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A common nutrient could supercharge cancer treatment

A simple nutrient from everyday vegetables could help supercharge the body’s fight against cancer. A common eye-health nutrient, zeaxanthin, may also help the body fight cancer more effectively. Scientists discovered it strengthens Tcells and enhances the impact of immunotherapy treatments. Found in everyday vegetables and supplements, it’s safe, accessible, and shows strong potential as a cancer therapy booster. Human trials are the next step.

Researchers at the University of Chicago have uncovered a surprising new role for zeaxanthin, a plant-based compound best known for supporting eye health. According to findings published in Cell Reports Medicine, this common carotenoid may also help the immune system fight cancer by enhancing the activity of key immune cells. The discovery points to zeaxanthin as a simple, widely available supplement that could improve how well cancer immunotherapies work.

“We were surprised to find that zeaxanthin, already known for its role in eye health, has a completely new function in boosting anti-tumor immunity,” said Jing Chen, PhD, Janet Davison Rowley Distinguished Service Professor of Medicine and senior author of the study. “Our study show that a simple dietary nutrient could complement and strengthen advanced cancer treatments like immunotherapy.”

Brain motion is driven by mechanical coupling with the abdomen

UNIVERSITY PARK, Pa. — The brain is more mechanically connected to the body than previously appreciated, scientists reported today (April 27) in Nature Neuroscience. Through a study using mice and simulations, the team found a potential biological mechanism underlying why exercise is thought to benefit brain health: abdominal contractions compress blood vessels connected to the spinal cord and the brain, enabling the organ to gently move within the skull. This swaying facilitates the surrounding cerebrospinal fluid to flow over the brain, potentially washing away neural waste that could cause problems for brain function.

According to Patrick Drew, professor of engineering science and mechanics, of neurosurgery, of biology and of biomedical engineering at Penn State, the work builds on previous studies detailing how sleep and neuron loss can influence how and when cerebrospinal fluid flushes through the brain.

“Our research explains how just moving around might serve as an important physiological mechanism promoting brain health,” said Drew, corresponding author on the paper. “In this study, we found that when the abdominal muscles contract, they push blood from the abdomen into the spinal cord, just like in a hydraulic system, applying pressure to the brain and making it move. Simulations show that this gentle brain movement will drive fluid flow in and around the brain. It is thought the movement of fluid in the brain is important for removing waste and preventing neurodegenerative disorders. Our research shows that a little bit of motion is good, and it could be another reason why exercise is good for our brain health.”

Drew, who also holds the title of associate director of the Huck Institutes of the Life Sciences, explained how in a hydraulic system, a pump creates pressure that drives fluid flow. In this case, the pump is the abdominal contraction — which can be as light as the tensing prior to sitting up or taking a step. The contraction puts pressure on the vertebral venous plexus, a network of veins that connect the abdominal cavity to the spinal cavity, causing the brain to move.

Abstract: Nature Neuroscience Brain motion is driven by mechanical coupling with the abdomen.

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The antimetastatic effects of calorie restriction are negated by voluntary exercise in an aggressive breast cancer mouse model

The role of lifestyle interventions in treatment success has become essential for nearly every disease. Healthy dietary habits, regular exercise, and stress management are key pillars that can improve quality of life during treatment, as well as delay disease onset and progression. In this study, we focus on the combination of mild calorie restriction (CR) and voluntary exercise as coadjuvants to chemotherapy in the treatment of triple-negative breast cancer using the 4T1 mouse model. In this model, voluntary exercise did not add benefits beyond chemotherapy plus CR in terms of primary tumor size, body composition, or physical performance, while dampening the antimetastatic effect of CR in the lungs of sedentary mice. These findings highlight the challenges of translating results from one preclinical model to another, and ultimately to humans.

Metabolic inflammation at the adipose-brain axis

Adipose-brain axis in metabolic inflammation.

White adipose tissue (WAT) in addition to storing excess energy also releases cytokines, lipid mediators, adipokines, and extracellular vesicles that influence brain physiology.

The inflammatory mediators disrupt key brain interfaces, including the blood-brain barrier (BBB), perivascular and glymphatic clearance pathways, promoting endothelial dysfunction, altered astrocyte-pericyte support, impaired amyloid-b clearance, and region-specific glial activation.

In the brain, obesity-associated neuroinflammation leads to various neuronal dysfunction including cognition.

The authors discuss the role of adipokines in adipose-brain communication during obesity including how they contribute to neuroinflammation and synaptic dysfunction.

The authors also discuss therapeutic strategies targeting the adipose-brain axis, including exercise and dietary interventions and pharmacological approaches such as orlistat and incretin-based therapies. sciencenewshighlights ScienceMission https://sciencemission.com/adipose-brain-axis


Scientists Develop New Antibody For Virus That Infects 95% of People

The Epstein-Barr virus (EBV) is one of the world’s most common viruses, thought to be lurking in 95 percent of adults. For most, it causes no obvious symptoms.

But EBV is more than a short-term infection.

Once it enters the body, EBV can stay for life, and it has been linked to several cancers, multiple sclerosis, and other severe health complications. Now, new research has given us a promising way to fight it.

Stealth switch in tuberculosis enzyme could open route to drug-resistant treatment

Recent research published in Communications Biology marks an advance in structural biology by enhancing understanding of protein regulation mechanisms in Mycobacterium tuberculosis (Mtb), a global health threat. The team led by the University of Melbourne combined several advanced techniques at the Australian Synchrotron and the National Deuteration Facility to reveal the hidden allosteric mechanism that activates a key enzyme, ICL2.

The study opens a target pathway to treat drug-resistant TB with modulators that can interfere with the enzyme’s “on switch.” Traditional drugs often targeted the enzyme’s active site, which is difficult to block effectively.

However, ICL2 is unique to mycobacteria and is essential for the survival of the TB bacterium during infection, especially when it is starved of sugar and forced to live on fats.

Mitochondrial dysfunction in cerebrovascular diseases

Opening of the mitochondrial permeability transition pore, Ca2+ overload, and mitochondrial fragmentation are early features of stroke-induced brain injury observed in experimental models.

Mitochondrial reactive oxygen species and activation of the cyclophilin D– reactive oxygen species–NLR family pyrin domain-containing 3–matrix metalloproteinase-9 axis are associated with intracranial aneurysm progression, linking mitochondrial stress to vascular wall instability.

Disruption of mitochondrial homeostasis exacerbates vascular pathology in intracranial atherosclerotic stenosis, arteriovenous malformations, and cavernous malformation, indicating a shared mitochondrial contribution across cerebrovascular disorders.

Pharmacological modulation of mitochondrial permeability, redox signaling, proprotein convertase subtilisin/ kexin type 9, and mechanistic target of rapamycin kinase pathways shows robust preclinical efficacy, while clinical outcomes remain heterogeneous.

Experimental studies support the feasibility of mitochondrial transplantation in models of cerebrovascular injury, including stroke. sciencenewshighlights ScienceMission https://sciencemission.com/Mito-dysfunction-in-CVD


Mitochondria are central regulators of cerebrovascular health through their control of energy metabolism, Ca2+ homeostasis, and redox signaling, and their dysfunction represents a convergent pathogenic mechanism across cerebrovascular diseases. In ischemic stroke, mitochondrial failure exacerbates neuronal injury via permeability transition pore opening, oxidative stress, and bioenergetic collapse, while altered mitochondrial dynamics and the release of mitochondrial damage-associated molecular patterns amplify neuroinflammation during reperfusion. Beyond stroke, mitochondrial dysfunction contributes to intracranial aneurysms, atherosclerotic stenosis, and vascular malformations, where oxidative stress, mitochondrial DNA instability, and cell type-specific metabolic reprogramming drive vascular remodeling and lesion progression.

Negative effects of artificial sweeteners may pass on to next-generation, study suggests

Health organizations are starting to raise concerns about the potential long-term impacts of artificial sweeteners, which taste sweet but—unlike sugar—contain no calories, suggesting they could interfere with energy metabolism and increase the eventual risk of diabetes or cardiovascular disease.

Now a new study in mice indicates that the popular sweeteners sucralose and stevia have negative effects on the gut microbiome and gene expression, potentially compromising metabolic health, which can be transmitted between generations.

“We found it intriguing that despite the growing consumption of these additives, the prevalence of obesity and metabolic disorders such as insulin resistance has not declined,” said Dr. Francisca Concha Celume of the Universidad de Chile, lead author of the article in Frontiers in Nutrition.

MRI reveals cerebrospinal fluid shifts after mild brain injury

Researchers at University of Tsukuba have found that cerebrospinal fluid (CSF) microdynamic motion shows region-specific alterations after mild traumatic brain injury (TBI). Using a specialized magnetic resonance imaging (MRI) technique, the team noninvasively visualized these CSF changes, which have been difficult to quantify with conventional imaging. The approach is expected to advance the understanding of the relationship between post-traumatic brain conditions and cognitive function. The study is published in Frontiers in Neuroscience.

The brain contains cerebrospinal fluid (CSF), which protects neural tissue and helps clear metabolic waste. Rather than being static, CSF exhibits continuous subtle motion, and this motion is thought to be closely linked to brain health. However, little has been known about how CSF motion is altered after a mild head injury.

The researchers employed a specialized magnetic resonance imaging (MRI) technique known as intravoxel incoherent motion (IVIM) MRI to evaluate CSF microdynamic motion through the incoherent movement of water molecules. The results showed that, after mild traumatic brain injury (TBI), CSF motion increased in some brain regions and decreased in others.

T cells secrete DNA to boost the immune system’s cancer-fighting ability

Activated immune cells secrete tiny capsules bearing DNA that can enter other immune and tumor cells to stimulate the body’s defense systems, according to a study led by investigators at Weill Cornell Medicine. The discovery extends the scientific understanding of the immune system, identifies a new strategy for boosting immunity against cancers and potentially offers a new tool for delivering genetic payloads to other cells.

Most animal cells secrete tiny capsules known as extracellular vesicles—nanoscale, membrane-bound particles—whose cargo can include proteins, snippets of DNA and other molecules. In the new study, published April 30 in Cancer Cell, the researchers discovered that vesicles secreted by activated T cells —major weapons of the immune system—carry DNA that enters immune cells and nearby tumor cells to enhance the immune response against the tumor. Preclinical experiments showed that this vesicle-associated DNA could be useful therapeutically, boosting T cell attacks against tumors that otherwise evoke little or no immune response.

“These findings reveal a natural mechanism for treating immunologically silent tumors and other diseases that stem from insufficient immune surveillance,” said study co-senior author Dr. David Lyden, the Stavros S. Niarchos Professor in Pediatric Cardiology and a member of the Gale and Ira Drukier Institute for Children’s Health and the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.

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