for the first time in a bacterium, opening new possibilities for the pigment’s use in a wide range of materials and cosmetics — from photoelectronic devices and thermal coatings to dyes and UV protectants. The new approach produces up to 1,000 times more material than traditional methods.

“We’ve developed a new technique that has sped up our capabilities to make a material, in this case xanthommatin, in a bacterium for the first time,” said Bradley Moore, the study’s senior author and a marine chemist with joint appointments at Scripps Oceanography and UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. “This natural pigment is what gives an octopus or a squid its ability to camouflage — a fantastic superpower — and our achievement to advance production of this material is just the tip of the iceberg.”

Published Nov. 3 in Nature Biotechnology, the study was funded by the National Institutes of Health, the Office of Naval Research, the Swiss National Science Foundation and the Novo Nordisk Foundation.

The study authors said their discovery is significant, not just for understanding this unique pigment — which sheds light into the biology and chemistry of the animal kingdom — but also because the technique they used could be applied to many other chemicals, potentially helping industries move away from fossil fuel-based materials toward nature-based alternatives.

A promising pigment

Beyond cephalopods, xanthommatin is also found in insects within the arthropod group, contributing to the brilliant orange and yellow hues of monarch butterfly wings and the bright reds seen in dragonfly bodies and fly eyes.

Despite xanthommatin’s fantastic color properties, it is poorly understood due to a persistent supply challenge. Harvesting the pigment from animals isn’t scalable or efficient, and traditional lab methods are labor intensive, reliant on chemical synthesis that is low yielding.

Researchers in the Moore Lab at Scripps Oceanography sought to change that, working with colleagues across UC San Diego and at the Novo Nordisk Foundation Center for Biosustainability in Denmark to design a solution, a sort of growth feedback loop they call “growth coupled biosynthesis.”

The way in which they bioengineered the octopus pigment, a chemical, in a bacterium represents a novel departure from typical biotechnological approaches. Their approach intimately connected the production of the pigment with the survival of the bacterium that made it.

“We needed a whole new approach to address this problem,” said Leah Bushin, lead author of the study, now a faculty member at Stanford University and formerly a postdoctoral researcher in the Moore Lab at Scripps Oceanography, where her work was conducted. “Essentially, we came up with a way to trick the bacteria into making more of the material that we needed.”

Typically, when researchers try to get a microbe to produce a foreign compound, it creates a major metabolic burden. Without significant genetic manipulation, the microbe resists diverting its essential resources to produce something unfamiliar.

By linking the cell’s survival to the production of their target compound, the team was able to trick the microbe into creating xanthommatin. To do this, they started with a genetically engineered “sick” cell, one that could only survive if it produced both the desired pigment, along with a second chemical called formic acid. For every molecule of pigment generated, the cell also produced one molecule of formic acid. The formic acid, in turn, provides fuel for the cell’s growth, creating a self-sustaining loop that drives pigment production.

“We made it such that activity through this pathway, of making the compound of interest, is absolutely essential for life. If the organism doesn’t make xanthommatin, it won’t grow,” said Bushin.

To further enhance the cells’ ability to produce the pigment, the team used robots to evolve and optimize the engineered microbes through two high-throughput adaptive laboratory evolution campaigns, which were developed by the lab of study co-author Adam Feist, professor in the Shu Chien-Gene Lay Department of Bioengineering at the UC San Diego Jacobs School of Engineering and senior scientist at the Novo Nordisk Foundation Center for Biosustainability. The team also applied custom bioinformatics tools from the Feist Lab to identify key genetic mutations that boosted efficiency and enabled the bacteria to make the pigment directly from a single nutrient source.

“This project gives a glimpse into a future where biology enables the sustainable production of valuable compounds and materials through advanced automation, data integration and computationally driven design,” said Feist. “Here, we show how we can accelerate innovation in biomanufacturing by bringing together engineers, biologists and chemists using some of the most advanced strain-engineering techniques to develop and optimize a novel product in a relatively short time.”

Traditional approaches yield around five milligrams of pigment per liter “if you’re lucky,” said Bushin, while the new method yields between one to three grams per liter.

Getting from the planning stages to the actual experimentation in the lab took several years of dedicated work, but once the plan was put into motion, the results were almost immediate.

“It was one of my best days in the lab,” Bushin recalled of the first successful experiment. “I’d set up the experiment and left it overnight. When I came in the next morning and realized it worked and it was producing a lot of pigment, I was thrilled. Moments like that are why I do science.”

Next steps

Moore anticipates that this new biotech methodology, which is fully nature-inspired and non-invasive, will transform the way in which biochemicals are produced.

“We’ve really disrupted the way that people think about how you engineer a cell,” he said. “Our innovative technological approach sparked a huge leap in production capability. This new method solves a supply challenge and could now make this biomaterial much more broadly available.”

While some applications for this material are far-out, the authors noted active interest from the U.S. Department of Defense and cosmetics companies. According to the researchers, collaborators are interested in exploring the material’s natural camouflage capabilities, while skincare companies are interested in using it in natural sunscreens. Other industries see potential uses ranging from color-changing household paints to environmental sensors.

“As we look to the future, humans will want to rethink how we make materials to support our synthetic lifestyle of 8 billion people on Earth,” said Moore. “Thanks to federal funding, we’ve unlocked a promising new pathway for designing nature-inspired materials that are better for people and the planet.”

Additional study authors are Tobias Alter, María Alván-Vargas, Daniel Volke, Òscar Puiggené and Pablo Nikel from the Novo Nordisk Foundation Center for Biosustainability; Elina Olson from UC San Diego’s Shu Chien-Gene Lay Department of Bioengineering; Lara Dürr and Mariah Avila from Scripps Institution of Oceanography at UC San Diego; and Taehwan Kim and Leila Deravi from Northeastern University.

Original Publication
Authors: Leah B. Bushin, Tobias B. Alter, María V. G. Alván-Vargas, Lara Dürr, Elina C. Olson, Mariah J. Avila, Daniel C. Volke, Òscar Puiggené, Taehwan Kim, Leila F. Deravi, Adam M. Feist, Pablo I. Nikel and Bradley S. Moore.
Journal: Nature Biotechnology
DOI: 10.1038/s41587-025-02867-7
Method of Research: Experimental study
Subject of Research: Animals
Article Title: Growth-coupled microbial biosynthesis of the animal pigment xanthommatin
Article Publication Date: 3-Nov-2025

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Heart failure (HF) is one of the leading causes of death and disability worldwide, affecting millions of people and placing an enormous burden on healthcare systems. The disease occurs when the heart can no longer pump blood efficiently, leaving patients short of breath, fatigued, and at risk of life-threatening complications. For decades, scientists have focused on studying cardiomyocytes—the heart’s muscle cells responsible for pumping blood—believing that these were the key drivers of the disease. But new research challenges this long-standing view by showing that another, often-overlooked group of cells plays a central role in HF progression.

A recent study published in Volume 4 of Nature Cardiovascular Research on September 10, 2025, reveals how a specialized type of cardiac fibroblast—cells that traditionally provide structural support—can actively worsen HF. A research team led by Professor Shinsuke Yuasa from the Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan, along with Dr. Jin Komuro from The University of Tokyo, Japan, discovered that these fibroblasts use a signaling pathway known as the MYC–CXCL1–CXCR2 axis to promote harmful changes in the heart.

“We were surprised to discover that fibroblasts, which were thought to be support players in the heart, can actually drive the worsening of HF,” said Prof. Yuasa. “They send out signals that disrupt the normal work of muscle cells, ultimately reducing the heart’s ability to pump effectively.”

To uncover this mechanism, the team studied both patient samples and experimental models of HF. By examining cardiac fibroblasts at a molecular level, researchers identified a fibroblast population unique to ‘failing hearts’ in mice models that expresses the gene Myc These fibroblasts release a chemokine (signaling molecule) CXCL1, which destroys cardiomyocyte function through its complimentary receptor CXCR2, expressed on cardiomyocytes. In simpler terms, fibroblasts communicate with other cells using chemical signals, but in HF, this communication becomes harmful. The signaling pathway and consequent chemical signals weaken heart muscle cells, leading to disease progression. Researchers found that blocking this pathway in mice models improved heart function, suggesting that fibroblasts could be a potential target for new therapeutic strategies.

The researchers further examined if these findings were applicable to human HF. They used cardiac biopsy samples from patients with HF and from healthy patients who served as controls. They found that MYC and CXCL1 were expressed in elevated amounts in the cardiac fibroblasts of patients with HF, suggesting that the MYC–CXCL1–CXCR2 axis in responsible for cardiac dysfunction in human hearts.

“This discovery opens new possibilities for treatment,” mentions Prof. Yuasa. Severe HF often leaves transplantation as the only option. By targeting fibroblasts and their signaling pathways, we may be able to develop therapies that slow disease progression and give patients more choices,” he explains.

The findings are important as they challenge the belief that HF research should focus mainly on cardiomyocytes. By showing that fibroblasts also contribute to cardiac dysfunction, the study expands opportunities for drug discovery. “This research is an extension of our long-standing studies on HF,” emphasized Prof. Yuasa. “We hope our research inspires a more multifaceted approach, where therapies address not just the muscle cells but also the support cells that shape the disease.”

This new perspective is especially valuable given the limited options currently available to patients with severe HF. Medications can help manage symptoms, but for many, a transplant remains the only hope. By identifying fibroblasts as a key causal factor, scientists may be able to develop drugs that target the signaling pathway used to damage the heart—offering a more direct approach to stop disease progression.

The researchers stress that while the findings are promising, more work is needed to translate them into clinical treatments. Future studies will focus on developing safe therapeutics that can block fibroblast signaling in humans and exploring whether these therapies can improve outcomes in patients with the less advanced form of the disease.

Overall, by uncovering the unexplored influence of fibroblasts, this study reshapes our understanding of HF and highlights a promising new avenue for the management of cardiac diseases.

About Okayama University, Japan

As one of the leading universities in Japan, Okayama University aims to create and establish a new paradigm for the sustainable development of the world. Okayama University offers a wide range of academic fields, which become the basis of the integrated graduate schools. This not only allows us to conduct the most advanced and up-to-date research, but also provides an enriching educational experience.

Website: https://www.okayama-u.ac.jp/index_e.html

About Professor Shinsuke Yuasa from Okayama University, Japan

Professor Shinsuke Yuasa, M.D., Ph.D., is a faculty member in the Department of Cardiovascular Medicine at the Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan. His research focuses on heart failure, arrhythmias, stem cell therapy, and cardiovascular imaging. He has also contributed to advancements in induced pluripotent stem cell-derived cardiomyocyte therapy and the use of artificial intelligence in regenerative medicine. With extensive academic and clinical experience, Prof. Yuasa continues to advance therapeutic strategies that shape the future of cardiovascular medicine.

Original Publication
Authors: Jin Komuro, Hisayuki Hashimoto, Toshiomi Katsuki, Dai Kusumoto, Manami Katoh, Toshiyuki Ko, Masamichi Ito, Mikako Katagiri, Masayuki Kubota, Shintaro Yamada, Takahiro Nakamura, Yohei Akiba, Thukaa Kouka, Kaoruko Komuro, Mai Kimura, Shogo Ito, Seitaro Nomura, Issei Komuro, Keiichi Fukuda, Shinsuke Yuasa and Masaki Ieda.
Journal: Nature Cardiovascular Research
DOI: 10.1038/s44161-025-00698-y
Method of Research: Experimental study
Subject of Research: Animals
Article Title: Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC–CXCL1–CXCR2 axis
Article Publication Date: 25-Sep-2025
COI Statement: Keiichi Fukuda is a founding scientist funded by the SAB of Heartseed Co., Ltd.
The other authors declare no competing interests.

Original Source: https://www.nature.com/articles/s44161-025-00698-y

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“Our flexible artificial tongue holds tremendous potential in spicy sensation estimation for portable taste-monitoring devices, movable humanoid robots, or patients with sensory impairments like ageusia, for example,” says Weijun Deng, the study’s lead author.

Currently, measuring flavor compounds in foods requires taste testers and complex laboratory methods.  As an alternative, scientists are developing artificial tongues, which can measure tastes including sweet and umami, among others. However, capsaicin in chili peppers, piperine in black pepper, and allicin in garlic produce stinging, tingling or burning sensations that are hard to replicate and measure with synthetic materials. Jing Hu and colleagues noted that the heat of peppers, for example, can be neutralized when their capsaicin is bound by casein proteins in milk. So, the team wanted to create an artificial tongue by adding casein to an electrochemical gel material and measuring spiciness through an electrical current change that occurs when casein binds to capsaicin.

The researchers created a tongue-shaped film by combining acrylic acid, choline chloride and skim milk powder, and then they exposed the solution to UV light. The resulting flexible and opaque gel conducted an electrical current. Ten seconds after the researchers added capsaicin on top of the film, the current decreased, showing its potential as an artificial, spice-detecting tongue. Initial tests showed that the milk-containing material responded to capsaicin concentrations ranging from below human detection to beyond levels perceived as painful (called the oral pain threshold). Additionally, the material detected other pungent-flavored compounds found in common hot sauce ingredients: ginger, black pepper, horseradish, garlic and onion.

As a proof-of-concept, the researchers tested eight pepper types and eight spicy foods (including several hot sauces) on the artificial tongue and measured how spicy they were by changes in electrical current. A panel of taste testers rated the spiciness of the same items. Results from the artificial tongue and the tasting panel matched well. Therefore, the researchers say that the casein-containing artificial tongue could be used to quickly test a food’s spiciness level — without putting one’s taste buds at risk.

The authors acknowledge funding from the National Natural Science Foundation of China and the Fund of Fujian Provincial Key Laboratory of Leather Green Design and Manufacture.

The paper’s abstract will be available on Oct.29 at 8 a.m. Eastern time here: http://pubs.acs.org/doi/abs/10.1021/acssensors.5c01329

###

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Original Publication
Authors: Weijun Deng, Jinzhi Yang, Huitao Wen and Jing Hu.
Journal: ACS Sensors
DOI: 10.1021/acssensors.5c01329
Article Title: A Soft and Flexible Artificial Tongue for Pungency Perception
Article Publication Date: 29-Oct-2025

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Lausanne, Switzerland – 28 October 2025. In a peer-reviewed article published today in Brain Medicine, a European research team presents a focused review of emerging neuromodulation techniques for treatment-resistant obsessive-compulsive disorder (OCD). The article, “Neuromodulation techniques in obsessive-compulsive disorder: Current state of the art,” examines how transcranial direct current stimulation (tDCS), repetitive transcranial magnetic stimulation (rTMS), and deep brain stimulation (DBS) are changing clinical approaches for patients who do not respond to traditional therapy or medication. Lead authors Dr. Kevin Swierkosz-Lenart and Dr. Carolina Viegas from Lausanne University Hospital, in collaboration with Prof. Luc Mallet from Paris-Est Créteil University, describe how each approach targets dysfunctional brain networks and how personalization, neuroimaging, and biomarker discovery could shape the next generation of psychiatric treatments.

Recalibrating the Circuits of Compulsion

OCD is a chronic neuropsychiatric disorder that affects roughly two percent of the population and often begins early in life. Many patients experience intrusive thoughts and repetitive actions that cause significant distress and impairment. Although serotonin reuptake inhibitors and cognitive behavioral therapy remain the standard of care, up to 60 percent of patients show incomplete or poor response.

This persistent challenge has prompted clinicians and neuroscientists to investigate the brain’s electrical systems directly. Neuromodulation techniques aim to normalize abnormal activity in the interconnected network that underlies decision-making, emotion regulation, and the sense of internal control. “We are witnessing a convergence of clinical psychiatry and systems neuroscience,” said Dr. Viegas. “Neuromodulation allows us to interact with the circuits that maintain obsessions and compulsions.”

The review traces this transformation from early experimental attempts to a robust field guided by imaging, electrophysiology, and computational modeling. The authors emphasize that these tools do not replace existing therapies but complement them, creating a continuum from noninvasive stimulation to targeted surgical interventions.

Transcranial Direct Current Stimulation: Gentle Current, Evolving Evidence

Transcranial direct current stimulation delivers low-intensity electrical current through scalp electrodes, altering the excitability of cortical neurons. By shifting resting membrane potentials, it can subtly influence the dynamics of cortical and subcortical circuits implicated in OCD.

In recent studies, researchers have explored whether applying anodal or cathodal currents over regions such as the pre-supplementary motor area (pre-SMA) or orbitofrontal cortex (OFC) can reduce hyperactivity in the cortico-striato-thalamo-cortical loops associated with compulsive behavior. Early trials have yielded mixed results. Some report modest improvements, while others show little difference from sham stimulation. The authors attribute these inconsistencies to variations in electrode placement, current intensity, and session duration across studies.

“tDCS remains appealing because it is accessible and safe,” said Dr. Swierkosz-Lenart. “But we need rigorous standardization and larger trials before it becomes part of mainstream clinical care.” According to the review, future progress will depend on high-quality randomized trials using electric-field modeling, and objective biomarkers such as neuroimaging measures of connectivity or electrophysiological changes.

The paper notes that tDCS is well tolerated, with side effects typically limited to transient tingling or mild redness of the skin. Its portability and cost-effectiveness make it an attractive candidate for home-based interventions under professional supervision, once validated protocols are established.

Repetitive Transcranial Magnetic Stimulation: Noninvasive Modulation with Growing Clinical Confidence

Repetitive transcranial magnetic stimulation (rTMS) uses rapidly changing magnetic fields to induce electric currents in specific cortical regions. Depending on frequency and site, stimulation can either increase or decrease neuronal activity. In 2018, the U.S. Food and Drug Administration approved deep rTMS for treatment-resistant OCD, targeting the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC).

Since then, a growing number of controlled trials and meta-analyses have confirmed that rTMS can produce significant symptom improvements, particularly when applied to the dorsolateral prefrontal cortex (DLPFC) or supplementary motor area (SMA). These targets are part of the brain’s cognitive control network, which plays a central role in regulating intrusive thoughts and behavioral inhibition.

“rTMS represents the first noninvasive neuromodulation technique to achieve regulatory approval for OCD,” said Dr. Viegas. “It has demonstrated clinical benefits, but we are still learning how to tailor parameters to the individual patient.”

The review highlights variability across stimulation protocols. Some studies suggest that low-frequency inhibitory stimulation over hyperactive regions such as the SMA yields the best results, while others point to high-frequency excitatory protocols over hypoactive prefrontal areas. This diversity underlines the need for personalized targeting, potentially guided by neuroimaging data and neurophysiological markers.

Side effects are generally mild and transient, including scalp discomfort, tingling, or headache. The risk of seizure is extremely low when safety guidelines are followed. The authors also discuss theta-burst stimulation (TBS) and accelerated rTMS protocols that aim to achieve faster clinical effects through condensed treatment sessions. Though promising, these approaches require further validation in OCD populations.

Deep Brain Stimulation: Precision Therapy for the Most Resistant Cases

For patients whose OCD remains severe and refractory to all other therapies, deep brain stimulation has become an established and clinically validated treatment option.. The procedure involves implanting thin electrodes into specific deep brain regions, which are then connected to an implanted pulse generator that continuously delivers electrical stimulation.

DBS has shown sustained efficacy in several randomized controlled trials. According to the Brain Medicine review, the most effective targets include the bed nucleus of the stria terminalis (BNST), ventral capsule/ventral striatum (VC/VS), nucleus accumbens (NAc), and subthalamic nucleus (STN). Across multiple studies, stimulation in these areas has led to symptom reductions ranging from 35 to 60 percent on the Y-BOCS scale, with long-term response rates of up to two-thirds of patients.

“DBS offers hope for individuals who have exhausted every other form of therapy,” said Dr. Swierkosz-Lenart.

Instead of focusing on a single anatomical location, researchers are now interested in diffusion tractography and connectomic mapping to identify the white-matter pathways most associated with clinical improvement. Stimulating along these optimized fiber bundles can produce better results, even if electrode placements vary slightly between patients.

The review also details the emerging field of closed-loop DBS, where implanted systems record neural signals in real time and automatically adjust stimulation in response to brain activity. This approach could reduce side effects and enhance precision. Early evidence suggests that specific patterns in low-frequency oscillations within OCD-related circuits may serve as biomarkers for symptom states, potentially enabling dynamic, adaptive therapy.

DBS is generally safe when performed in specialized centers. The most common complications are minor and reversible, such as transient mood changes or local discomfort. Serious adverse events like hemorrhage or infection are rare. The authors caution that extensive follow-up and multidisciplinary management remain essential, especially as adaptive technologies evolve.

Personalization, Ethics, and the Next Decade

The review concludes that neuromodulation represents one of the most exciting frontiers in psychiatry, but also one of the most complex. A central theme across all three modalities is personalization—the idea that stimulation parameters, targets, and protocols should be adjusted to match each patient’s unique brain anatomy and symptom profile.

“Moving forward, we must integrate neuroimaging, electrophysiology, and computational modeling into daily clinical decision-making,” said Dr. Viegas. “That is how we will achieve true precision psychiatry.”

The authors call for harmonized international standards to enable cross-study comparisons and improve reproducibility. They also highlight the importance of addressing ethical considerations surrounding invasive interventions, data privacy, and informed consent. Access and equity remain key concerns, as high costs and specialized infrastructure can limit availability outside major academic centers.

Despite these challenges, the tone of the review is cautiously optimistic. With the increasing use of imaging-based targeting and adaptive stimulation, the field is poised to enter a phase of more individualized, data-driven therapy. “We are moving,” the authors write, “toward a model of psychiatry that listens to the brain directly—one that adapts treatment as neural activity changes.”

The Review Article in Brain Medicine titled “Neuromodulation techniques in obsessive-compulsive disorder: Current state of the art,” is freely available via Open Access on 28 October 2025 in Brain Medicine at the following hyperlink: https://doi.org/10.61373/bm025y.0125.

About Brain Medicine: Brain Medicine (ISSN: 2997-2639, online and 2997-2647, print) is a peer-reviewed medical research journal published by Genomic Press, New York. Brain Medicine is a new home for the cross-disciplinary pathway from innovation in fundamental neuroscience to translational initiatives in brain medicine. The journal’s scope includes the underlying science, causes, outcomes, treatments, and societal impact of brain disorders, across all clinical disciplines and their interface.

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Original Publication
Journal: Brain Medicine
DOI: 10.61373/bm025y.0125
Method of Research: Literature review
Subject of Research: People
Article Title: Neuromodulation techniques in obsessive-compulsive disorder: Current state of the art
Article Publication Date: 28-Oct-2025
COI Statement: The contributors have confirmed that no conflict of interest exists.

Original Source: https://doi.org/10.61373/bm025y.0125

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Understanding Liver Fibrosis

Liver fibrosis occurs when prolonged liver damage — often from factors like alcohol abuse or unhealthy lifestyles — causes fibrous scar tissue to replace healthy liver tissue. This progressive scarring disrupts liver function and can lead to cirrhosis, liver failure, or even cancer. Despite affecting an estimated 3–4% of the population in its advanced stages, effective treatments remain scarce.

Targeting the Root Cause: Hepatic Stellate Cells

A key player in fibrosis development is the hepatic stellate cell (HSC). Under normal conditions, HSCs help maintain liver stability. However, during liver injury, they become overactive and produce excess collagen and fibrous tissue, impairing the liver’s natural functions.

Discovering Lawsone: The Healing Component in Henna

The research team led by Associate Professor Tsutomu Matsubara and Dr. Atsuko Daikoku at Osaka Metropolitan University’s Graduate School of Medicine developed a chemical screening system to find compounds that directly act on activated HSCs. Through this method, they identified Lawsone — a chemical component found in Lawsonia inermis (henna) — as a potential inhibitor of HSC activation.

Promising Results in Laboratory Tests

When Lawsone was administered to mice, researchers observed a significant decrease in liver fibrosis markers such as YAP, αSMA, and COL1A. At the same time, the expression of cytoglobin — a marker linked with antioxidant functions in HSCs — increased, suggesting that the activated cells were reverting to their normal, non-fibrotic state.

Toward the First Fibrosis-Reversing Drug

The findings suggest that Lawsone-based treatments could not only halt the progression of fibrosis but also promote liver recovery.

“We are currently developing a drug delivery system capable of transporting drugs to activated HSCs and ultimately hope to make it available for patients with liver fibrosis,” Matsubara said. “By controlling fibroblast activity, including HSCs, we could potentially limit or even reverse the effects of fibrosis.”

Summary: Key Takeaways

• Discovery: Researchers identified Lawsone, a natural compound in henna, as a promising inhibitor of liver fibrosis.
• Mechanism: Lawsone acts on activated hepatic stellate cells (HSCs), reducing fibrosis markers and promoting cell recovery.
• Results: Mouse studies showed reduced liver scarring and increased antioxidant activity.
• Future Potential: The team aims to develop a targeted drug delivery system to bring this treatment to human patients.

Original Publication
Authors: Atsuko Daikoku, Tsutomu Matsubara, Misako Sato-Matsubara, Miku Ando, Chiho Kadono, Sayuri Takada, Naoshi Odagiri, Hideto Yuasa, Hayato Urushima, Katsutoshi Yoshizato, Norifumi Kawada and Kazuo Ikeda.
Journal: Biomedicine & Pharmacotherapy
DOI: 10.1016/j.biopha.2025.118520
Method of Research: Experimental study
Subject of Research: People
Article Title: Lawsone can suppress liver fibrosis by inhibition of YAP signaling and induction of CYGB expression in hepatic stellate cells
Article Publication Date: 4-Sep-2025
COI Statement: The authors declare that they have no known competing financial interests or personal relationships.

Original Source: https://www.omu.ac.jp/en/

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