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Comment by Dr. Krishna Kumari Challa 6 hours ago

Inflammation is involved in the earliest stages of atherosclerosis

Atherosclerosis begins decades before it causes a heart attack or stroke. During that time, arteries progressively accumulate fatty plaques and inflammatory cells without producing symptoms.
Inflammation plays an important role in the development of atherosclerosis from its earliest stages, long before the onset of symptoms or cardiovascular events such as heart attack or stroke. This is the main conclusion of a study led by a team at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) and published in the European Heart Journal. The research shows that systemic inflammation contributes to disease development independently of traditional cardiovascular risk factors such as elevated cholesterol and hypertension.

In 3,471 adults without known cardiovascular disease followed for six years, systemic inflammation was associated with early atherosclerosis burden and progression independently of LDL cholesterol and blood pressure. White blood cell count was the inflammatory biomarker most closely associated with disease presence and progression.

The results show that inflammation contributes to the development of atherosclerosis independently of LDL cholesterol and blood pressure, two of the most important cardiovascular risk factors. The study also identifies white blood cell count as the inflammatory biomarker that best reflects the presence and progression of early atherosclerotic disease.
The research also shows that incorporating inflammatory biomarkers into cardiovascular risk assessment could complement the information provided by traditional risk factors and contribute to more personalized prevention.

Guiomar Mendieta et al., Inflammation and early atherosclerosis beyond traditional risk factors: an imaging study, European Heart Journal (2026). DOI: 10.1093/eurheartj/ehag846

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Comment by Dr. Krishna Kumari Challa 7 hours ago

When a food-triggered reaction isn't a food allergy

It can be scary to have a reaction to something you've eaten and believe the symptoms indicate a food allergy. But for some, the cause of symptoms may be a different condition that can go unnoticed for years. Two new studies being presented at the American College of Allergy, Asthma and Immunology (ACAAI) Annual Scientific Meeting look at how eosinophilic esophagitis (EoE) diagnoses are on the rise and how EoE symptoms can be mistaken for a food allergy.

EoE is an allergic condition of the esophagus, the tube that carries food from your mouth to your stomach. In people with EoE, a type of white blood cell called an eosinophil builds up in the esophagus. This causes swelling and irritation. Over time, it can make it hard to swallow and can cause food to get stuck.

The first study looked at 29 adults who had been sent to an allergist because doctors thought they had experienced anaphylaxis, a severe allergic reaction, after eating certain foods. On average, each patient had gone to the emergency room three times, and most had been given at least one dose of epinephrine.

Their symptoms included a tight throat, trouble swallowing, chest pain, drooling and food getting stuck in their esophagus. But testing did not show a true food allergy. Instead, tissue samples taken from their esophagus showed that the patients had EoE. On average, it took more than five years for them to get the right diagnosis.
So not every frightening reaction after eating is anaphylaxis.
Eosinophilic esophagitis can closely mimic food allergy and may lead to repeated emergency visits before the correct diagnosis is made. When throat tightness, difficulty swallowing or food impaction recur, especially with negative food allergy testing, we should think about EoE. Early recognition can prevent years of uncertainty and progressive esophageal damage.

The second study used health records from more than 300 million patients in the U.S., making it the largest study of EoE in the country to date. Researchers found more than 500,000 people with an EoE diagnosis.

Key findings include:

The number of people diagnosed with EoE has increased about sevenfold since 2009.
EoE was most often first diagnosed in two age groups: teenagers and people in their 40s.
Males were more likely to have EoE than females.

People with several allergic conditions, such as asthma, hay fever, eczema and food allergies, were much more likely to have EoE. Among food allergies, wheat allergy had the strongest link.

When Anaphylaxis Is Not Anaphylaxis: Eosinophilic Esophagitis Mimicking Food Allergy, Annals of Allergy Asthma & Immunology (2026).

Epidemiology and Clinical Features of Eosinophilic Esophagitis: Analysis Using the COSMOS Database, Annals of Allergy Asthma & Immunology (2026).

Comment by Dr. Krishna Kumari Challa 7 hours ago

Why we may feel the cold more as we age

Researchers from City of Hope have uncovered the biological reason why we become more sensitive to cold as we get older. Unlike white fat, which primarily stores energy, thermogenic fat is a special type of body fat that burns calories to produce heat and helps us stay warm. Thermogenic fat tends to become less active with age, which may explain why older people are more sensitive to cold.

How the body turns up the heat

The mix of thermogenic fat cells may give the body a built-in way to adjust to changing temperatures. When more warmth is needed, signals from the nervous and immune systems prompt less-active cells to increase heat production. When the need passes, the system can dial that activity back.

In older mice, however, this response became sluggish. Their thermogenic fat could still increase heat production, but it took longer. As a result, the animals had more difficulty maintaining their body temperature during cold exposure.

The researchers were able to restore some heat production in older mice by blocking one part of the biological pathway behind this slowdown. The treated animals produced more heat and burned more energy.
The drug used in the experiment, mifepristone, affects many parts of the body, so it is not a treatment for age-related cold sensitivity. But the results suggest that the decline in thermogenic fat activity could be reversed.

Anying Song et al., Bistable regulation of adipocyte heterogeneity governs thermogenesis, Nature (2026). DOI: 10.1038/s41586-026-11308-7

Comment by Dr. Krishna Kumari Challa 7 hours ago

Parasites of parasites! Fungus infects powdery mildew

In the fungal kingdom, no one is safe from parasites—not even other parasites. A new study from North Carolina State University finds that Ampelomyces, an intracellular fungus that infects the plant disease powdery mildew, is far more common than previously known. By screening museum samples of powdery mildews up to about 150 years old, researchers discovered that not only is Ampelomyces quite common, but many specimens labeled as Ampelomyces are misidentified.

Because powdery mildews cannot be cultured, researchers screened more than 600 dried samples from the NC State herbarium (a collection of plant and/or fungal samples) to collect data on the prevalence of Ampelomyces. These samples were collected across 28 countries over the past 150 years and were analyzed alongside samples available on GenBank, a public database of DNA sequences used by scientists to share and study genetic data. Researchers found that about 7% of all powdery mildew specimens analyzed were infected by this parasite.

Understanding hyperparasites (parasites of parasites) could open doors to better control methods for the fungi they infect.

By understanding hyperparasite diversity and how many different strains are out there, it might give us insights on if some are better at controlling the fungus than others. There is a degree of host specificity to these hyperparasites, and if we are able to delve deeper they may be very useful in containing this plant disease.

Jacklyn Thomas et al., Parasites of parasites: Herbaria as archives of hidden ecological interactions, Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2026.1772

Comment by Dr. Krishna Kumari Challa 9 hours ago

Previous studies may also have underestimated how often important genes mutate.
We'd expect natural selection to rapidly remove mutations when they occur in more important genes, because these mutations are more likely to be harmful to the organism. This can create the illusion that important genes have fewer mutations when, in reality, some mutations have simply disappeared before we have a chance to analyze them—what you can think of as 'ghost mutations'."
To overcome these problems, the researchers used data from "mutation accumulation" experiments in E. coli and baker's yeast, designed to minimize the effects of natural selection. Three separate tests found no evidence that natural selection had substantially skewed the results.
The researchers then asked whether important genes really do mutate less often. They compared mutation rates with experimental evidence showing what happens when individual genes are removed. Some genes are essential, meaning that removing them kills the cell, while the loss of others has little or no effect.
The team also considered other ways of measuring a gene's importance, including how much of its protein a cell produces and the strength of natural selection acting on it over evolutionary time.

They found that genes producing more abundant proteins don't have lower mutation rates. Nor does the way genes evolve over thousands of years predict how frequently they mutate.
The researchers did, however, find that some features of the genome can affect mutation rates—for example, genes copied later during DNA replication tend to mutate more frequently.

Sofia Radrizzani et al., The importance of genes does not predict their mutation rate, PLOS Biology (2026). DOI: 10.1371/journal.pbio.3004089

Part 2

Comment by Dr. Krishna Kumari Challa 9 hours ago

Large mutation analysis challenges claim that evolution shields important genes from changes
The idea that important genes mutate less frequently than others was first proposed in 1972 as a challenge to the traditional view of evolution. But the claim has remained contentious. Now, new research by scientists finds the evidence behind that theory to be flawed.

In a new paper published in PLOS Biology, researchers analyzed the largest collection to date of spontaneous mutations in two microorganisms: the bacterium Escherichia coli (E. coli) and the single-celled fungus baker's yeast (Saccharomyces cerevisiae).
The researchers say their study debunks the idea that natural selection might protect important genes by reducing their mutation rates—a theory that has repeatedly resurfaced since it was first proposed, most recently in 2023.

The claim that mutation is slower for important genes is a triumph of hype over substance, they claim. It's a really old suggestion and is reinvented in various forms routinely.
Classically, evolution is seen as a two-step process. First, mutations generate genetic variation. Then, forces such as natural selection act on that variation, favoring some traits over others. In other words, natural selection is like a sieve that traps larger objects while letting finer ones through.

Darwin's finches—first encountered by Charles Darwin on the Galápagos Islands in 1835—provide a famous example: differences in the finches' beaks allow them to exploit different sources of food. While random mutation generates beaks of different sizes, when conditions favour particular foods, birds whose beaks are better suited to them are more likely to survive and reproduce, making those traits more common over generations.
However, some researchers argue that mutation may not be as random as traditionally assumed and that important genes (such as those involved in replicating DNA or maintaining basic cellular machinery) are protected from mutation, while genes where change could aid adaptation (such as those in which mutations give bacteria resistance to antibiotics, or change beak dimensions) mutate more frequently.

The idea that organisms might protect important genes from mutation seems helpful. If mutations in an important gene are likely to cause serious harm or genetic disease, why would evolution not reduce that gene's mutation rate?

However, there are theoretical problems with this idea. Gene mutation rates are already so low that reducing them further for individual genes would bring very little benefit, making it difficult for natural selection to favour such a system.

Part 1

Comment by Dr. Krishna Kumari Challa 9 hours ago

Despite substantial individual-level heterogeneity, atrophied regions in most MCI patients were functionally connected to a common episodic memory-associated impaired network," wrote the research authors in their paper. "This phenomenon was not significant in SCD patients. Both lesion-memory network mapping and cross-dataset validation confirmed consistency across cohorts. Critically, rTMS can modulate the impaired network in MCI patients, primarily reflected by enhanced functional connectivity within this network."

The team's findings suggest that the difficulties in remembering past events experienced by people with MCI could be associated with cortical thinning linked to the same neural network. In addition, the researchers showed that for people with MCI, functional connectivity within this network increased after rTMS.

Anxing Huang et al., Episodic memory-associated weighted atrophy network mapping in mild cognitive impairment and subjective cognitive decline: a multi-center study, Translational Psychiatry (2026). DOI: 10.1038/s41398-026-04539-9.

Part 2

Comment by Dr. Krishna Kumari Challa 9 hours ago

Brain imaging uncovers a shared memory network linked to mild cognitive impairment
As they age, many individuals can struggle to remember recent events or what they meant to say next during a conversation, while also frequently losing or misplacing objects. In some cases, cognitive tests detect these memory impairments. In others, people notice and report a decline even though their test scores remain within the normal range.
The term mild cognitive impairment (MCI) refers to measurable difficulties with memory or other thinking skills in people who remain largely independent in daily life. Subjective cognitive decline (SCD), on the other hand, is a perceived decline despite normal performance on standard cognitive tests. Understanding the neural underpinnings of both could potentially help researchers develop and test interventions for cognitive decline.
Researchers recently compared brain scans and memory test scores using data collected from more than 1,000 people. Their paper, published in Translational Psychiatry, suggests that different areas of cortical thinning in people with MCI could map to a shared memory network, while the same pattern was not statistically significant in people with SCD.
The researchers analyzed data from 1,312 people across three independent cohorts, including brain scans and scores on tests assessing episodic memory, the ability to recall specific events or experiences. They used structural magnetic resonance imaging (MRI) to measure cortical thickness and a reference map based on resting-state functional MRI (fMRI) to estimate how activity in different brain regions typically varies together.
When they analyzed the structural scans, the team specifically looked at the thickness of each participant's cerebral cortex. This allowed them to identify regions whose thickness was linked to episodic memory scores.
The team found that areas of cortical thinning varied from person to person. In most participants with MCI, however, these areas mapped to a common network associated with episodic memory.

The team did not find statistically significant evidence of the same shared network pattern in participants with SCD. Yet this does not necessarily mean that those participants had no cortical thinning or other brain changes.
They also carried out another experiment involving 25 participants with MCI and 13 with SCD. The experiment used a four-week course of repetitive transcranial magnetic stimulation (rTMS). This is a technique that delivers repeated magnetic pulses through a coil placed against the scalp.

The researchers found that the rTMS intervention was linked to changes in the functional connectivity of people with MCI. Specifically, after stimulation, signals from regions within the identified network varied more closely together.
Part 1

Comment by Dr. Krishna Kumari Challa yesterday

The Lloyds Bank coprolite is a 9th-century fossilized human stool (palaeofaeces) discovered in 1972 by construction workers and archaeologists from the York

Size: Measures 20 cm (8 in) long and 5 cm (2 in) wide, making it one of the largest recorded examples of preserved human faeces.
Diet and Health: Analysis shows the Viking-era producer lived mostly on a diet of meat and coarse bread, and suffered from a heavy intestinal parasite infestation (including whipworms and maw-worms).
Value: In 1991, York Archaeological Trust palaeoscatologist Andrew Jones famously appraised the specimen for insurance purposes, stating it is "as precious as the crown jewels" (with modern estimates valuing it around $39,000).
Current Location: After accidentally breaking into three pieces in 2003, it was repaired and is now on display in a glass case at the Jorvik Viking Centre in York.

Comment by Dr. Krishna Kumari Challa yesterday

Sudden confusion in the hospital may signal higher dementia risk later in life

Hospitalized older adults can suddenly become disoriented and struggle to make sense of their surroundings. This condition, known as delirium, disrupts attention, awareness and clear thinking. The confusion can set in abruptly or come and go, sometimes changing in severity over time. It is far from rare, as it affects up to 30% of older hospital patients and as many as 80% of those in intensive care units (ICUs). There are several factors that can trigger such a state, including an infection, surgery or even certain medications.
A recent study set out to explore if delirium during hospitalization could have lasting consequences for memory and thinking. The researchers followed 3,501 older adults all of whom had experienced at least one hospital stay between 2004 and 2023, but none had dementia before being hospitalized.

The team kept track of their cognitive health for a median of 7.2 years, putting participants through in-person memory and thinking tests every 15 months. Neurologists and neuropsychologists assessed whether they developed mild cognitive impairment (MCI) or dementia over this period.

According to results published in JAMA Neurology, the consequences of delirium appeared to extend far beyond the hospital walls. Older adults who experienced an episode during or shortly after hospitalization were more likely to face more severe cognitive impairment and faster cognitive decline. Their risk of developing dementia was 5.39 times that of patients who had not experienced delirium.

An episode of delirium is not just a temporary disturbance in mental functioning; it does have the potential to impact overall brain health in the long run. Studies have found that it could also increase the risk of dementia and speed up cognitive decline.

Analysis of data collected across repeated 15-month follow-ups, spanning 4.1 years for some participants and more than a decade for others, showed that patients who experienced delirium had 3.67 times the risk of developing MCI, an early stage of noticeable memory and thinking difficulties. Memory and thinking test scores dropped much more rapidly over time in patients with delirium.

The researchers suggest delirium be treated as a medical emergency due to its lasting effects on the cognitive health of older adults.

Allyson K. Palmer et al., Delirium and Long-Term Cognitive Trajectories in Cognitively Unimpaired Adults, JAMA Neurology (2026). DOI: 10.1001/jamaneurol.2026.4001

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