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  • Dr. Krishna Kumari Challa

    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

  • Dr. Krishna Kumari Challa

    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

  • Dr. Krishna Kumari Challa

    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