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Comment by Dr. Krishna Kumari Challa 5 hours ago

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 9 hours ago

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

Comment by Dr. Krishna Kumari Challa 9 hours ago

About 15,000 land vertebrate species could lose habitat to sea-level rise by 2100
The rate of sea-level rise is now more than 4 millimeters (0.16 inches) per year, having more than doubled since 1993–2002. Scientists estimate that this figure may go up to 10 millimeters (0.39 inches) per year in the near future. The inundation of coastlines and islands will affect human and animal habitats alike.
A new study, published in Science, has laid out projections of which land animals and habitats will be most affected by rising sea levels. The study seeks to provide guidance for conservation efforts by pointing out important refuges for affected animals.
The study found that roughly 14,300–15,300 of the 34,120 species studied could experience partial habitat inundation, depending on the emissions scenario. The researchers say that 57%–63% of birds, 47%–52% of mammals, 28%–36% of reptiles and 20%–24% of amphibians would be affected. Under the highest-emissions scenario, 109 species could lose more than 10% of their habitat by 2100, compared with 18 by 2050.
The study also identified specific regions with the most at-risk species. Southeast Asia emerged as a major hotspot for threatened and small-range species, largely due to inundated areas harboring high numbers of threatened species. The Amazon delta leads in the number of species whose habitats overlap projected flooding, with more than 1,000 square kilometers (386 square miles) of inland area inundated by 2050.

Islands are also at a greater risk due to smaller geographic ranges for habitats.

Zhong-Wen Jiang et al., Safeguarding global terrestrial vertebrate species from future sea level rise, Science (2026). DOI: 10.1126/science.aed5772

Comment by Dr. Krishna Kumari Challa 9 hours ago

Parkinson's-linked protein may sabotage the brain's waste disposal system

A protein's shape can make all the difference between keeping the body running smoothly and contributing to disease. A protein called α-synuclein (α-syn), under normal conditions, helps neurons release neurotransmitters by interacting with tiny structures called synaptic vesicles at the ends of nerve cells. The accumulation of misfolded versions of the same protein can lead to Parkinson's disease, a nervous system disorder that affects movement and gets worse over time. The clumped-up protein also collects in the cerebrospinal fluid (CSF) surrounding the brain and in the brain's outer border tissue, known as the dura mater.
A recent study published in the Journal of Experimental Medicine explores how the buildup of α-syn at the brain's borders impairs central nervous system functions such as waste clearance.

To investigate this, researchers examined donated CSF and dura mater from people with Parkinson's disease and healthy controls, looking for forms of α-syn prone to clumping. They also developed mouse models to study what happens when the brain's waste-clearance system fails.

They saw that the toxic aggregates accumulated not only inside the brain, CSF and dura mater but also immediately adjacent to the meningeal lymphatic vessels, which are responsible for draining fluid and waste out of the skull. In the mouse models, the misfolded protein buildup in these layers altered the behaviour of immune cells and threw the brain's waste-clearance system off balance.
The results show how α-syn affects the tissues along the brain's borders and point to meningeal immune activity as another factor behind impaired waste clearance in Parkinson's disease.

Taylor J. Stevenson et al., Cerebrospinal fluid and dural accumulation of α-synuclein impairs CNS clearance in Parkinson's disease, Journal of Experimental Medicine (2026). DOI: 10.1084/jem.20251245

Comment by Dr. Krishna Kumari Challa on Tuesday

Childhood cancers may spread by 'shape-shifting' rather than mutating

A review proposes that some childhood cancers spread through reversible changes in cell state without acquiring additional mutations. Changes in gene activity may exploit developmental flexibility to enable metastasis and treatment resistance. The model requires further validation and does not establish a new treatment.

Developmental plasticity as a framework for paediatric cancer metastasis, Trends Open (2026).

Comment by Dr. Krishna Kumari Challa on Tuesday

Researchers reveal how inhaled nanoplastics trigger lung inflammation

Everyday plastic products, including water bottles, disposable cups and packaging, can break down over time into tiny fragments known as nanoplastics. These particles are invisible to the naked eye and can become airborne, raising concerns about their potential to reach deep into the lungs when inhaled.
The researchers prepared PE and PP nanoparticles and compared their effects with those of diesel exhaust particles. Using a mouse model in which particles were delivered directly into the trachea, they evaluated lung inflammation and investigated the biological processes underlying the response.

Both types of nanoplastics caused acute lung inflammation. Importantly, their relative inflammatory potency depended on how the particle dose was measured.

When compared by mass, PE nanoplastics produced an inflammatory response at least as strong as that of diesel exhaust particles. When the researchers compared doses based on particle surface area, both PE and PP nanoplastics showed greater inflammatory potential than diesel exhaust particles.
The team also examined alveolar macrophages, immune cells that act as the lungs' cleanup crew. Exposure to the nanoplastics increased the production of reactive oxygen species (ROS), highly reactive molecules that can damage cells when produced in excess.

ROS production was closely associated with the inflammatory response, helping explain how nanoplastics can promote the recruitment of additional immune cells and contribute to lung tissue injury. Gene expression analysis also revealed changes in pathways involved in inflammation and immune regulation.
The findings show that nanoplastics can actively disrupt immune responses in the lungs under the experimental conditions tested. They also suggest that assessing airborne particles by mass alone may underestimate the inflammatory potential of nanoplastics.

Polyethylene and polypropylene nanoplastics caused acute lung inflammation after intratracheal delivery in mice. Both were more inflammatory than diesel particles at equal surface-area doses. Inflammation was associated with increased reactive oxygen species in alveolar macrophages. Mass-based dosing alone may underestimate nanoplastic inflammatory potential.

Eunsol Bae et al., Comparative toxic potential of polypropylene and polyethylene nanoplastics using a mouse intratracheal instillation model, Journal of Hazardous Materials Advances (2026). DOI: 10.1016/j.hazadv.2026.101625

Comment by Dr. Krishna Kumari Challa on Tuesday

Very strong El Niño episodes are associated with over 100,000 additional heat-related deaths worldwide per year
Very strong El Niño episodes were associated with an estimated 107,035 additional heat-related deaths and 112,681 fewer cold-related deaths annually worldwide versus neutral conditions. These changes largely offset globally, but combined heat- and cold-related mortality increased in lower-resource countries.

Natalia Shartova et al., Global temperature-related mortality associated with El-Nino Southern Oscillation, Nature Medicine (2026). DOI: 10.1038/s41591-026-04793-w

Comment by Dr. Krishna Kumari Challa on Tuesday

Maps of inflammaging reveal the heart does not age evenly

Scientists have long known that aging drives inflammation in the heart, but exactly how those changes are distributed throughout the organ has remained unclear. Now, a research team has pinpointed hotspots where these "inflammaging" signals concentrate, providing a new map of cardiac aging and a foundation for future studies of cardiovascular health and decline.
In a study of mouse hearts published in Aging Cell, JAX researchers found that cellular signatures associated with age-related inflammation and scarring concentrated in the aortic valves and aortic root, where immune and connective tissue cells interact in ways that change with age and may influence the health of the surrounding heart muscle.
Rather than finding signs of aging evenly distributed, the researchers discovered hotspots of inflammation and fibrosis (or scarring) concentrated in the valves and aortic root. They concluded that these regions may serve as hubs of cardiac aging, where inflammation and aging signals concentrate, potentially influencing surrounding muscle tissue.
Together, the findings reinforce evidence that the valves and aortic root may function as localized hubs of cardiac aging.

Aleksandra Aljakna Khan et al., Alterations in the Immune‐Fibrotic Axis Are Spatially Localized in the Aging Heart, Aging Cell (2026). DOI: 10.1111/acel.70768

Comment by Dr. Krishna Kumari Challa on Tuesday

The brain's 'dimmer switch' could help explain why attention drifts

Researchers have discovered that serotonin, a brain chemical best known for its role in mood and mental health, also helps regulate attention. These findings suggest serotonin-producing neurons deep in the midbrain act like a dimmer switch on attention.
More than a century of research has revealed how attention shapes behaviour.
Everyone has moments of sharp focus and moments of drift. This work identifies a specific brain chemical that selectively controls the moment-to-moment strength of attention to salient stimuli.
In the study, when researchers reduced serotonin activity, the mice in the experiment focused better. Increasing serotonin had the opposite effect. That was surprising because it's often assumed that increasing a brain signal will improve performance.
The results suggest the level of serotonin helps control the moment-to-moment strength of attention. Rather than turning attention on or off, serotonin appears to act more like a dimmer switch, dialing its strength up or down.

These insights could help researchers better understand such conditions as ADHD. They also raise new questions about how medications that act on serotonin—including common antidepressants—may affect the brain.

While people often think of distraction as a problem, occasional lapses in focus may serve an important purpose.

From an evolutionary perspective, the ability to quickly shift attention to a new threat or opportunity was probably beneficial for survival.
Today, that same system may be at work when you're focused on your job but still monitoring your phone for an important message. The challenge is finding the right balance between focusing strongly and remaining responsive to changes around us.

Jonas Lehnert et al., Rapid dynamics of dorsal raphe serotonin neurons regulate the strength of visual attention, Nature Communications (2026). DOI: 10.1038/s41467-026-70658-y

Comment by Dr. Krishna Kumari Challa on Tuesday

Their analysis revealed that cancer cells naturally undergo −1 ribosomal frameshifting, in which ribosomes slip backward by one genetic letter at specific codon pairs, such as AGAACG and ACGAGA. This often produces detectable peptides or proteins, such as gasdermin D (GSDMD-N), from the altered genetic instructions.

The researchers traced this slippage to elevated phosphorylation of ribosomal protein S6 (pRPS6), which pushes paused ribosomes into an alternative reading frame. This phosphorylation is driven by the mTOR and MAPK growth signalling pathways, which are often overactive in cancer cells.
The researchers designed FAST to exploit the frameshifting tendency of cancer cells. They placed a fragment of GSDMD-N responsible for forming pores in the −1 reading frame, just behind the codon sequence that triggers ribosomes to slip backward.

When cancer cells underwent the shift, they produced a protein fragment that punched holes in their membranes, causing the cells to burst and die through an inflammatory process called pyroptosis. Normal cells, which read the sequence in the usual way, remain unharmed.

When delivered intravenously into a mouse model, FAST triggered substantial tumor regression in colorectal cancer (MC38) and spontaneous pancreatic cancer (KPC mice). It also curbed the spread of cancer to the liver and lungs. FAST also boosted immune activity within tumors and proved more effective when combined with immune checkpoint inhibitors. Tests in mice found no inflammation or organ toxicity in healthy tissues of major organs.

These findings offer hope that frameshifting-triggered gene circuits could, with further research, provide a way to selectively target cancer cells.

Qiuyi Wang et al., Cancer-selective gene circuits via intrinsic ribosomal frameshifting, Nature (2026). DOI: 10.1038/s41586-026-11200-4

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