Many of us may have taken ibuprofen, sometimes two pills at once, especially when we are struggling with menstrual cramps. Well, as good these pills may be in treating the pain, they are not recommended for your health, especially if you are someone who consumes it on a daily basis or frequently. Gastroenterologist Trisha Pasricha, MD, writes in The Washington Post about why should you avoid taking nonsteroidal anti-inflammatory drugs, or NSAIDs, such as ibuprofen, naproxen and aspirin.

What happens when you consume pain killers?

She writes that NSAIDs are great in treating short term pain. They comprise of a group of drugs that inhibit the production of prostaglandins, which serve as a variety of purposes in the body. Some of which also includes contracting the uterus during menses and regulating blood flow in our vessels.

While one to two doses every now and then is okay, following a regular dosage routine, which could range from several times a month, or twice in an hour or so could lead to health risk. NSAIDs are well known to increase intestinal permeability. This means, these painkillers could damage the lining of your gut.

A 2018 review by Ingvar Bjarnason et. al., also writes about how NSAIDs can reduce the blood flow in the tiny vessels that feeds our guts. It can also disrupt the intestinal cells forming a barrier between the outside world and your insides.

What can be done?

While people with conditions like migraines, chronic back pain or bad period cramps can find NSAIDs to be helpful. It is always advisable to have a chat with your physicians to explore NSAID alternatives.

Pasricha suggests acetaminophen.

However, if someone is in dire need of NSAID, her tip is to take the pill right at the start of your symptoms. She says that the drug can do a far better job at stopping things at the source than chasing after all prostaglandins.

Why is it a concern?

NSAIDs are available as over the counter drug, which means people do not need a prescription for it and can make medical decision about them without the guidance of a physician.

A 2018 study published in the Official Journal of the International Society for Pharmacoepidemiology by David W Kaufman, et.al., found that 15% of adult ibuprofen users in the US have exceeded the maximum recommended daily dose. The study also mentions that more than a third of ibuprofen users were taking other NSAIDs, like aspirin and naproxen, while consuming ibuprofen at the same time. Out of these, 61% did not realise that they were using NSAIDs.

Pasricha talks about how it ruptures the gut wall, as she herself has rushed to the hospital in the middle of the night "far more times than" she can count "to perform an emergency endoscopy on someone who was bleeding profusely from an ulcer caused by NSAID".

Another 2009 study published in the American Journal of Gastroenterology states that as many as 1 in 4 chronic NSAID users will get an ulcer and about 4% will bleed or rupture through the gut wall.

An older study from 2005 titled A quantitative analysis of NSAID-induced small bowel pathology by capsule enteroscopy, found that as 75 percent of people regularly using NSAIDs develop low-grade inflammation in their small bowels. NSAIDs can also lead to development of fatty liver disease. This happens because your gut lining becomes more permeable, more toxins and bacteria from the outside world enters your liver and leads to inflammation.

A 2011 study titled Haemoglobin decreases in NSAID users over time: an analysis of two large outcome trials, states that as many as 6% of people taking NSAIDs regularly have found their blood count dropping within a few months of starting the medicines, this suggests that this is due to the small, slow amount of bleeding in the gut overtime.

Bird flu viruses pose a particular danger to people because they can continue multiplying even at temperatures that would normally stop most infections. Fever is one of the body’s natural ways to slow viruses, yet new research from the universities of Cambridge and Glasgow shows that avian strains can survive what should be a hostile environment.

The study, published in Science, identifies a key gene that influences how well a virus copes with heat. This same gene moved into human flu strains during the 1957 and 1968 pandemics, allowing those viruses to spread more easily.

How Flu Viruses Thrive In The Body

Human influenza viruses infect millions each year. The seasonal strains we see most often fall under influenza A and tend to do well in the cooler temperatures of the upper respiratory tract, which is close to 33°C. They are less suited to the warmer, deeper parts of the lungs, where temperatures reach about 37°C.

As per Science Daily, when the body cannot slow an infection, the virus continues to multiply and spread, which can lead to more serious illness. Fever acts as a protective response, pushing body temperature as high as 41°C. Until now, the exact reason why fever slows some viruses but not others has been unclear.

Avian influenza behaves differently. These viruses usually grow in the lower respiratory tract, and in their natural hosts, such as ducks or seagulls, they often infect the gut. Temperatures in these areas can reach 40°C to 42°C, which helps explain their greater tolerance to heat.

How Fever Limits Infection and Why Bird Flu Can Resist It

If left unchecked, a virus can move through the body and cause significant harm. Fever is one of the body’s most familiar defence responses and can raise the core temperature to levels that inhibit many pathogens. Scientists have long known that some viruses withstand these temperatures, but the reason behind this resistance has remained uncertain.

Avian flu strains show a clear advantage in hotter environments. They thrive in the lower airways and, in birds, survive in the high heat of the gut. These features distinguish them from human influenza strains, which prefer cooler tissue.

Earlier studies in cell cultures hinted that avian flu copes better with fever-range temperatures than human strains. The new research offers direct evidence from animal experiments, helping explain why fever is effective against some types of influenza but far less useful against others.

Experiments Show Why Fever Slows Human Flu but Not Avian Flu

Researchers from Cambridge and Glasgow recreated fever-like conditions in mice to examine how different viruses responded. They worked with a lab-adapted human influenza strain known as PR8, which does not pose a threat to people.

Mice do not typically develop a fever from influenza A, so the scientists raised the temperature of the environment to lift the animals’ body temperature.

The findings were striking. When body temperature rose to fever levels, the human-origin virus struggled to replicate, and the infection weakened. Avian influenza behaved very differently. Raising the temperature did not stop the virus from multiplying, and a small increase of only 2°C was enough to turn a normally severe human-origin infection into a mild one.

The PB1 Gene Helps Bird Flu Withstand Fever

The study also identified the PB1 gene as a major reason why bird flu can tolerate heat. PB1 helps the virus copy its genetic material inside infected cells. When viruses carried an avian-type PB1 gene, they were able to endure high temperatures and still cause severe disease in mice. This matters because avian and human flu viruses can exchange genes when they infect the same host, such as pigs.

Dr. Matt Turnbull, the study’s first author from the Medical Research Council Centre for Virus Research at the University of Glasgow, explained that this gene swapping remains a major concern for emerging influenza strains. He noted that similar exchanges occurred in 1957 and 1968, when human flu viruses replaced their PB1 gene with one from an avian strain. According to the researchers, this may help explain why those pandemics were so severe.

In moments where life seems to slip away, many people describe seeing a bright tunnel with a strong light shining at the end. The image feels almost otherworldly. Whether it happens during major surgeries, car crashes, or sudden accidents, people from different places and backgrounds share accounts that sound strikingly alike. Films, novels, and personal stories often mention this same vision during a near-death experience. While some link it to a glimpse of the afterlife, there may be a scientific explanation for why the mind creates this scene.

Is it a sign of something beyond the physical world, a reaction of the mind in distress, or part of how the brain behaves as it shuts down? Here is what researchers have learnt.

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Do You Really See A Tunnel Of Light When You Die?

Yes. Scientists agree that many people do report seeing a tunnel of light when death is close. Even though death is certain, much about it still feels unclear. For generations, people have tried to understand what takes place in those last moments. Only in recent years, as medical care has advanced, have researchers been able to look more closely at near-death experiences, also known as NDEs, which occur when someone comes dangerously close to dying.

One of the most repeated features of NDEs is the bright tunnel, a sight described by millions. It is not a quick trick of the mind. People often speak of it as deeply emotional and unforgettable. This leads to difficult questions. Does this vision suggest something beyond physical life, or is the brain responding to extreme stress in its final effort to survive?

Why Do You See A Tunnel Of Light During Near-Death Experiences?

When someone nears death, the body begins to change very quickly. Vital functions start to drop. The heart may slow, reducing the amount of oxygen that reaches the brain. Body temperature can fall, and breathing may become weak or uneven. Along with these physical changes, the brain also reacts in its own way.

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Tunnel Of Light During Death Experiences: What Scientists Found

A team at the University of Michigan studied what happens in the brain as a person dies. They examined four people who were removed from life support and found that two of them showed a strong surge of brain activity right before death.

The pattern of activity was similar to what occurs when a person is awake and using higher thought. These bursts were produced by gamma waves, which are linked to conscious processing. In one patient, the rise in gamma activity was nearly three hundred times higher than normal.

Jimo Borjigin of the University of Michigan suggested that this might show a form of hidden awareness that becomes active just before death.

Professor Borjigin explained that some people near death may recall seeing or hearing things or may feel as though they are watching their body from above, or even moving through space. She said her team may have identified the basic brain steps connected to this type of hidden consciousness.

She added that future research needs to involve people who survive such events, so their brain activity can be compared with their own descriptions of what they experienced.

Another study in the Journal of the Missouri State Medical Association also explores how consciousness may shape near-death experiences. The researchers note that there is still much to learn about how the brain creates awareness and how that awareness influences what people see or feel as they approach death.

A team of Indian scientists has uncovered a rare mutation in the USP18 gene that appears to drive repeated neurological deterioration in children. This unusual mutation offers important clues about a disorder previously seen in only 11 cases worldwide, now identified for the first time in India.

The work was carried out by specialists at the Indira Gandhi Institute of Child Health in Bangalore, along with researchers from Ramjas College, University of Delhi, and Redcliffe Labs. But what does this neurological condition involve?

The study, featured in the journal Clinical Dysmorphology, describes a never-before reported variant, c.358C>T (p.Pro120Ser), adding to what is known about Pseudo-TORCH syndrome type 2.

What Is Pseudo-TORCH Syndrome Type 2?

Pseudo-TORCH syndrome type 2 is an extremely uncommon inherited disorder that affects how a child’s brain forms and functions. The symptoms often resemble those caused by congenital infections, though no actual infection is present.

According to the researchers, it is marked by serious brain abnormalities such as intracranial calcifications, a smaller-than-usual head size, and white matter injury. These problems can lead to seizures, stiffness of the limbs, and often early death. The condition results from recessive mutations in genes like USP18.

What Is The USP18 Gene?

The USP18 gene provides instructions for making the Ubiquitin-Specific Peptidase 18 protein, which helps regulate the body’s type I interferon response. It performs two major tasks. It works as an enzyme that removes ISG15 tags from certain proteins, and it also dampens interferon signaling by attaching to the IFNAR2 receptor. Disturbances in this gene are linked to interferon-related disorders and some cancers, according to the National Institutes of Health.

In a healthy state, USP18 keeps the immune response balanced so the body does not produce unnecessary inflammation. When the gene is altered, this control weakens and the immune system reacts in an exaggerated way, which can damage the developing brain.

“The finding shows how clinical experience combined with advanced genetic tools can change outcomes. For years, we treated symptoms without a clear explanation, but identifying this new USP18 mutation has changed both the diagnosis and the child’s path forward,” said Dr. Vykuntaraju K. Gowda from the Department of Pediatric Neurology, IGICH, speaking to IANS.

What Doctors Found?

The investigation began with an 11-year-old girl who had shown symptoms since infancy, including repeated episodes of febrile encephalopathy, meaning fever-associated unconsciousness, along with seizures, developmental delays, and microcephaly. Her brain scans over time showed growing calcium deposits in several regions.

To trace the cause of her recurring neurological episodes, the doctors advised detailed genetic analysis. Using exome sequencing combined with mitochondrial genome testing, the team uncovered a previously unknown alteration in the USP18 gene, finally providing an explanation after years of uncertainty.

This new mutation changes the USP18 protein’s shape, reducing its ability to keep inflammation under control. The overly active immune response offers a clear reason for the child’s repeated fever-linked neurological decline. Recognising this link is important because it helps clinicians spot early signs, avoid unnecessary infection-related treatments, and pay closer attention to conditions caused by immune overactivity instead.

“This is also the first reported instance of a USP18-related disorder showing up as recurrent febrile encephalopathy,” said Dr. Himani Pandey, part of the research team.

The study underscores the value of early genetic testing in children with unexplained neurological issues and suggests new possibilities for more focused care in the years ahead.