All Posts in "News Staff"

Sex differences in brain gene activity could explain why some disorders affect men and women differently

The physical differences between men and women are all too obvious, but the biological divide goes right down to the cellular level in the brain, according to a new study published in the journal Science.

While we have known for a long time that men and women face different risks for brain disorders such as depression and Alzheimer’s, we haven’t always known why. Although this latest research doesn’t directly answer this, it could help us better understand the underlying biology.

Most previous research has focused on broad sections of brain tissue, but in this study, a team of researchers analyzed more than one million nuclei from six different cortical regions from 30 donors.

Decoding brain differences

Previous MRI scans of these brain regions had shown physical differences in size or volume between the sexes. The scientists wanted to see if gene activity matched the physical differences seen on the scans.

The technique they used was single-nucleus RNA sequencing, which allows researchers to examine the genetic instructions within individual cells. Specifically, the focus was on how gene expression varies across different cell types and regions.

The study identified more than 3,000 genes that differ in expression between males and females. These differences included how genes are turned on or off and how active genes are in producing RNA messages that guide protein production. What’s more, they aren’t spread evenly across the brain, as the team explains, “Broader effects of sex on autosomal expression are captured in 13 core signatures with varying cell type versus region specificity.”

For example, the differences were much stronger (a higher number of genes were behaving differently) in certain areas like the fusiform cortex, which is a part of the brain involved in face recognition and complex visual processing.

Some of the strongest variations were seen in glial cells, which insulate neurons, but perhaps not surprisingly, the biggest differences were in the sex chromosome genes (X and Y). However, hundreds of genes across the entire genome are also influenced by sex.

Disease risk

When it comes to disease risk, the study found that some of the genes showing sex differences are the same ones linked to brain conditions that affect men and women differently, such as autism, ADHD, Alzheimer’s disease and mood disorders. “This study substantially advances the breadth, depth, and granularity of knowledge on sex differences in the human brain,” added the team.

The researchers explain that while their study has provided a massive amount of data, it is just the beginning. Future research could focus on when the changes appear and how they are influenced by the environment.

News Staff by — April 19, 2026 By News Staff in Uncategorized
3D-printed brain sensors may unlock personalized neural monitoring

Soft electrodes designed to perfectly match a person’s brain surface may help advance neural interfaces for neurodegenerative disease monitoring and treatment, according to a new study led by Penn State researchers. Neural interfaces are powered by tiny sensors capable of tracking biophysical signals, known as bioelectrodes. These sensors are usually made from stiff materials in a one-size-fits-all design that struggles to match the brain’s complex structure. The researchers have created a novel approach to 3D printing bioelectrodes that can stretch and morph to fit the minor differences that make every brain unique.

Simulating unique brain structures

The team used software to simulate detailed brains based on MRI scans taken from 21 human patients, shaping a set of electrodes tailored for brains’ specific structures before 3D printing the electrodes and models of the brains. In a paper published in Advanced Materials, they reported that their electrodes better fit the structure of the brain than traditional designs, while remaining effective and biologically compatible, even in tests done in rats.

The folds in the human brain are created through a process known as gyrification, where the cortical sheet on the outer wall of the brain bunches up into ridges, known as gyri, and grooves, known as sulci. This helps cells across the brain communicate at high speeds, and allows for a relatively large organ to fit compactly in the skull—a spread-out adult brain would be around 2,000 square centimeters, or about the size of two large pizzas.

Why one-size-fits-all falls short

Although the major cortical folds are consistent across individuals, the precise layout of the brain’s gyri and sulci changes substantially from person to person, according to Tao Zhou, Wormley Family Early Career Professor, assistant professor of engineering science and mechanics and corresponding author on the paper. However, traditional bioelectrode designs don’t take this into account.

“Each person has a different brain structure, depending on their height, weight, age, sex and more,” said Zhou, who also holds an affiliation in biomedical engineering and the center for neural engineering at Penn State. “Despite this, we try to fit neural interfaces onto brains like they have identical structures. This motivated us to create electrodes that are tailored for each individual, based on the structure of their brain.”

Hydrogel and honeycomb design

The electrodes are built mainly from a water-rich material known as hydrogel to better match the soft tissues and patient-specific geometry of a brain. Furthermore, the team used a novel honeycomb-inspired structure that offers flexibility and strength, while remaining cost-effective and quick to print, according to Zhou.

“The honeycomb structure helps us significantly reduce the stiffness of the electrodes, without sacrificing their mechanical strength,” Zhou said. “What’s more, the structure helps us reduce the overall material used during fabrication, reducing production time, cost and environmental impact.”

From MRI scan to 3D-printed match

Production starts by taking an MRI scan of a patient’s brain, which is used to conduct finite element analysis—a process that creates a detailed simulation of a person’s neural structure. This analysis is then rendered as a 3D model of the patient’s brain, where the team uses computer software to tailor a bioelectrode specifically morphed to fit the ridges and grooves of the cerebral cortex.

After shaping, the team 3D prints the hydrogel electrode using direct ink printing, a technique that can create electrodes capable of monitoring and transmitting brain signals over a relatively small surface. For this study, the team 3D printed models of 21 different participant brains, applying their electrodes and physically measuring how accurately the electrodes could fit the brain surface. Zhou explained how traditional fabrication approaches require specialized facilities like clean rooms, making them incredibly expensive to customize—3D printing allows the team to personalize and manufacture electrodes much faster, for a fraction of the price.

Softer contact, stronger brain signals

Compared to traditional approaches, the hydrogel-based electrodes follow the structure of the brain more precisely. Zhou said their approach produces electrodes that exhibit nearly perfect connectivity to electrical signals present in the brain. Additionally, because the stretchy gel is so malleable, it can be applied to the soft brain tissue without causing damage, compared to the stiff materials comprising other designs that could damage tissue.

According to Zhou, the softness of their electrodes enables closer and more stable contact with the brain, in turn facilitating higher-quality, more reliable monitoring. Moreover, bioelectrodes made with this approach don’t impact fluid transport around the brain, a critical aspect of brain function that many traditional electrodes disrupt.

“Personalizing the electrodes to the brain’s specific structure substantially improves their reliability,” Zhou said. “Because they conform to the brain better, the signal quality itself is significantly improved.”

Testing in rats and future use

To further study their electrodes, the team placed them onto the brains of rat models over a period of 28 days. The rats did not exhibit any immune response to the printed electrodes, a key consideration in biodevice development, Zhou said. Additionally, the electrodes did not exhibit performance degradation, while offering sensitive and accurate readings of the electric and physiological signals in the brain.

Zhou said he believes that this printing method could serve as a framework for the commercial-scale printing of bioelectrodes customized for specific patients. Although these systems are traditionally used for monitoring neural activity, the team plans to explore how personalized electrodes may contribute to neurological treatments.

“We are looking to further improve this technology to optimize the electrodes to monitor for specific diseases,” Zhou said. “In the future, we would really like to work with patients to see how this approach could support brain monitoring and disease treatment in clinical settings.”

News Staff by — April 19, 2026 By News Staff in Global News
Gene discovery opens new path for disease-resistant rice breeding

Bacterial blight (BB) is a serious plant disease that mainly affects rice plants, especially in warm, humid regions. Due to the severity of BB, discovering and applying BB-resistance genes is strategically important for ensuring stable rice production in Asia. However, genetic strategies to improve disease resistance face a trade-off between crop yield and immunity to disease—since better immunity may be associated with lower yield.

To date, most BB resistance genes (Xa) that have been “cloned”—i.e., identified, isolated, and functionally validated—either originate from wild rice relatives or are loss-of-function mutations in susceptibility genes, suggesting that BB resistance may have been negatively selected during rice domestication.

Despite this finding, researchers have recognized the importance of elucidating how resistance genes and their regulatory networks are differentially selected during domestication in order to guide disease resistance breeding in rice.

To achieve this goal, Prof. He Zuhua’s team from the Center for Excellence in Molecular Plant Sciences of the Chinese Academy of Sciences, along with Prof. Chen Gongyou’s team from Shanghai Jiao Tong University and Prof. Deng Yiwen’s team from Zhejiang University, have cloned the broad-spectrum BB resistance gene Xa48. They elucidated a new model for broad-spectrum, durable BB resistance involving an NLR immune receptor and its cognate effector, and revealed the molecular mechanism by which XA48 coordinates growth and immunity during crop domestication.

Through large-scale germplasm mining, the researchers identified a novel BB resistance gene, Xa48, in the indica rice variety Shuangkezao (SKZ). Combining map-based cloning with GWAS analysis, they cloned the gene and showed that it encoded an NLR receptor protein. Screening and functional characterization identified its pathogenic cognate effector, XopG, and demonstrated that XA48 directly recognized XopG, thus triggering immune responses.

Systematic genetic, biochemical, and cell biology studies revealed that upon XopG recognition, XA48 promoted degradation of the downstream immune suppressor OsVOZ1/2, ultimately activating immune responses. This discovery provides a foundation for breeding high-yielding, disease-resistant rice varieties.

Moreover, the researchers investigated the domestication trajectory of XA48 to understand how it balances growth and immunity. They discovered that the gene encoding the downstream transcription factor, OsVOZ1, has evolved into two allelic variants: OsVOZ1A and OsVOZ1S. Japonica rice carries only OsVOZ1A, while indica rice has retained both.

The combination of Xa48 and OsVOZ1A imposed a reproductive penalty in japonica—an effect not seen in indica, ultimately leading to the functional loss of Xa48 in japonica. Accordingly, Xa48 was present only in indica (regardless of the OsVOZ1 variant), which is primarily grown in Southeast Asia, a region with high BB incidence. This geographic distribution was consistent with negative selection acting on the resistance gene in japonica, which is traditionally grown in Northeast Asia with lower BB incidence.

Furthermore, the researchers established an immune research platform centered on two major plant immune pathways—pattern-triggered immunity (PTI), mediated by RaxX-XA21, and effector-triggered immunity (ETI), mediated by AvrXa48-XA48—to systematically investigate their synergistic effects during pathogen infection. They developed a comprehensive PTI+ETI platform that integrates these immune networks to improve BB resistance. They also reconstituted broad-spectrum resistance from wild rice into modern rice, offering a novel strategy for sustainable control of crop diseases.

This study lays the foundation for advancing plant protection and crop breeding in China by providing genetic resources and technical support for improving crop disease resistance as part of rice breeding programs.

News Staff by — April 19, 2026 By News Staff in Biotechnology Today
For regrowing human limbs, this salamander gene could hold the key

Investigating a common gene in three very different species—salamanders, mice and zebrafish—scientists have discovered the potential for a novel gene therapy aimed at eventually regrowing limbs in humans, according to new research published this week.

“This significant research brought together three labs, working across three organisms to compare regeneration,” said Wake Forest Assistant Professor of Biology Josh Currie, whose lab studies the Mexican axolotl, a salamander. “It showed us that there are universal, unifying genetic programs that are driving regeneration in very different types of organisms, including salamanders, zebrafish and mice.”

The research, now published in the Proceedings of the National Academy of Sciences, included David A. Brown, a plastic surgeon who studies digit regeneration in mice at Duke University, and Kenneth D. Poss, who studies fin regeneration in zebrafish at the University of Wisconsin–Madison.

Each year, around the world, more than 1 million limb amputations occur because of vascular diseases such as diabetes, traumatic injuries, cancer or infections, according to annual Global Burden of Disease statistics. The number is expected to rise with the aging population and the increase in diabetes diagnoses.

That looming challenge has inspired Brown, Currie and Poss to search for a treatment beyond prosthetics, for something that could replace the complex senses and motor skills of an actual limb.

They might have found the start of a solution in something called SP genes, which the scientists discovered are vital for limb regeneration and shared by the mouse, zebrafish and axolotl.

Therapy makes up for missing gene

The scientists chose to study these three animals for specific reasons:

  • The axolotl excels at regeneration, with the ability to regrow complete limbs; tails, including the spinal cord; parts of the heart, brain, liver, lungs and jaw.
  • Zebrafish offer one of the best models for appendage regeneration because their tail fins regrow rapidly and have unlimited capacity for regrowth. The zebrafish also can regenerate its heart, spinal cord, brain, retinas, kidneys and pancreas.
  • Mice represent mammals like humans, and they already can regenerate the tips of their digits. Humans, too, can regrow their fingertips when an injury preserves the nailbed. That allows regrowth of flesh, skin and bone.

Currie said that once the scientists determined the regenerating epidermis, or skin, of all three species expressed the SP genes SP6 and SP8, they set out to test what the genes do and how they work.

Biology Ph.D. student Tim Curtis Jr. contributed to the research in the Currie lab, with assistance from undergraduate researcher Elena Singer-Freeman, a Goldwater Scholar and 2025 Wake Forest biochemistry and molecular biology graduate.

Emulating the abilities of salamander genes

In salamanders, SP8 does the work in regenerating limbs. Using CRISPR gene-editing technology, Currie’s lab removed SP8 from the axolotl genome. Without SP8, the axolotl could not properly regenerate the limb bones; a similar result occurred with the mouse digits missing SP6 and SP8.

With that information in hand, Brown’s lab used a tissue regeneration enhancer found in zebrafish to develop a viral gene therapy.

That therapy delivered a secreted molecule called FGF8, a gene that is usually turned on by SP8, to encourage digit bone regrowth and partially restore the regenerative effects of the missing SP genes in mice.

Human limbs don’t have that kind of regenerative power—but might someday, with a therapy that emulates the abilities of SP genes.

“We can use this as a kind of proof of principle that we might be able to deliver therapies to substitute for this regenerative style of epidermis in regrowing tissue in humans,” Currie explained.

Building the foundation for human therapies

Although it will require much more research to take the findings from mouse digits to human limbs, Currie called this study foundational in the search for therapies to regrow limbs after injury or disease.

“Scientists are pursuing many solutions for replacing limbs, including bioengineered scaffolds and stem cell therapies,” Currie explained. “The gene-therapy approach in this study is a new avenue that can complement and potentially augment what will surely be a multidisciplinary solution to one day regenerate human limbs.”

He said the decision to collaborate among scientists studying such different animals made all the difference in this research.

“Many times, scientists work in their silos: we’re just working in axolotl, or we’re just working in mice, or just working in fish,” Currie said. “A real standout feature of this research is that we work across all these different organisms. That is really powerful, and it’s something that I hope we’ll see more of in the field.”

News Staff by — April 19, 2026 By News Staff in Biotechnology Today
Brain Circuits Underlying Placebo Pain Relief Identified in Mice

Though the placebo effect is a well documented phenomenon, the neurological mechanisms that underlie the process are still not fully understood. Now scientists from multiple institutions led by a team at the University of California San Diego (UCSD) have pinpointed the brain circuitry in mice that they believe is responsible for placebo pain relief. Details of their findings are published in a new paper in the journal Neuron. In it, they describe brain regions that support placebo effects and highlight sites where endogenous opioid neuropeptides send signals that are important for placebo pain relief.

The paper is titled “Top-down control of the descending pain modulatory system drives multimodal placebo analgesia.” According to the team, theirs is the first study to establish placebo mechanisms by adapting a protocol used for humans to work in mice. Working alongside labs at the University of Pennsylvania, University of California Irvine, and elsewhere, the UCSD team detected activity in parts of the mouse brain that correspond to those previously implicated in human studies. Furthermore, by precisely mapping neural pathways and brain activity in the mice, the team identified essential roles for neural circuits that link the cortex to the brainstem and spinal cord during placebo pain relief.

They also found that training mice to exhibit a placebo effect with one type of pain results in relief from several different types of pain including pain from injuries. That is particularly notable because it has “direct implications for how placebo training in humans might be used to produce resilience to future pain that results from injury,” explained Matthew Banghart, PhD, an associate professor in UCSD’s neurobiology department and lead author on the study. The findings also open a door to “expectancy-driven” placebo effects as a substitute for addictive painkillers, he noted, meaning that it might be possible to use placebo conditioning to train patients to build preemptive resilience to pain.

Full details of the findings and methods used are provided in the paper. In it, the teams explain that they used sensor technology and a light-activated drug developed in the Banghart lab to study the role of naturally-occurring opioid peptides in the brain. Specifically, they used the sensors to detect opioid peptide signaling in the ventrolateral periaqueductal gray (vlPAG) region, a known hub for pain signaling, during placebo trials. They then used the light-activated drug called photoactivatable naloxone, or PhNX, to establish that these opioid peptides actually drive pain relief in a manner similar to drugs like morphine. The light allowed the scientists control and timing of the opioid signaling interference. Using PhNX, they confirmed that both morphine-induced pain relief and placebo pain relief use the same opioid signaling pathway in the vlPAG region of the brain.

Essentially, “we trained a mouse brain to create its own broad-spectrum painkillers on demand, precisely where they are needed to treat pain, without the off-target effects of opioid-based painkillers,” said Janie Chang-Weinberg, a PhD student in the biological sciences graduate program at UCSD and one of the first authors on the study.

Future studies planned by the team will dig more deeply into how placebo learning unfolds in the brain and evaluate different placebo training strategies in mice with an eye towards developing protocols that readily translate to produce placebo pain resilience in people living with chronic pain.

News Staff by — April 19, 2026 By News Staff in Bio Space
Advances in Stem Cell‑Derived Insulin‑Producing Cells for Type 1 Diabetes

Researchers at Karolinska Institutet and KTH Royal Institute of Technology have developed an improved method for creating insulin-producing cells from human stem cells. In a newly published study, the team demonstrated that these cells effectively regulate blood sugar levels in laboratory tests and can reverse diabetes in mice.

“We have developed a method that reliably produces high-quality insulin-producing cells from multiple human stem cell lines,” said Per-Olof Berggren, PhD, professor at the Department of Molecular Medicine and Surgery, Karolinska Institutet. “This opens up opportunities for future patient-specific cell therapies, which could reduce immune rejection.” Berggren and Siqin Wu, PhD, researcher at Spiber Technologies AB (formerly at Karolinska Institutet), are co-corresponding authors of the researchers’ published paper in Stem Cell Reports, titled “An optimized protocol for efficient derivation of pancreatic islets from multiple human pluripotent stem cell lines.”

Type 1 diabetes (T1D) occurs when the immune system destroys insulin-producing cells in the pancreas, meaning the body can no longer absorb glucose from the blood and regulate blood sugar levels. “In type 1 diabetes (T1D), autoimmune destruction of β cells results in loss of glycemic control,” the authors wrote.

One possible treatment strategy is to replace these cells with new ones. However, previous methods of producing such cells from stem cells have often yielded mixed results. Stem cell therapy for type 1 diabetes is already being tested in several clinical trials. However, a challenge with previous methods is that the stem cells often develop into a combination of the desired and undesired cell types, increasing the risk of complications. Another challenge is that the insulin-producing cells created are often not mature enough to respond well to glucose.

“The success of cell therapy for type 1 diabetes (T1D) depends on reliable differentiation of stem cells into functional pancreatic islets,” the authors noted. They pointed out that previous protocols have exhibited variable efficiency across different human pluripotent stem cell (hPSC) lines. “Differentiation beyond the stage (S) 4 pancreatic progenitor (PP) stage frequently yields heterogeneous cultures containing proliferative non-endocrine cells and immature endocrine cells … increasing the risk of cyst or tumor formation,” the team further commented.

The newly optimized production process reported by Berggren and colleagues yields more mature and purer insulin-producing cells than previous methods. In a laboratory setting, the cells were able to secrete insulin and responded strongly to glucose. When the researchers transplanted these cells into streptozotocin (STZ)-induced diabetic mice, the animals gradually regained the ability to regulate their blood sugar. “By adjusting the culture steps and allowing the cells to form three-dimensional clusters themselves, many unwanted cell types are eliminated and the cells gain a better ability to respond to glucose, according to the researchers. “Single-cell analyses show that the SC-islets are free of non-endocrine cell populations before and after transplantation,” the team stated.

The transplantation was performed in the anterior chamber of the eye (ACE) which provides a transparent and accessible site for noninvasive monitoring of engrafted SC-islets through the cornea, the team pointed out. Transplantation into this compartment is also straightforward and minimally invasive. In their paper, the team noted, “Intraperitoneal glucose tolerance tests (IPGTT) at three, four, and six months post-transplantation showed improved glucose handling over time … SC-islet transplantation reversed hyperglycemia by three months, and by five–six months blood glucose levels fell slightly below pre-STZ baselines.”

Berggren commented, “This is a technique we use to monitor the development and function of the cells over time in a minimally invasive way. We observed that the cells gradually matured after transplantation, retaining their ability to regulate blood sugar for several months, which demonstrates their potential for future treatments.”

Fredrik Lanner, PhD, professor at the Department of Clinical Science, Intervention and Technology, Karolinska Institutet, and last author of the paper, added, “This could solve several of the problems that have previously hindered the development of stem cell-based treatments for type 1 diabetes. Building on this, we will work towards clinical translation aiming at treating type 1 diabetes.” In their report the authors concluded, “Our protocol generated glucose-responsive SC-islets from all eight hPSC lines tested … demonstrating potential for autologous applications … Our efficient differentiation protocol represents a key step toward autologous cell therapy, though further work is required to realize this goal.”

News Staff by — April 19, 2026 By News Staff in Bio Space
How a tiny circle of repeat offenders poisoned 100s of gold-standard medical trials for over a decade

Randomized Controlled Trials (RCTs) are the gold standard of medical research as random assignment approach helps eliminate bias and yields the most reliable evidence on whether a treatment truly works. Since RCTs sit at the top of the evidence hierarchy, retractions can send ripple effects across the entire system. A fraudulent study with fabricated data or results can influence the credibility of systematic reviews and meta-analyses, and those distortions can quietly shape clinical practice guidelines that influence real-world medical care.

In a recent study, researchers set out to investigate how many retracted randomized clinical trials were linked to superretractors (authors with the most retractions) and to highly cited authors with multiple retractions.

They found that just 6 superretractors were co-authors on 22% of all retracted clinical trials studied, 5 were based in Japan, and 1 was from Germany. Also, a group of 18 top-cited scientists were involved in 25% of all retracted trials. The retractions were highly concentrated in specific areas like anesthesiology, endocrinology and metabolism.

The findings are published in JAMA Network Open, as well as an Invited Commentary.

Identifying the superretractor concentration

To become a superretractor, first, a researcher must produce large volumes of unreliable, duplicate, or fabricated work, often fueled by the publish or perish system of academia that rewards output over rigor and lacks strong oversight. Second, that misconduct has to be uncovered through investigation and exposure.

Superretractors can also act as superspreaders of contaminated research. When flawed or fabricated trials enter systematic reviews and meta-analyses, they are amplified and woven into widely used evidence summaries. By the time a study is retracted, it has often already shaped these studies referenced for developing clinical guidelines that doctors rely on. The result is a cascade of distorted evidence that can translate into incorrect, even harmful, decisions in patient care.

A major concern is the rise of zombie studies—research that appears fake or lacks credible data yet remains in medical literature, often without being retracted by journals as it should be.

By pinpointing a small group of highly cited, influential authors behind many retractions, researchers can more quickly flag fraudulent and zombie literature at scale and trace related problematic studies through their co-author networks.

So, in this study, the researchers used a dataset called VITALITY, which includes 1,330 randomized clinical trials (RCTs) that have been retracted as of late 2024. They focused on three particular groups of scientists: superretractors on the Retraction Watch Leaderboard, scientists who are 2% of their subfield and have 10 or more retractions not due to editor or publisher errors, and top-cited scientists in 2024 who also have 10 or more such retractions.

They found that a very small group of people were responsible for a disproportionately large number of retracted medical trials. Of the 30 global superretractors, six individuals were involved with coauthoring 290 retracted trials and among the 163 highly influential scientists, just 18 were linked to 327 retracted trials.

Also, papers written by these high-profile authors remained in the scientific literature far longer before being retracted, taking an average of about 14 years, compared with just over a year for other researchers. As a result, these papers accumulated far more citations, allowing potentially flawed findings to spread more widely through the scientific community. Many of these authors also collaborated with other scientists whose papers were retracted, as co-authors.

These findings point to a clear need for systematic approaches to actively trace how untrustworthy data spreads and to prevent its continued contamination of the scientific record. The information highlighted in this study can guide journal editors, funders, and institutions in identifying high-risk authors and fields, directing attention where it is needed most.

News Staff by — April 18, 2026 By News Staff in Global News
Cutting calories to slow aging—without compromising health

Restricting calorie intake in species such as mice, rhesus monkeys, and fruit flies has been shown to extend their lifespans. In some cases, these animals not only live longer, but are also free of disease. But when pushed too far, calorie restriction can have negative impacts. Mice that undergo a 40% reduction in calorie intake, for example, are more susceptible to infections, less likely to reproduce, and experience stunted growth.

Scientists have wondered whether there is a way to reap the longevity benefits of calorie restriction in humans without its negative repercussions. And in a new study published in Nature Aging, they found a potential answer in an immune-related protein called complement component 3 (C3).

Yale researchers have previously shown that people who undergo moderate calorie restriction—a 14% reduction in calorie intake—for two years developed better immune defense without any growth or reproductive trade-offs.

“This concept demonstrates that aging is actually malleable and a process that can be targeted,” says senior author Vishwa Deep Dixit, Ph.D., Waldemar Von Zedtwitz Professor of Pathology, professor of immunobiology and of comparative medicine, and director of the Yale Center for Research on Aging (Y-Age) at Yale School of Medicine.

Calorie restriction reduces inflammation-related protein

In the new study, Dixit and his colleagues at YSM analyzed the plasma samples of 42 individuals who took part in a two-year trial called the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy or CALERIE.

“It’s the only trial of its kind that has been done with such rigor and control and demonstrates relevance to human physiology,” Dixit says. During the trial, participants were able to reduce their calorie intake by 11 to 14% without feeling deprived.

In their analysis, the researchers detected more than 7,000 proteins in the longitudinal plasma samples. Among them was an immune-related protein called C3 that was significantly reduced following calorie restriction. C3 was of particular interest to the scientists as prior studies have suggested that activation of the complement system—a network of proteins involved in the defense against pathogens—could drive chronic inflammation, a major hallmark of aging and age-associated diseases.

“But the causal effects of C3 in aging and chronic inflammation have not been identified. So, we were very excited to find that in our study,” says Hee-Hoon Kim, Ph.D., a postdoctoral associate in the Dixit lab and a co-first author of the paper.

A target to slow aging

When comparing the protein levels before and after two years of calorie restriction, the researchers identified white adipose tissue—the main type of fat tissue in mammals—as the primary site affected by calorie restriction.

The researchers confirmed their findings in animals. As with the human plasma, they found that C3 expression increased with age in mice. Further biochemical analyses showed that visceral white adipose tissue was responsible for an increase in C3 during aging.

“We were not expecting that because these proteins are mainly synthesized in the liver,” says Manish Mishra, Ph.D., a postdoctoral associate in the Dixit lab and a co-first author of the study.

Single-cell RNA sequencing further revealed that the protein is produced by age-associated macrophages—essential white blood cells—within the adipose tissues.

“This whole process was unknown in the beginning,” Mishra says. “Just to narrow it down to the subtypes of macrophages responsible for this complement protein production was very challenging.”

Macrophages are the body’s first line of immune defense, mostly known for their role in engulfing pathogens. These immune cells also help maintain the balance of tissue functions, Dixit adds.

The question is whether the benefits gained from a reduction in C3 can be achieved without weight loss.

The researchers initially suspected that the shedding of adipose tissue or body fat due to weight loss may have stalled C3 production and slowed down the aging process. After all, most of the study participants lost about 18 pounds after two years of moderate calorie restriction.

However, when the researchers analyzed the body mass index of the study participants, they did not observe any correlation between weight loss and a decrease in complement proteins.

“This suggests that calorie restriction has a beneficial effect that is unique to adipose tissues and is likely independent of weight loss,” Kim says.

Further, when the researchers inhibited C3 activation using a drug to mimic the effect of calorie restriction, the mice experienced less age-related inflammation.

The finding demonstrates that what is beneficial early on in life can be detrimental later on, Dixit says. This theory, known as antagonistic pleiotropy, was first proposed by biologist Peter Medawar in 1952 to describe the aging process. A prime example of this theory is growth hormone production, which is essential in early development but could also drive cancer later in life.

Proteins like C3 are evolutionarily designed to protect us from infections, but as humans live much longer than their ancestors, these molecules can come back to harm us. Lowering the level of C3 proteins may be the key to enhancing health span, Dixit says.

The researchers are now investigating whether they could hold back C3 production to slow down aging in humans using FDA-approved inhibitor drugs. “The idea is not to remove complement systems that are required for us to fight infections,” Dixit says. “Instead, the goal is to restore the balance.”

News Staff by — April 18, 2026 By News Staff in Global News
Two bacteria join forces to turn chemical signals into electricity, opening up low-cost sensing options

Bacterial sensors usually rely on emitting light to transfer information about what they’re sensing, but that method isn’t practical in many settings. That’s why most information transmission is done via electricity. And while electricity-emitting bacteria exist, manipulating them into useful sensors has been quite challenging. Rice University professor Caroline Ajo-Franklin’s group, working in collaboration with researchers from Tufts University and Baylor College of Medicine, recently developed a flexible bioelectrical sensor system called electroactive co-culture sensing system (e-COSENS). The study is published in Nature Biotechnology.

“Bioelectrical sensing is by no means a new concept,” said Ajo-Franklin, the Ralph and Dorothy Looney Professor of Biosciences and corresponding author on this paper. “But e-COSENS is the first system that allows us to easily engineer bioelectronic sensors in a modular manner, like assembling Legos, allowing us to potentially use them to monitor everything from human health to environmental contaminants.”

Bioelectrical sensing requires bacteria that produce electricity and are easy for researchers to manipulate to respond to different substances. Ideally, the bacteria would be able to live in a variety of different places so that the system could be used in environments ranging from rivers to milk.

The challenge was finding bacteria that met all three conditions. E. coli, for example, is simple to engineer but doesn’t produce electricity. L. plantarum, a common food bacterium, produces electricity using a molecule called quinone but is incredibly difficult to engineer.

“Instead of forcing a single bacterium to do everything, we split the job between two bacteria,” said Siliang Li, the first author on this study and postdoctoral fellow. “That division of labor is what makes e-COSENS so flexible and powerful.”

The key to e-COSENS is quinone, the molecule L. plantarum uses to create electricity. L. plantarum cannot create its own quinone; it has to be provided by the environment. This means the quinone can be used as a signal, or trigger, to turn electricity on or off.

The researchers revealed that they could easily manipulate bacteria like E. coli, a bioengineering workhorse, to make quinone only in the presence of a specific substance called an analyte. Once E. coli released the quinone in the environment, L. plantarum would use it to send an electrical signal, which could be read by an electrode—in this case, a current meter.

To test this system, the researchers designed systems to look for four different analytes in four different environments. They used E. coli to sense heavy metal ions in bayou water and inflammation markers in artificial saliva, and L. lactis, another quinone-producing bacterium, to sense antimicrobial peptides in human fecal-derived samples provided by Baylor and an antibiotic in milk from the grocery store. They placed each sample and bacterial system into individual reactors connected to current meters. Within a few hours, all four current meters showed an electrical charge, revealing the bacteria were responding to the analytes—some in as few as 20 minutes.

All four versions of the system were successful, but the large reactors they used wouldn’t easily translate from the lab to the outdoors. Luckily, their collaborators at Tufts had a solution: a compact electronic disk roughly the size of a quarter which can be paired with commercially available digital multimeters.

“This simplified hardware dramatically lowers the barrier to using bioelectronic sensors outside the lab and opens possibilities for low-cost, field-ready diagnostics,” Li said. The researchers had also identified multiple other bacteria that could either send or receive a quinone signal, increasing the number of possible environments e-COSENS could be used in.

“The strength of e-COSENS is the flexibility derived from sharing the work across multiple cells,” said Ajo-Franklin, director of the Rice Synthetic Biology Institute, which focuses on supporting interdisciplinary research. “In the same manner, the success of this research hinged on sharing expertise and work among my research group and our partners, Duolong Zhu and Robert Britton at Baylor and Kundan Saha and Sameer Sonkusale at Tufts.”

News Staff by — April 18, 2026 By News Staff in Biotechnology Today
Shrink, remove and modify: Team successfully ‘trims’ wheat chromosomes

For the first time, a research team at the Leibniz Institute of Plant Genetics and Crop Plant Research (IPK) has succeeded in reducing the size of, or even completely removing, chromosomes in plants with large genomes, such as wheat. They achieved this by using the CRISPR/Cas gene-editing tool to target highly repetitive sections of DNA. The results of the study, published today in the journal Plant Communications, could significantly accelerate breeding processes.

While the targeted manipulation of entire chromosomes is well established in model organisms such as Arabidopsis thaliana, it has posed a significant challenge in crops with large genomes, such as wheat. The IPK research team has now set out to determine whether highly repetitive DNA sequences known as satellite DNA are suitable targets for the CRISPR gene-editing system. The idea was that cutting many of these identical sequences simultaneously could affect the entire chromosome. The team introduced CRISPR components into the plants using a virus-based system. This approach bypasses lengthy traditional transformation processes and enables highly efficient chromosomal modifications.

“In our study, we were actually able to demonstrate for the first time that chromosomes can be efficiently reduced in size by making targeted cuts in satellite DNA,” says Dr. Jianyong Chen, the study’s first author. This is a significant breakthrough, as such changes had previously only occurred by chance. You can think of it like a rope. If you cut a rope in several places at once, it becomes unstable and eventually snaps. The same thing happens to chromosomes when many cuts are made simultaneously.

In some cases, the method resulted in the loss of entire chromosomes. “If too many breaks occur, the cell can no longer repair the chromosome efficiently—it is lost entirely,” explains Prof. Dr. Andreas Houben, head of the IPK’s research group “Chromosome Structure and Function.”

Faulty repair processes can also create new forms of chromosomes, called isochromosomes. “These changes can generate new genetic variants, opening pathways for breeding resistant wheat and other crops,” explains Prof. Dr. Houben. This innovation potential should inspire optimism about future crop improvements.

The study shows that plant genomes can be modified with unprecedented precision. Notably, satellite DNA, once considered “genetic ballast,” is now an effective target for modern breeding tools. “This approach enables efficient manipulation of chromosomes, paving the way for transferring valuable traits from wild relatives into cultivated wheat,” say the IPK scientists, encouraging a sense of empowerment in future crop development.

News Staff by — April 18, 2026 By News Staff in Biotechnology Today