Asthma has long been a formidable foe for many people, causing symptoms that can range from mild discomfort to life-threatening attacks. While powerful biological drugs have significantly improved the lives of those with severe asthma, a recent study has shed light on why these symptoms often return despite treatment.

Biological drugs, or biologics, have become a crucial tool in managing severe asthma by helping patients keep their symptoms under control. However, researchers at Karolinska Institutet in Sweden discovered that certain immune cells, which play a significant role in asthma inflammation, do not disappear during treatment as previously thought. Instead, these inflammatory cells increase in number.

This finding suggests that biologics might not address the root cause of asthma, but rather manage its symptoms. As such, continued treatment may be necessary to keep the disease under control. This is particularly concerning considering that little is still known about the long-term effects of biologics like mepolizumab and dupilumab, which have been prescribed to asthmatics for less than ten years.

The study analyzed blood samples from 40 patients before and during treatment, using advanced methods such as flow cytometry and single-cell sequencing. Researchers were surprised to find that the levels of inflammatory cells in these patients increased rather than decreased. This could explain why inflammation of the airways often returns when the treatment is tapered or discontinued.

It is essential for researchers and medical professionals to understand the long-term immunological effects of biologics, as this knowledge can lead to more effective treatments and better outcomes for patients with severe asthma. The next stage of the study will involve analyzing samples from patients with a long treatment history and studying lung tissue to see how immune cells are affected in the airways.

The findings of this study have significant implications for the management and treatment of asthma, highlighting the need for continued research into the effects of biologics on the immune system.

Now, let me rewrite the article to make it more accessible and engaging for a general audience:

Breathe with Identity: The Surprising Link Between Your Breath and You

Imagine if your breath could reveal not only your health but also your identity. Sounds like science fiction? Think again! A recent study published in the journal Current Biology has shown that scientists can identify individuals based solely on their breathing patterns with an astonishing 96.8% accuracy.

The research was led by Noam Sobel and Timna Soroka from the Weizmann Institute of Science, Israel. They were intrigued by the connection between our brain and breathing, which is processed during inhalation in mammals. Since every brain is unique, wouldn’t each person’s breathing pattern reflect that?

To test this idea, the team developed a lightweight wearable device that tracks nasal airflow continuously for 24 hours using soft tubes placed under the nostrils. This innovative approach revealed that people’s respiratory patterns are as distinctive as fingerprints – and just as reliable.

In an experiment with 100 healthy young adults, the researchers asked them to go about their daily lives while wearing the device. The collected data allowed them to identify individuals with high accuracy, rivaling the precision of some voice recognition technologies. What’s more, the study found that these respiratory “fingerprints” correlated with various aspects of a person’s life, such as:

* Body mass index (BMI)
* Sleep-wake cycle
* Levels of depression and anxiety
* Behavioral traits

For instance, participants who scored relatively higher on anxiety questionnaires had shorter inhales and more variability in the pauses between breaths during sleep. This suggests that long-term nasal airflow monitoring may serve as a window into physical and emotional well-being.

But here’s the really interesting part: what if the way we breathe affects our mental and emotional states? Could changing our breathing patterns actually change those conditions? The researchers are already investigating this possibility, aiming to develop a more discreet and comfortable version of the device for everyday use.

Sobel notes, “We intuitively assume that how depressed or anxious you are changes the way you breathe. But it might be the other way around. Perhaps the way you breathe makes you anxious or depressed. If that’s true, we might be able to change the way you breathe to change those conditions.”

This study opens up exciting possibilities for using respiratory monitoring as a tool for improving mental and emotional well-being. And who knows? Maybe one day, your breath will be the key to unlocking a healthier, happier you!

The diabetes pill dapagliflozin has shown promising results in reducing liver scarring in a clinical trial published in The BMJ. The study found that treatment with dapagliflozin improved metabolic dysfunction-associated steatohepatitis (MASH), a condition where excess fat accumulates in the liver, leading to inflammation, and liver fibrosis, a build-up of scar tissue.

The trial involved 154 adults diagnosed with MASH after a liver biopsy at six medical centers in China. Almost half had type 2 diabetes, and almost all had liver fibrosis. The participants were randomly assigned to receive either 10 mg of dapagliflozin or a matching placebo once daily for 48 weeks.

The results showed that treatment with dapagliflozin improved MASH in 53% of participants without worsening of fibrosis, compared to 30% in the placebo group. Resolution of MASH without worsening of fibrosis occurred in 23% of participants in the dapagliflozin group, compared to 8% in the placebo group.

Fibrosis improvement without worsening of MASH was also reported in 45% of participants in the dapagliflozin group, compared to 20% in the placebo group. The percentage of participants who discontinued treatment due to adverse events was 1% in the dapagliflozin group and 3% in the placebo group.

The researchers acknowledged that the trial was conducted in a Chinese population, which limits its broader generalizability, and that female and older patients were under-represented. However, they pointed out that results were consistent after further analyses, suggesting they are robust.

The study’s findings indicate that dapagliflozin may affect key aspects of MASH by improving both steatohepatitis and fibrosis. Large-scale and long-term trials are needed to further confirm these effects.

In the coming years, researchers expect exciting developments in the field of pharmacological treatment for MASH, with more drugs becoming available and therapeutic decisions becoming increasingly tailored to individual patient profiles. Ideally, such treatments should provide cardiovascular benefit, have an established safety profile, and be accessible to broad and diverse patient populations.