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Comment by Dr. Krishna Kumari Challa on August 21, 2025 at 9:21am

Since such heterogeneity is important, they used a series of single cell sequencing techniques to study gene expression and chromatin structure in individual mTECs, instead of using traditional bulk sequencing tools that average the results over thousands of cells.

Chromatin is the complex of DNA and proteins in the nucleus that packages long stretches of DNA into more compact structures. When chromatin is more loosely packed, or open, genes are more poised to be activated than if it's tightly coiled.

When the researchers analyzed the data, they did not find links between peak levels of chromatin accessibility and the expression of tissue-specific genes. Instead, they saw a lot of accessibility "noise" that gave cells the potential to activate genes solely expressed in other specialized tissues. This "ectopic expression" in turn helped train T cells to discriminate between self and non-self.

Chromatin is usually tightly regulated to sequester regions that encode other cell fates and focus accessibility for regions pertinent for the established cell identity.
In this work context, the researchers found the genomic regions that should be tightly packed were more labile or 'jiggly," allowing more opportunities for factors to access and activate genes specific to different cell types."
The team then tried to understand how this "chromatin noise" is amplified in cells. They found that the activity of the tumor suppressor protein p53, known as "the guardian of the genome," is repressed by mTECs prior to their genome becoming noisy. p53 is usually activated when DNA is damaged and can trigger cell death or stop tumor cell growth.

So, it made sense to the researchers that it would be implicated in a process where epithelial cells promiscuously express genes dedicated to other tissues and organs.
When the researchers genetically engineered p53 activity to be enhanced in mTECs, their chromatin became more stable, epigenetic noise was turned down, and the cells could no longer activate tissue-specific genes. This ultimately resulted in the escape of self-reactive T cells from the thymus to cause multi-organ autoimmune disease.
This suggests that thymic epithelial cells adopt deviant states that should normally trigger p53 activation and cell death.But because p53 is downregulated, the cells survive and facilitate this ectopic gene expression to promote the self/non-self discrimination.
It's a fascinating idea to think that cells are programmed to loosen their grip on genes to give them more freedom to get creative and solve problems like preventing T cells from attacking their own tissues.
The researchers extended their studies and found that epigenetic noise also allows lung cancer to sample more of the genome once p53 is deleted. This activates programs specific to other tissues to develop into more aggressive, malignant states. They hope to continue studying whether other cancer types exploit similar mechanisms for tumorigenesis.
Part 2

Comment by Dr. Krishna Kumari Challa on August 21, 2025 at 9:17am

Epigenetic noise: Unappreciated process helps cells change identity

All cells in the body contain the same DNA, but different cell types express different genes; skin cells express genes for the skin, liver cells express liver genes, and so on. This coordination is crucial to help cells differentiate into their assigned roles, but a new study by researchers shows how cells can randomly "shake up" regions of the genome to express genes normally reserved for other cell types.

The study, "Thymic epithelial cells amplify epigenetic noise to promote immune tolerance," published in Nature, suggests that randomness or variability in the way DNA is packaged can create a kind of "epigenetic noise," enabling cells to take on the identity of different cell types. This flexibility plays an important role in tissue repair and the immune system but can also be exploited for the development of tumors.

The researchers worked with an incredibly resourceful group of cells called medullary thymic epithelial cells (mTECs). These cells are found in the thymus, a small, specialized organ of the immune system located just above the heart. They are one of the few cell types in the body that can express a wide variety of genes and alter their identity to mirror cell types from other tissues.

mTECs play an important role in training the immune system to prevent autoimmunity. They present proteins that are normally expressed only in specialized tissues and organs to T cells developing in the thymus. Then, the T cells that react too strongly to molecules from the body's own cells are purged so they don't later trigger an autoimmune response.

The capability to express almost any gene and alter their identities makes mTECs a great candidate for studying how cells can change their fates.

Each individual cell does not express the entire genome. Instead, they express only a unique subset of the tissue-specific genes at any given snapshot. There's a great deal of heterogeneity, so the researchers thought that it was really important to look cell-by-cell to uncover the mechanisms that allow the activation of each subset of tissue-specific genes.

Part 1

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 12:09pm

“Logic will get you from A to B.  Imagination will take you everywhere.” –Albert Einstein

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 12:08pm

Imagination won't take you everywhere—study reveals limitations of the mind's eye

Our imagination might not be as powerful as we think when it comes to holding visual images, according to a first-of-its-kind study by psychologists.

 The research found that people can remember more items when they've seen them, compared to when they must imagine them.

While short-term visual memory can hold three to four items at once, our imagination can manage only two items before becoming less accurate.

Across a series of five experiments, more than 150 participants were asked to either remember or imagine the locations of objects on a grid.

Researchers examined how accurately participants could detect changes in specific locations under various conditions, including timing, cueing, display type, and object complexity. They then compared the number of items participants could correctly remember after viewing them with the number they could accurately imagine and recall without having seen them.

Findings showed that even when given more time or simpler images, people still imagined fewer items than they could remember visually.

The study, "The relation between the capacities of imagination and visual memory in the short-term," published in the Journal of Experimental Psychology: Human Perception and Performance, offers the first direct comparison of how much information people can hold in visual imagination versus visual memory.

Imagination and memory use similar parts of the brain, but this is the first time scientists have measured exactly how they differ when it comes to capacity. These findings demonstrate that actually seeing something, even a brief glimpse, gives our brain extra sensory support that bolsters our memory. In fact, researchers estimate that 17–35% of visual memory capacity depends on sensory input. When we imagine something from scratch, we don't have that input from our eyes, so it's harder to hold detailed images.

We use imagination constantly in everyday life, as imagery is seen as essential for navigating and predicting our environment and is involved in decision-making and emotion regulation, but the study reveals that our capacity to visualize is surprisingly limited, and this might affect how we make decisions, remember plans, or follow instructions when we rely on mental imagery alone.

Christopher Atkin et al, The relation between the capacities of imagination and visual memory in the short term., Journal of Experimental Psychology: Human Perception and Performance (2025). DOI: 10.1037/xhp0001364

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 11:37am

Hight-salt diet sparks brain inflammation that could explain stubborn high blood pressure

A new study finds that a high-salt diet triggers brain inflammation that drives up blood pressure. 

The research suggests the brain may be a missing link in certain forms of high blood pressure—or hypertension—traditionally attributed to the kidneys.

This is new evidence that high blood pressure can originate in the brain, opening the door for developing treatments that act on the brain.

Hypertension affects two-thirds of people over 60 and contributes to 10 million deaths worldwide each year. Often symptomless, the condition increases the risk of heart disease, stroke and other serious health problems.

About one-third of patients don't respond to standard medications, which primarily target the blood vessels and kidneys based on the long-standing view that hypertension begins there.

The study, published in the journal Neuron, suggests the brain may also be a key driver of the condition, particularly in treatment-resistant cases.

How salt disrupts the brain

To mimic human eating patterns, rats were given water containing 2% salt, comparable to a daily diet high in fast food and items like bacon, instant noodles and processed cheese.

The high-salt diet activated immune cells in a specific brain region, causing inflammation and a surge in the hormone vasopressin, which raises blood pressure. Researchers tracked these changes using cutting-edge brain imaging and lab techniques that only recently became available.

The brain's role in hypertension has largely been overlooked, in part because it's harder to study.

The researchers used rats instead of the more commonly studied mice because rats regulate salt and water more like humans. That makes the findings more likely to apply to people.

Next, the scientists plan to study whether similar processes are involved in other forms of hypertension.

Ning Gu et al, Microglia regulate neuronal activity via structural remodeling of astrocytes, Neuron (2025). DOI: 10.1016/j.neuron.2025.07.024

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 11:31am

To examine the mechanisms behind the link between cardiovascular disease and cancer growth, the study authors developed a mouse model with breast tumors and induced temporary ischemia in one hind limb. The team then compared cancer growth in mice with and without impaired blood flow.

Their findings build on the nature of the immune system, which evolved to attack invading bacteria and viruses, and, under normal conditions, to detect and eliminate cancer cells. These protective functions rely on stem cell reserves in the bone marrow, which can be activated as needed to produce key white blood cell populations throughout life.

Normally, the immune system responds to injury or infection by ramping up inflammation to eliminate threats, then scaling back to avoid harm to healthy tissue. This balance is maintained by a mix of immune cells that either activate or suppress inflammation.

The researchers found that reduced blood flow disrupts this equilibrium. It reprograms stem cells in the bone marrow to favor the production of "myeloid" immune cells (monocytes, macrophages, neutrophils) that dampen immune responses, while reducing output of lymphocytes like T cells that help to mount strong anti-tumor responses.

The local environment within tumors showed a similar shift, accumulating more immune-suppressive cells– including Ly6Chi monocytes, M2-like F4/80+ MHCIIlo macrophages, and regulatory T cells—that shield cancer from immune attack.

Further experiments showed that these immune changes were long-lasting. Ischemia not only altered the expression of hundreds of genes, shifting immune cells into a more cancer-tolerant state, but also reorganized the structure of chromatin–the protein scaffolding that controls access to DNA–making it harder for immune cells to activate genes involved in fighting cancer.
results reveal a direct mechanism by which ischemia drives cancer growth, reprogramming stem cells in ways that resemble aging and promote immune tolerance.
These findings open the door to new strategies in cancer prevention and treatment, like earlier cancer screening for patients with peripheral artery disease and using inflammation-modulating therapies to counter these effects."

Moving forward, the research team hopes to help design clinical studies that evaluate whether existing inflammation-targeted therapies can counter post-ischemic changes driving tumor growth.

Ischemic Injury Drives Nascent Tumor Growth via Accelerated Hematopoietic Aging, JACC CardioOncology (2025). DOI: 10.1016/j.jaccao.2025.05.016

Part 2

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 11:30am

Restricted blood flow speeds tumor growth by aging the immune system, study finds

Cutting off blood flow can prematurely age the bone marrow, weakening the immune system's ability to fight cancer, according to a new study .

Published online in JACC-CardioOncology, the study showed that peripheral ischemia–restricted blood flow in the arteries in the legs–caused breast tumors in mice to grow at double the rate seen in mice without restricted flow. These findings build on a 2020 study by the same team that found ischemia during a heart attack to have the same effect.

Ischemia occurs when fatty deposits, such as cholesterol, accumulate in artery walls, leading to inflammation and clotting that restrict the flow of oxygen-rich blood. When this happens in the legs, it causes peripheral artery disease, which affects millions of people, and can increase the risk of heart attack or stroke.

This new study  shows that impaired blood flow drives cancer growth regardless of where it happens in the body.

This link between peripheral artery disease and breast cancer growth underscores the critical importance of addressing metabolic and vascular risk factors as part of a comprehensive cancer treatment strategy.

Importantly, the research team found that restricted blood flow triggers a shift toward immune cell populations that cannot efficiently fight infections and cancer, mirroring changes seen with aging.

Part 1

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 8:56am

How HPV reprograms immune cells to help cancer grow

The most common cancer-causing strain of human papillomavirus (HPV), HPV16, undermines the body's defenses by reprogramming immune cells surrounding the tumor, according to new research.

In mice, blocking this process boosted the ability of experimental treatments for HPV to eliminate cancer cells. The results were published in the Journal for ImmunoTherapy of Cancer.

HPV16 causes more than half of cervical cancer cases and roughly 90% of HPV-linked throat cancers. It can be neutralized with the preventive vaccine Gardasil-9, but only if vaccination occurs prior to HPV exposure.

Researchers are now working to develop "therapeutic vaccines," which can be taken after HPV exposure—for instance, following an abnormal pap smear or cancer diagnosis—to trigger an immune response against infected cells by T-cells, a type of "fighter" cell that helps defend the body from disease. But these vaccines, now in clinical trials, have limited effectiveness—and the new study helps explain why.

The research focuses on a signalling protein in the immune system with inflammatory properties called Interleukin-23 or IL-23. While IL-23 was previously implicated in cervical and throat cancers, its exact role was unclear.

In a series of tests in mice and cell cultures,  researchers found that two HPV proteins, E6 and E7, prompt nearby cells to release IL-23, which in turn prevents the body's T-cells from attacking the tumor.

In order to eliminate the cancer, T-cells need to proliferate and destroy infected cells. But IL-23 stops them from working effectively, so the tumor keeps growing.

HPV16 E6 and E7 expressing cancer cells suppress the anti-tumor immune response by upregulating KLF2 mediated IL-23 expression in macrophages, Journal for ImmunoTherapy of Cancer (2025). DOI: 10.1136/jitc-2025-011915

Comment by Dr. Krishna Kumari Challa on August 20, 2025 at 8:49am

Maize plants use a volatile gas to fight off pests in densely crowded fields

When maize fields become too crowded, the plants signal each other to boost their defenses. A research team found that in crowded conditions, maize plants release a volatile gas called linalool into the air. When it reaches neighboring plants, the gas triggers a defensive response in their roots.

While planting crops close together can increase harvest size, it also increases the risk of pathogens and pests such as caterpillars and the African maize stalk borer. When this happens, maize crops don't stand idly by. It was already known that the plants can change their shape in crowded conditions, such as growing taller to get more sunlight, but less was known about their immune response.

The research team reports that in dense fields, linalool acts like an alarm bell, triggering the roots of neighboring plants to increase production of jasmonate and other plant hormones. This, in turn, leads to more benzoxazinoids leaking into the soil around the roots.

This class of plant chemical defense compounds alters the bacterial composition of the soil, thereby protecting the plants from pests. And the protective response is a speedy one, with increased defense against caterpillars observed after just three days of growth in high-density conditions.

However, as the researchers note from their field studies, there is a catch. This defensive boost comes at the cost of reduced growth as the plants put more of their resources into defense rather than growing.

The scientists also showed that soil modified by densely planted maize crops offered ongoing protection for new crops even against different pests. Later plantings were protected from nematodes and other pathogens, not just insects. This suggests that maize defense readiness persists in the soil long after the initial crop is harvested.

Dongsheng Guo et al, Linalool-triggered plant-soil feedback drives defense adaptation in dense maize plantings, Science (2025). DOI: 10.1126/science.adv6675

Niklas Schandry et al, The scent of a crowd, Science (2025). DOI: 10.1126/science.adz7633

Comment by Dr. Krishna Kumari Challa on August 19, 2025 at 1:45pm

Early lead exposure could result in memory issues later in life

A new study has found that people who lived in areas with high levels of leaded gasoline emissions in the 1960s and '70s are more likely to report memory problems today—a finding that researchers say could deepen our understanding of environmental risks tied to dementia.

The study and others presented in July at the 2025 Alzheimer's Association International Conference used data from more than 600,000 participants .

Participants who lived in areas with higher estimated lead emissions—often tied to dense traffic and industrial zones—were significantly more likely to report poor memory. 

Lead has long been known to affect brain development in children. But research into its long-term effects on aging brains is still emerging.

Lead is bad for lots of things. There's been some studies that suggest it's related to IQ generally, and also aggression and lots of other things in animal model studies.

IQ is not the only area where lead exposure damages us. Instead, it often overlaps with other social determinants of health, like poverty and poor housing, making it difficult to isolate one factor. Higher levels of exposure and living near environmental pollutants often correlate to those with lower incomes.

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