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Comment by Dr. Krishna Kumari Challa 19 hours ago

Menstrual cycle found to affect women's reaction time, but not as much as being active

Women performed best on cognitive tests during ovulation but physical activity level had a stronger influence on brain function, according to a new study .

The study, published in Sports Medicine–Open, explored how the different phases of the menstrual cycle and physical activity level affected performance on a range of cognitive tests designed to mimic mental processes used in team sports and everyday life, such as the accurate timing of movements, attention, and reaction time.

Researchers found that women had the fastest reaction times and made the fewest errors on the day of ovulation, when the ovaries release an egg ready to be fertilized (and when women's fertility is at its peak).

But while cognitive performance fluctuated across the menstrual cycle, much greater differences were observed between those who were active and those who weren't. Compared to active participants, inactive participants had reaction times on average around 70 milliseconds slower and made around three times as many impulsive errors, regardless of cycle phase.

The researchers say the findings are particularly relevant to women's sport, where slightly quicker reaction times of around 20 milliseconds may make the difference between sustaining or avoiding an injury like concussion. Previous research on elite athletes has suggested injuries are more common at certain points during the menstrual cycle, and the authors say that these changes in cognition might partially explain this occurrence.

However, while a difference of 20 milliseconds is likely to be inconsequential in everyday life, the much larger difference between active and inactive groups is more significant, where 70 milliseconds could determine whether we regain balance after tripping over an obstacle or not.

Menstrual cycle and athletic status interact to influence symptoms, mood, and cognition in females, Sports Medicine–Open (2025). DOI: 10.1186/s40798-025-00924-8

Comment by Dr. Krishna Kumari Challa 19 hours ago

Blood cancer: Scientists reprogram cancer cell death to trigger immune system

The aim of immunotherapy strategies is to leverage cells in the patient's own immune system to destroy tumor cells. Using a preclinical model, scientists successfully stimulated an effective anti-tumor immune response by reprogramming the death of malignant B cells. They demonstrated an effective triple-therapy approach for treating forms of blood cancer such as certain lymphomas and leukemias which affect B cells. The study was published on August 15 in the journal Science Advances. 

Immunotherapy strategies represent a major breakthrough in cancer treatment. They aim to harness the patient's immune system so that their own cells can recognize and specifically eliminate tumor cells. Immune cells can act like sentinels, scanning the body and identifying all residual tumor cells to reduce the risk of relapse. Various novel immunotherapy strategies are emerging, one of which makes use of a cell death mechanism known as necroptosis. Unlike apoptosis, which results in silent cell death, necroptosis releases warning signals that attract and stimulate immune cells so that they can kill any remaining tumor cells.

Scientists set out to explore the effectiveness of this necroptosis-based immunotherapy strategy on hematological malignancies. They began by observing that necroptosis cannot be easily induced in malignant B cells because of the absence of the MLKL protein.

To overcome this hurdle, the scientists combined administration of three drugs already used in clinical practice. They confirmed induction of necroptosis and observed a strong immune response leading to the complete elimination of leukemia in a preclinical model. 

The triple therapy they used forces cancer cells to die in a way that activates the immune system.

The results were observed in preclinical models using an innovative intravital imaging technique. The scientists were able to monitor the interactions between immune cells and cancer cells in real time for the different types of cell death induced.

"This novel immunotherapy strategy, successfully tested in preclinical models, turns tumor cells into triggers for the immune system, pointing to a potential therapeutic avenue for certain cancers, such as lymphomas or leukemias affecting B cell.

Ruby Alonso et al, Reprogramming RIPK3-induced cell death in malignant B cells promotes immune-mediated tumor control, Science Advances (2025). DOI: 10.1126/sciadv.adv0871

Comment by Dr. Krishna Kumari Challa on Friday

The researchers then examined the underlying mechanisms driving these changes. They found that air pollution had triggered significant changes in the regulation of DNA in brown fat cells.

This included modifications in DNA methylation patterns and changes in how accessible certain genes were for being turned on or off—a process known as chromatin remodeling. These epigenetic changes affect how cells function by regulating gene activity without altering the genetic code itself.

Two enzymes were identified as main drivers of this process: HDAC9 and KDM2B. These enzymes are involved in modifying histones, the proteins around which DNA is wrapped. They were found to bind to specific regions of the DNA in brown fat cells of the mice exposed to PM2.5, leading to a reduction in key chemical tags, or methyl groups, that normally promote gene activity.

When these enzymes were experimentally suppressed, brown fat function improved, whereas increasing their activity led to further declines in metabolism.
The study shows that long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat. This occurs through complex changes in gene regulation controlled by epigenetic mechanisms.

Rengasamy Palanivel et al, Air pollution modulates brown adipose tissue function through epigenetic regulation by HDAC9 and KDM2B, JCI Insight (2025). DOI: 10.1172/jci.insight.187023

Part 2

Comment by Dr. Krishna Kumari Challa on Friday

Study suggests air pollution can contribute to obesity and diabetes

Long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat in mice. A study co-led by the University of Zurich shows that this occurs through complex changes in gene regulation driven by epigenetic mechanisms. The results demonstrate how environmental pollutants contribute to the development of insulin resistance and metabolic diseases.

There is growing evidence that air pollution is not just harmful to our lungs and heart, but also plays a significant role in the development of metabolic disorders like insulin resistance and type 2 diabetes.

For their investigation, the researchers exposed laboratory mice to either filtered air or concentrated PM2.5 for six hours a day, five days a week, over a period of 24 weeks. This setup was designed to closely mimic chronic urban exposure in humans.
Particular attention was paid to brown adipose tissue, a special type of fat that helps the body generate heat and burn calories, and therefore plays a key role in energy balance and glucose metabolism. After the exposure period of about five months, the mice that had inhaled PM2.5 showed signs of disrupted metabolism, including impaired insulin sensitivity.

Further examination revealed that the function of brown fat had been significantly altered. In particular, they found that the expression of important genes in brown adipose tissue which regulate its ability to produce heat, process lipids and handle oxidative stress were disturbed. These changes were accompanied by increased fat accumulation and signs of tissue damage and fibrosis within the tissue.

Part 1

Comment by Dr. Krishna Kumari Challa on Friday

For cancer patients, this discovery suggests simple changes, like eating more foods rich in OA (such as olive oil, avocados and nuts) and cutting back on PA (found in processed foods, palm oil and fatty meats), could improve the effectiveness of cancer treatments. The study also points to novel strategies, like combining dietary changes with specific drugs to further boost the immune system.

Yanmei Zhang et al, Oleic acid restores the impaired antitumor immunity of γδ-T cells induced by palmitic acid, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02295-8

Part 2

Comment by Dr. Krishna Kumari Challa on Friday

Certain dietary fatty acids can supercharge cancer-fighting immune cells

A research team has discovered that certain dietary fatty acids can supercharge the human immune system's ability to fight cancer. The team found that a healthy fatty acid found in olive oil and nuts, called oleic acid (OA), enhances the power of immune γδ-T cells, specialized cells known for their cancer-fighting properties.

Conversely, they found that another fatty acid, called palmitic acid (PA), commonly found in palm oil and fatty meats, diminishes the ability of these immune cells to attack tumors.

Their study, published in the journal Signal Transduction and Targeted Therapy, offers an innovative approach using dietary OA supplementation to strengthen the antitumor immunity of γδ-T cells.

Dietary fatty acids are essential for health, helping with growth and body functions. They may also play a role in cancer prevention and treatment, but understanding how they affect cancer is challenging because of the complexity of people's diets and the lack of detailed studies.
Recently, scientists have learned that fatty acids can influence the immune system, especially in how it fights cancer. Specialized immune cells, called γδ-T cells, are particularly good at attacking tumors. These cells, once activated, have helped some lung and liver cancer patients live longer.
However, this therapy is not effective for all patients, partly because the variation of metabolic status, such as fatty acid metabolism, can influence its efficacy in the patients.

The research team identified a correlation between PA and OA levels and the efficacy of cancer therapies. The research suggests that dietary fatty acid supplementation, particularly with foods rich in OA, such as olive oil and avocados, could enhance γδ-T cell immunosurveillance, leading to more effective cancer treatments.

The team also discovered that another fatty acid, called PA, can weaken these immune cells and how OA can counteract this.

The results indicate that cancer patients should avoid PA and consider OA supplementation in their diets to improve clinical outcomes of γδ-T cell-based cancer therapies.

By analyzing blood samples, the researchers confirmed that the levels of these fatty acids are linked to the outcome of cancer immunotherapy.

Part 1

Comment by Dr. Krishna Kumari Challa on Friday

Nanoparticle vaccine prevents multiple cancers and stops metastasis in mice

A new study by researchers demonstrates that their nanoparticle-based vaccine can effectively prevent melanoma, pancreatic and triple-negative breast cancer in mice. Not only did up to 88% of the vaccinated mice remain tumor-free (depending on the cancer), but the vaccine reduced—and in some cases completely prevented—the cancer's spread.

By engineering these nanoparticles to activate the immune system via multi-pathway activation that combines with cancer-specific antigens, they could prevent tumor growth with remarkable survival rates.

The first test paired their nanoparticle system with well-characterized melanoma peptides (called an antigen, similar to how a flu shot typically contains parts of the inactivated flu virus). The formulation activated immune cells called T cells, priming them to recognize and attack this type of cancer. Three weeks later, the mice were exposed to melanoma cells.

Eighty percent of these "super adjuvant" vaccinated mice remained tumor-free and survived until the completion of the study (250 days). In comparison, all of the mice vaccinated with traditional vaccine systems, non-nanoparticle formulations or unvaccinated mice developed tumors; none survived longer than 35 days.

The vaccine also protected against the spread of cancer to the lungs. When exposed to melanoma cells systemically, which mimics how cancer metastasizes, none of the nanoparticle-vaccinated mice developed lung tumors, while all of the other mice did.

The tumor-specific T-cell responses that the researchers are able to generate—that is really the key behind the survival benefit. 

There is really intense immune activation when you treat innate immune cells with this formulation, which triggers these cells to present antigens and prime tumor-killing T cells. This robust T-cell response is possible because of the particular nanoparticle design of the vaccine.

The researchers say that their design offers a platform approach that could be used across multiple cancer types.

"Super adjuvant" nanoparticles for platform cancer vaccination, Cell Reports Medicine (2025). DOI: 10.1016/j.xcrm.2025.102415. www.cell.com/cell-reports-medi … 2666-3791(25)00488-4

Comment by Dr. Krishna Kumari Challa on Friday

Schizophrenia is linked to iron and myelin deficits in the brain, neuroimaging study finds

Schizophrenia is a severe and debilitating psychiatric disorder characterized by hallucinations, disorganized speech and thought patterns, false beliefs about the world or oneself, difficulties concentrating and other symptoms impacting people's daily functioning. While schizophrenia has been the topic of numerous research studies, its biological and neural underpinnings have not yet been fully elucidated.

While some past brain imaging studies suggest that schizophrenia is associated with abnormal levels of iron and myelin in the brain, the results collected so far are conflicting. Iron is a metal known to contribute to healthy brain function, while myelin is a fatty substance that forms a sheath around nerve fibers, protecting them and supporting their conduction of electrical signals.

Researchers  recently set out to further explore the possibility that schizophrenia is linked to abnormal levels of iron and myelin in the brain. Their findings, published in Molecular Psychiatry, uncovered potential new biomarkers of schizophrenia that could improve the understanding of its underlying brain mechanisms.

Iron is essential for many neuronal processes but excess causes oxidative damage, so brain levels are kept in a delicate balance. Iron-sensitive MRI studies focusing on schizophrenia have yielded conflicting results, with both increases and decreases reported. As myelin—which increases brain signal transmission—influences iron-sensitive MRI, myelin variation could complicate interpretation.

Researchers  examined the brains of 85 individuals diagnosed with schizophrenia and 86 matching control subjects. To study the brains of the study participants, they used iron-sensitive and myelin-sensitive magnetic resonance imaging (MRI), imaging techniques that allow researchers to detect iron and myelin levels in specific regions of the brain.

The researchers' results suggested iron and myelin anomalies that affected specific regions in the brains of individuals diagnosed with schizophrenia, including the caudate, putamen, and globus pallidus. Their findings are aligned with those of some earlier studies and could help to paint a clearer picture of disease pathophysiology.

They found that patients with schizophrenia had lower magnetic susceptibility, higher mean diffusivity, and lower magnetic susceptibility anisotropy, suggesting that both iron and myelin brain levels are lower in schizophrenia.

This was most significant in regions rich in oligodendrocytes. As oligodendrocytes utilize iron to synthesize myelin, this links oligodendrocyte dysfunction to schizophrenia, highlighting the mechanism underlying this as an important research area.

Luke J. Vano et al, The role of low subcortical iron, white matter myelin, and oligodendrocytes in schizophrenia: a quantitative susceptibility mapping and diffusion tensor imaging study, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03195-7.

Comment by Dr. Krishna Kumari Challa on Thursday

Novel blood test for chronic fatigue achieves 96% accuracy

Scientists  have developed a high accuracy blood test to diagnose chronic fatigue syndrome, also known as myalgic encephalomyelitis (ME/CFS).

The debilitating long-term illness affects millions worldwide but is poorly understood and has long lacked reliable diagnostic tools.

With 96% accuracy, the new test offers new hope for those living with the condition—which is often misunderstood and misdiagnosed. It is hoped that the breakthrough could pave the way for a similar blood test to diagnose long COVID.

Chronic fatigue syndrome is not a genetic disease you're born with. That's why using EpiSwitch 'epigenetic' markers—which can change during a person's life, unlike a fixed genetic code—was key to reaching this high level of accuracy.

The team discovered a unique pattern that appears consistently in people with ME/CFS that is not seen in healthy people.

The researchers also found signs of immune system and inflammation pathways involved in the disease, which may help guide future treatments and identify patients more likely to respond to specific therapies.

'Development and validation of blood-based diagnostic biomarkers for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) using EpiSwitch® 3-dimensional genomic regulatory immuno-genetic profiling, Journal of Translational Medicine (2025). translational-medicine.biomedc … 6/s12967-025-07203-w

Comment by Dr. Krishna Kumari Challa on Thursday

New type of diabetes discovered in babies

Advanced DNA sequencing technologies and a new model of stem cell research have enabled an international team to discover a new type of diabetes in babies.

The researchers established that mutations in the TMEM167A gene are responsible for a rare form of neonatal diabetes.

Some babies develop diabetes before the age of six months. In over 85% of cases, this is due to a genetic mutation in their DNA. Research  found that in six children with additional neurological disorders such as epilepsy and microcephaly identified alterations in a single gene: TMEM167A.

To understand its role, the researchers  used stem cells differentiated into pancreatic beta cells and gene-editing techniques (CRISPR). They found that when the TMEM167A gene is altered, insulin-producing cells can no longer fulfill their role. They then activate stress mechanisms that lead to their death.

This discovery shows that the TMEM167A gene is essential for the proper functioning of insulin-producing beta cells, but also for neurons, whereas it seems dispensable for other cell types. These results contribute to a better understanding of the crucial steps involved in insulin production and could shed light on research into other forms of diabetes, a disease which today affects almost 589 million people worldwide.

Enrico Virgilio et al, Recessive TMEM167A variants cause neonatal diabetes, microcephaly and epilepsy syndrome, Journal of Clinical Investigation (2025). DOI: 10.1172/jci195756

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