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Comment by Dr. Krishna Kumari Challa on June 10, 2026 at 11:01am

Some drugs 'fail' because of unrealistic testing conditions, scientists discover

A drug once dismissed as ineffective suddenly worked—when scientists tested it under more realistic conditions that mimic the human body. In this surprising new discovery, scientists uncovered a hidden rule of drug behaviour. A medicine's effectiveness can change dramatically depending on the conditions inside our cells.

Drug efficacy can change significantly depending on physiological conditions such as body temperature and intracellular calcium levels, which affect protein structure and drug binding. Testing drugs under more realistic cellular environments revealed previously undetected activities and even opposite effects for some compounds. These findings suggest that drug screening should incorporate physiological variables to improve therapeutic design and predictability.
In the new study, scientists found that two fundamental features of human biology—body temperature and calcium levels inside cells—can change how drugs interact with their targets, sometimes even flipping a drug's effect entirely.

The findings could help explain why some drug candidates look promising in early lab tests but fail later in development. They also could point toward a smarter way to design more effective medicines with fewer unwanted side effects.
Drugs don't act in isolation. They act within the physiological environment of the cell. By incorporating temperature and calcium into their experiments, researchers uncovered drug activities that were completely invisible before.
In early evaluations, researchers commonly test drugs in simplified laboratory conditions—often at room temperature and in artificial chemical environments that do not necessarily reflect the realities inside the human body.
But proteins are dynamic, shape-shifting molecules. Their structure can change in response to their surroundings, including temperature and chemical signals like calcium. Because drugs often work by binding to proteins, even small structural shifts can dramatically change a drug's ability to work. In other words, if the protein changes its shape, the drug's effectiveness can change too.
To better understand this connection, the Northwestern team focused on TRPM4, a protein channel involved in heart rhythm, immune responses and other essential biological functions. They test triphenylphosphine oxide (TPPO), a small synthetic molecule, on cells expressing the TRPM4 channel.

In lab tests under simplified conditions, TPPO appeared inactive, showing no effect on TRPM4. But when the Northwestern team tested it at body temperature (37°C / 98.6°F) and with realistic calcium levels, the supposedly inactive compound powerfully activated the TRPM4 channel.

This completely overturned what they thought they knew. It shows that they may be overlooking important drug candidates simply because they are not testing them under the right conditions.
In another set of experiments, the team uncovered yet another surprise. This time, the researchers tested a compound called Necrocide-1 (NC1), which is known to activate TRPM4. At low calcium levels, NC1 behaved as expected, switching the protein channel on. But when calcium levels increased—as they often do when cells are stressed, injured or diseased—the same molecule largely lost its effect.

Simply put: The cell's internal environment determined whether the drug worked.
This tells us drug behaviour is not fixed. The same molecule can behave very differently depending on the biological context.
part 1

Comment by Dr. Krishna Kumari Challa on June 10, 2026 at 10:31am

'Technostress': Why many older people feel shut out by the digital world
Older adults experience technostress due to rapid digitalization, facing barriers such as inaccessible interfaces, inadequate support, and increased scam risks. While technology can enhance independence and social connection, it also causes distress and exclusion, particularly when digital tools are not age- or culturally-responsive. Digital inclusion requires more than willingness; equitable access, skills, and support are essential to prevent widening disparities.

original article.

Comment by Dr. Krishna Kumari Challa on June 10, 2026 at 10:26am

Asexual reproduction slowed the pace of evolution to a crawl

The way that Earth's first animals reproduced held back life's diversity for millions of years, until stress and competition led to the development of sexual reproduction, which in turn accelerated the pace of evolution.
Researchers from the University of Cambridge studied fossils from the oldest-known animals on Earth, dating from 574 million years ago, and found that asexual reproduction slowed the pace of evolution to a crawl, since it limited competition between different groups.

Their results, reported in the journal Nature Ecology & Evolution, could help explain a longstanding puzzle in paleontology: why animal life appeared on Earth but then barely changed for millions of years, before a second wave of diversification gave evolutionary progress a major boost.

After billions of years of microbial life, during the Ediacaran period, between 635 and 539 million years ago, life exploded in size and the first animals appeared. Some of these earliest animals, such as Fractofusus, could grow as tall as two meters, although most were much smaller.

The influence of reproductive mode on resource competition and diversity patterns in Ediacaran early animal communities, Nature Ecology & Evolution (2026). DOI: 10.1038/s41559-026-03094-2

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Comment by Dr. Krishna Kumari Challa on June 10, 2026 at 10:18am

Dino-killing asteroid may have fueled underground life for 8 million years

The asteroid that caused the extinction of the dinosaurs also created an underground environment suited to supporting new life, and new research suggests it lasted for millions of years longer than previously suspected.

Analysis of feldspar samples from the Chicxulub crater indicates that the impact-generated hydrothermal system persisted for at least 8 million years, significantly longer than previous estimates. This prolonged subsurface environment, sustained by heat, rock permeability, and geothermal conditions, could have supported microbial life and informs understanding of life's origins and potential habitats on other planetary bodies.

The finding has surprised the international team of researchers behind it, who came to their conclusions by pairing sophisticated new analysis of samples taken from the Chicxulub crater in Mexico with computer modeling of the geological effects of the asteroid impact that formed the crater 66 million years ago.
The research, published in the journal Communications Earth & Environment, casts new light on how life may have first been incubated in hydrothermal systems in the earliest chapters of Earth's history and could help direct the search for life on other planets.

Despite the devastation the asteroid's impact caused on the surface, the immense heat brought together fractured rocks and hot water underground, creating a hydrothermal system beneath the crater. The researchers provide evidence that the system persisted for at least 8 million years, around four times longer than previous estimates, making it the longest-lived impact-generated hydrothermal system yet documented.

Annemarie E. Pickersgill et al, A long-lived impact-generated hydrothermal system at the Chicxulub impact structure, Communications Earth & Environment (2026). DOI: 10.1038/s43247-026-03618-5

Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 1:11pm

HIV enters the brain and doesn't leave, drugs intended to reduce brain inflammation increase virus levels
HIV persists in the brain, where standard antiviral drugs have limited efficacy due to poor penetration of the central nervous system. Attempts to reduce brain inflammation by blocking integrins, specifically alpha-4, inadvertently increased viral loads by reducing killer T cell migration while allowing helper T cells to continue introducing HIV. Precision-targeted immune therapies may be necessary to control HIV-associated neurodegeneration without exacerbating viral persistence.

original article.

Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 1:08pm

Hay fever, antihistamines and the evidence on dementia risk

For millions of people around the world, pollen season means weeks of sneezing, itchy eyes, and a blocked or runny nose. The timing varies depending on where you live and which plants are in flower, but grass pollen is one of the most common triggers.
Hay fever, also known as seasonal allergic rhinitis, is an allergic reaction to airborne pollen. Many people manage their symptoms with antihistamines bought from a pharmacy. But recent headlines have raised a worrying question: could some of the medicines used to relieve hay fever symptoms increase the risk of dementia?

Antihistamines block histamine, a chemical released by the immune system during an allergic reaction. Histamine causes symptoms such as itching, sneezing, and a runny nose.

Older, first-generation antihistamines, such as diphenhydramine and chlorphenamine, are more likely to cause drowsiness. Newer, second-generation antihistamines, such as cetirizine, loratadine, and fexofenadine, are generally less sedating.

Some older antihistamines also reduce the activity of acetylcholine, a chemical messenger involved in attention, learning, and memory. Medicines that block the action of acetylcholine are described as having anticholinergic effects.
These older medicines should be used cautiously, particularly in later life. They can cause drowsiness and concentration problems, increasing the risk of falls. People should also take care when driving if a hay-fever medicine makes them sleepy, as highlighted in recent reports.
Some studies have found an association between prolonged use of medicines with strong anticholinergic effects and a higher risk of dementia. These include some treatments for depression, Parkinson's disease, and bladder problems, as well as certain older antihistamines.

There is a plausible reason for concern: acetylcholine plays an important role in memory and thinking. Some medicines used to treat symptoms of Alzheimer's disease work by increasing the amount of acetylcholine available in the brain. Anticholinergic medicines reduce its activity.
One large observational study found that people with the highest exposure to strong anticholinergic medicines had a greater risk of dementia. But observational studies can identify patterns without proving that one factor causes another. People who take these medicines may differ from those who do not in other ways that affect their dementia risk. Some may have underlying health conditions, while others may have been prescribed medication for symptoms linked to the early stages of dementia.

A 2024 study of people with allergic rhinitis also found that dementia risk appeared to increase with higher cumulative doses of antihistamines, meaning the total amount taken over time. The association was stronger for first-generation medicines but was also seen, to a lesser extent, with newer second-generation antihistamines.

That finding was puzzling since second-generation antihistamines are less likely to cross the blood-brain barrier, the protective boundary separating the bloodstream from the brain. They also tend to have fewer anticholinergic effects.
Prolonged use of first-generation antihistamines with strong anticholinergic effects is associated with an increased risk of dementia, while evidence does not support a similar risk for second-generation antihistamines. Confounding factors, such as allergy severity and inflammation, complicate interpretation of these associations. Newer antihistamines are generally preferred due to fewer side effects and lower dementia risk.

original article.

Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 12:06pm

Excessive bite force does not cause alveolar bone loss but significantly worsens it when combined with periodontitis, report researchers in a new study. While traumatic occlusion has long been suspected to exacerbate periodontitis, the molecular mechanisms behind this link were poorly understood. Now, using mouse models of both conditions separately and combined, the researchers conducted comprehensive gene expression analysis across multiple periodontal tissues, identifying key inflammatory pathways upregulated in bone when both conditions were present.
Periodontitis, or inflammation of the tooth-supporting tissues, is one of the most common chronic diseases worldwide and a leading cause of tooth loss in adults. It develops when bacterial buildup around the teeth triggers persistent inflammation, gradually destroying their supporting bone and tissue structures. While bacterial infection is the primary driver of periodontitis, other factors also influence how severely and quickly the condition progresses. These include lifestyle habits such as alcohol consumption and smoking, autoimmune disorders, and—as researchers have long suspected—the way teeth come together when biting or grinding.

When teeth are repeatedly subjected to abnormal or excessive bite forces, known as "traumatic occlusion," supporting structures come under intense mechanical stress. For decades, dentists and scientists have hypothesized that this overload can worsen periodontitis excessively, so that occlusal adjustment (reshaping of the biting surfaces) is already used in clinical practice as a part of gum disease treatment.
Using advanced imaging techniques, including micro-computed tomography, the team measured bone loss around the teeth. They also performed transcriptome analysis to examine the activity of thousands of genes in gum tissue, bone, and the periodontal ligament shortly after disease induction. This enabled them to capture early changes in gene expression associated with each condition. Additionally, they investigated the effects of long-term traumatic occlusion alone over a period of eight weeks.

Interestingly, mice exposed only to traumatic occlusion did not show significant bone loss, even after prolonged exposure. However, when traumatic occlusion was combined with periodontitis, bone loss became significantly more severe.
This confirms that excessive bite force does not directly cause damage but instead amplifies the destructive effects of existing dysregulation caused by periodontitis.

Yosuke Tsuchiya et al, Traumatic Occlusion Exacerbates Bone Resorption by Modifying Gene Expression in the Bone Tissue of Ligature‐Induced Periodontitis in Mice, Journal of Clinical Periodontology (2026). DOI: 10.1111/jcpe.70112

Part 2

Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 12:02pm

How mechanical stress can accelerate bone destruction in periodontitis
Mechanical stress from excessive bite force alone does not cause alveolar bone loss but significantly accelerates bone destruction when combined with periodontitis. Gene expression analysis in mouse models showed that key inflammatory and bone metabolism pathways are upregulated only when both conditions coexist, indicating that mechanical overload amplifies periodontitis-induced bone loss through enhanced inflammatory signalling.

Part 1

Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 11:59am

How often do people pass gas?

Flatulence, or farting, is something people often joke about or find embarrassing when it happens unexpectedly. It is, however, an essential bodily function that allows the digestive system to keep pressure within the intestinal tract low and prevents painful stretching of the stomach and intestines. Even though it is normal to fart, it remains unclear what counts as a healthy number.

A study by researchers from the Commonwealth Scientific and Industrial Research Organisation wanted to measure how many times people pass gas in a day. So they designed a mobile phone application, Chart Your Fart, that allowed more than 6,400 Australians to log their farting patterns in real time.

They found that most people, on average, passed gas five times a day, with men doing it more often than women. Flatulence patterns were not the same throughout the day.

They observed a gradual increase that typically peaked between 6 p.m. and 10 p.m., coinciding with the time when people generally consume the most calories and fiber.

When we fart, our body releases a mixture of gases accumulated from two very different origins. The first is the air that sneaks in when you are eating or drinking, and the second is the gases churned out by the billions of bacteria living in the gut during digestion.

The swallowed air is harmless and odorless, but the byproduct of the bacterial breakdown of food contains sulfurous compounds that are responsible for the notorious smell associated with flatulence.

Some food groups, such as fiber, can often lead to more frequent passing of gas, and so can gastrointestinal problems such as irritable bowel syndrome, or IBS. While too much can be an issue, too little is actually the bigger concern. A sudden inability to pass gas, especially alongside stomach pain or bloating, can signal a blockage or other serious gut problem that needs medical attention.

Researchers have not yet been able to clearly define what counts as excessive, too little or normal passing of gas. Without solid data on how often healthy people actually pass gas in daily life, it is difficult to know what is healthy and what is a potential digestive problem. Past studies usually looked at small groups of people or focused only on those with stomach problems.

In the study nearly 80% of participants fell within a range of two to seven times daily. The youngest group, ages 14 to 25, reported passing gas less often than all other age groups, while men averaged 5.2 times per day compared with 4.8 times for women. The number of recordings remained low during midday and began to rise after 6 p.m., when people are more likely to start eating their highest-calorie meals.

The researchers highlight that this study might be one of the first to describe real-time flatulence habits in a large, general population. Establishing what is normal for flatulence can not only provide a helpful starting point for discussions about symptoms at both ends of the spectrum, but also help monitor gut health and change social attitudes toward flatulence.

Emily Brindal et al, Regular Flatulence Patterns Among Community-Dwelling Individuals in Australia, JAMA Network Open (2026). DOI: 10.1001/jamanetworkopen.2026.15637

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Comment by Dr. Krishna Kumari Challa on June 9, 2026 at 11:16am

Why does the Y chromosome retain UTY?

The human Y chromosome has lost many of its ancestral genes over millions of years of evolution. Yet a small number of genes, including UTY, have been evolutionarily retained despite their weak expression and reduced enzymatic activity. Why these genes persist has remained a longstanding question in chromosome biology.

A study, published in the journal Development, is the first to precisely map endogenous UTY occupancy across the human genome and demonstrate that UTY remains functionally involved in transcriptional regulation during early human development.
UTY is retained on the Y chromosome because it continues to contribute to transcriptional regulation during early human development, co-occupying active cis-regulatory elements with its X homolog UTX and supporting pluripotency-associated transcription factor localization. Despite weaker expression and occupancy than UTX, UTY maintains residual, largely noncatalytic regulatory functions, suggesting it is in an evolutionary transition phase rather than being fully redundant or lost.

Tomohiko Akiyama et al, Functional redundancy between UTY and UTX in regulating the localization of transcription factors involved in pluripotency, Development (2026). DOI: 10.1242/dev.205328

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