Recently on December 11, the British government indefinitely banned puberty blockers for children with gender dysphoria. This step was taken after independent experts found that there was an unacceptable safety risk involved when prescribing this medication.

Before getting into the "why" of the ban, let's understand what gender dysphoria is and what puberty blockers do.

Gender Dysphoria

As per the National Health Service (NHS), UK, gender dysphoria is a term that describes a sense of unease that a person may have because of a mismatch between their biological sex and their gender identity. The NHS writes, "Most people identify as "male" or "female". These are sometimes called "binary" identities. However, some people feel their gender identity is different from their biological sex. For example, some people may have male genitals and facial hair but do not identify as a male or feel masculine."

NHS notes that children show their interest through the choice of toys and clothes that are often associated "societally" with the opposite gender.

Puberty Blocker

They are a type of medication that delays the changes of puberty in gender-diverse youth. They are called gonadotrophin-releasing hormone (GnRH).

How does it work?

Sex hormones get affected once you consume this medicine. Sex hormones determine the sexual organs present at birth, which are also known as the primary sex characteristics. They include the penis, scrotum and testicles, and the uterus, ovaries and vagina. In contrast, the secondary sex characters are the organs or physical changes that occur in our body after we hit puberty. For instance, facial hair, development of breasts, etc.

So what do puberty blockers do?

It delays puberty, which can combat the symptoms, as noted by NHS, which can occur if someone experiences gender dysphoria. The symptoms include:

• low self-esteem
• becoming withdrawn or socially isolated
• depression or anxiety
• taking unnecessary risks
• neglecting themselves

The puberty blocker by delaying the development of secondary sex character helps with the:

• improving mental well-being
• ease depression and anxiety
• improve social interactions with others
• lower the need for future surgeries
• ease thoughts or actions of self-harm

So, why is it banned?

The UK stated that this decision will be revisited in 2027, till then the ban remains effective. However, it goes against standards held by medical groups including the European and World Professional Associations for Transgender Health and American Medical Association and the American Academy of Pediatrics.

The ban was put in place by the Conservative government and has been extended by the Labour government too. The announcement comes after a judge upheld an emergency ban in a ruling that said this treatment could be potentially harmful. However, NHS also stopped prescribing puberty blockers at gender identity clinics stating that there was not enough evidence found for either benefits or harms.

However, in July, Justice Beverley Lang said that the review commissioned by the NHS found "very substantial risks and very narrow benefits” to the treatment. The confusion exists because the British Medical Association further noted that the NHS review was controversial and included patients, academics, scientists and legal experts among its critics. However, the group that challenged the court - TransActual criticized the decision and said that evidence of danger from 40 years of puberty blocker cannot be tracked.

Banning medicines with no evidence of serious harm, only for trans people … is discrimination plain and simple,” said Keyne Walker, the group’s strategy director. “Evidence of the harm of the temporary ban continues to emerge, and will grow now that it has been made permanent.”

Why the ban in Scotland?

The Scottish government also confirmed that as the medicine policy is reserved to Westminster, the ban would also apply across England, Scotland and Wales.

However, the ban is not on those who are already consuming the medicine for gender dysphoria, but on the "new children and young people aged under 18 years from beginning to take puberty blockers for the purposes of gender incongruence and/or gender dysphoria. under the care of private or non-UK prescribers".

Liga Deportiva Univerrsitaria (LDU) has confirmed a new injury to its roster this Sunday. Defender José "Choclo" Quintero has a grade 3A muscle injury. This has been confirmed by team's official statement which has come from the club's medical department.

The player is currently undergoing rehabilitation and will begin strength training and physical therapy sessions. The official statement says that "Choclo" will have a reasonable amount of time before he returns to the field. He has so far played 19 matches and his return will depend on his progress.

A List Of Injuries

He had earlier suffered a skull fracture from August 30 2021 to October 4 2021 and as a result had missed three games in the season 21/22. Previously too in the season 16/17, he was in rehabilitation for 173 days due to a knew medial ligament tear, as a result of which he missed 31 games.

What Is A 3A Muscle Injury?

As per the 2014 study published in Translational Medicine @ UniSa, Official Journal of the Medical School of the University of Salerno, a 3A muscle injury is part of the structural injuries, which are divided into 3 sub-groups as per the "entity of the lesion within the muscle".

A type 3A lesion is a minor partial lesion, which involves one or more primary fascicles within a secondary bundle.

Symptoms

It usually is characterized by sharp pain, especially during a specific movement. The pain is, however, localized, and is easy to "appreciate on palpation and, at times, preceded by a snap sensation. On palpitation, it is not possible to detect the structural defect as it is too small and the contraction against manual resistance is painful," notes the study.

Diagnosis

Another study from 2016, published in the journal Joints, a 3A involves a minor partial muscle tear with small maximum diameter and could be detected through MRI that shows fiber disruption.

A 2019 study published in the journal Sport and Exercise Medicine Switzerland, notes that Type 3A are of less than 5mm in size. Thus, it includes 1-5 primary muscle bundles. The study also notes that such injuries usually heal without defect, however, injury to the perimysium and the aponeurosis is found in type 3b injuries (> 5 mm), which is the cause for intermuscular hematoma formation.

What Are The Common Muscle Injuries Among Football Players?

Type 3B injuries are moderate partial lesion, which involves at least a secondary bundle, with less than 50% of breakage surface. A Type 4 lesion is a sub-total tear with more than 50% of breakage surface or even a complete tear of the muscle. It also involves the muscle belly or the musculotendinous junction.

While these comprise structural injuries, Type 1 and Type 2 comprise the non-structural injuries.

It is the non-structural injuries, which are the most common and accounts for 70% of all muscle injuries in football players, mentions the 2014 study.

While the lesion may not be readily recognized in these injuries, they cause more than 50% of days of absence away from sport matches and training, the study notes. When they are ignored, they could turn into structural injuries.

Non-structural muscle injuries are classified into different types based on their underlying causes. Here's a breakdown of common types and what triggers them:

Type 1A Injury

These injuries are often the result of fatigue or sudden changes in training routines, running surfaces, or high-intensity activities. The muscle strain occurs due to the body not being fully adapted to new or excessive demands.

Type 1B Injury

This type of injury is linked to prolonged and excessive eccentric muscle contractions — when the muscle lengthens while under tension. This repeated strain can lead to overuse and damage.

Type 2A Injury

Type 2A injuries are typically associated with spinal issues. Often misdiagnosed, they stem from minor intervertebral disorders that irritate spinal nerves. This nerve irritation disrupts the normal control of muscle tone in specific “target” muscles. In such cases, treating the underlying spinal disorder becomes the main focus of care.

Type 2B Injury

These injuries are caused by a breakdown in the balance of the neuro-musculoskeletal system, particularly the mutual inhibition mechanism controlled by muscle spindles. When this balance is disrupted, the regulation of muscle tone suffers. Specifically, when the inhibition of agonist muscles is reduced, those muscles may become overly contracted to compensate — leading to dysfunction and injury.

For decades, lung cancer has been synonymous with smoking. But the data is shifting—and fast. Today, 10–20% of lung cancer cases in the U.S. are found in people who have never smoked a single cigarette. A new large-scale international study has now unearthed some of the strongest evidence yet that air pollution may be a major culprit—and it’s leaving a genetic trail behind.

Researchers have discovered that fine particulate matter in polluted air, commonly from traffic, industrial emissions, and smog, is strongly associated with DNA mutations that are also found in smokers’ lung tumors. These mutations may be key drivers of lung cancer development in never-smokers.

The research, involving whole-genome sequencing of lung tumors from 871 never-smokers across 28 regions in four continents, found that individuals living in highly polluted environments had significantly more driver mutations—the kind that directly trigger cancer.

The investigators matched tumor samples with long-term air pollution exposure estimates, using ground and satellite data for fine particulate matter (PM2.5). They found that non-smokers exposed to high levels of pollution were nearly four times more likely to exhibit the SBS4 mutational signature—a genetic fingerprint commonly linked to tobacco smoke.

Additionally, they identified a 76% increase in a separate signature associated with accelerated biological aging. This is alarming, considering these were individuals with no direct tobacco exposure.

What makes this finding even more significant is that researchers discovered TP53 and EGFR mutations—both known to be aggressive lung cancer markers—more frequently in people living in polluted areas. These genetic changes are typically hallmarks of cancers in smokers.

This implies that air pollution could be triggering similar molecular pathways to those activated by cigarette smoke.

But there was a twist: a new mutational signature, SBS40a, was found in 28% of never-smokers but not in smokers. The origin of this marker remains unclear, but it suggests that pollution may not be the only hidden risk.

Rise of Environmental Carcinogens

The study adds to a growing body of evidence that air pollution is not just an irritant—it’s a carcinogen. Fine particles can be inhaled deep into the lungs, where they may damage DNA directly or trigger chronic inflammation that promotes tumor growth.

Even more surprising, another carcinogen showed up in the data: aristolochic acid, found in some traditional Chinese herbal remedies. This compound was associated with a distinct mutational signature in patients from Taiwan, hinting at a possible secondary environmental risk factor for lung cancer in never-smokers.

The rise of lung cancer in non-smokers is especially noticeable in East Asia, where rates remain disproportionately high—particularly among women. While genetic predisposition may play a role, this new evidence points clearly to environmental exposures as a key contributor.

And it’s not just an Asian problem. In Western countries, urban dwellers are also exposed to dangerously high levels of air pollution. The World Health Organization estimates that 99% of the world’s population breathes air that exceeds safe pollution thresholds. This means the risk is truly global.

The power of this new research lies in its use of whole-genome sequencing to link pollution to DNA changes. These mutational signatures act as a kind of molecular journal, recording every environmental insult a cell has endured.

The ability to map those changes and match them to known pollutants gives researchers a more precise way to trace cancer origins—not just infer them from epidemiological studies.

While this study can’t definitively prove causation, the strong correlation between pollution exposure and cancer-driving mutations makes it clear that dirty air is more than just a nuisance—it's a potential trigger for deadly disease.

Researchers acknowledge some limitations. Pollution estimates were regional, not personal, meaning it’s unclear how much exposure each participant had. Self-reported smoking histories can also be unreliable.

Still, the pattern is unmistakable. Air pollution behaves like a mutagen, leaving behind signatures that align with known cancer mechanisms. And it appears to affect never-smokers in a strikingly similar fashion to tobacco users—down to the very DNA damage.

This study raises serious public health questions: If environmental exposure to polluted air can cause DNA mutations tied to cancer, what safeguards are in place to protect those most vulnerable?

Governments and public health agencies may need to reconsider air quality regulations, urban zoning, and access to clean air—especially in densely populated cities where pollution levels remain dangerously high.

Healthcare systems might also need to adapt. Traditional lung cancer screenings focus on long-time smokers, but this research could shift how we think about early detection in non-smokers, especially those living in high-risk environments.

Lung cancer has long been viewed through the lens of personal responsibility: if you smoked, you knew the risks. But this research changes that narrative. The air we breathe—something no one can fully avoid—is now emerging as a significant threat.

For non-smokers around the world, especially women and urban residents, this is a wake-up call. Your lungs may be at risk not because of personal choices, but because of public ones—decisions about pollution control, urban planning, and clean energy.

The future of lung cancer prevention may lie not just in quitting cigarettes, but in cleaning up the air we all share.

Every year, thousands of seemingly healthy people—often young, active, and without obvious warning signs—die suddenly due to cardiac arrest. For decades, doctors have struggled to reliably identify which patients with heart conditions are at high risk and who might be unnecessarily undergoing invasive interventions. That may be about to change.

In a breakthrough that could transform how we predict—and prevent—sudden cardiac death, scientists at Johns Hopkins University have developed an artificial intelligence model that vastly outperforms current clinical standards in identifying people most at risk. Their new system, known as MAARS (Multimodal AI for Arrhythmia Risk Stratification), not only forecasts risk with up to 93% accuracy in vulnerable age groups, but also explains why someone is high risk—something most algorithms fail to do.

The focus of the study is hypertrophic cardiomyopathy (HCM), one of the most common inherited heart conditions. It affects around 1 in 200 to 500 people globally and is a leading cause of sudden cardiac death in athletes and young adults. While most individuals with HCM live normal lives, a subset is at high risk for lethal arrhythmias—heart rhythm disturbances that can cause the heart to stop without warning. And here’s the catch: right now, doctors only have a 50-50 shot at predicting who will be affected.

“Currently we have patients dying in the prime of their life because they aren’t protected,” said Dr. Natalia Trayanova, senior author of the study and a leading figure in AI cardiology research. “And others are putting up with defibrillators for the rest of their lives with no benefit.”

Trayanova is referring to implantable cardioverter defibrillators (ICDs)—tiny devices inserted into the chest that deliver electric shocks to correct abnormal heart rhythms. They save lives in the right patients but come with physical, emotional, and financial burdens when used unnecessarily.

The need for a more precise, personalized tool has never been greater.

What the AI Model Does Differently?

Published in Nature Cardiovascular Research, the new model represents a significant departure from traditional clinical guidelines used across the US and Europe.

MAARS doesn’t rely on a single data source. Instead, it analyzes a multimodal spectrum of information—ranging from electronic health records and patient histories to contrast-enhanced cardiac MRI images that reveal scarring, or fibrosis, within the heart.

Scarring is a key factor in determining sudden death risk in HCM. But interpreting these raw images is extremely challenging for even seasoned cardiologists. That’s where AI has the edge.

“People have not used deep learning on those images,” Trayanova explained. “We are able to extract this hidden information in the images that is not usually accounted for.”

The AI essentially spots dangerous patterns in the heart’s scar tissue that the human eye—and even conventional software—can’t see.

How Accurate Is It?

In clinical tests involving real-world patients from Johns Hopkins Hospital and Sanger Heart & Vascular Institute in North Carolina, the results were staggering:

• Traditional clinical guidelines correctly predicted sudden cardiac death risk only 50% of the time.
• The MAARS model achieved an overall accuracy of 89%.
• In patients aged 40 to 60—a group particularly vulnerable to undetected risk—the model was 93% accurate.

What makes this even more valuable is its ability to provide explanations. The system doesn't just say "this patient is high risk"—it breaks down the why, giving cardiologists critical information to tailor treatment plans.

“This significantly enhances our ability to predict those at highest risk compared to our current algorithms,” said co-author Dr. Jonathan Crispin, a Johns Hopkins cardiologist. “It has the power to transform clinical care.”

Why This Could Be Transformative?

MAARS isn't the first AI model from Trayanova’s lab. In 2022, her team built another tool that provided survival predictions for patients with prior heart attacks, known as infarcts. But this latest model breaks new ground by tackling one of the most elusive forms of cardiac risk—arrhythmias caused by scarring in inherited heart conditions. The potential benefits are wide-ranging:

• Lives saved by identifying at-risk patients who might otherwise be missed.
• Better quality of life for patients who avoid unnecessary ICD implantation.
• More personalized treatment plans based on detailed, AI-generated insight.

Importantly, the model was trained and validated across diverse demographics, showing consistent performance regardless of age, gender, or ethnicity.

The researchers aren’t stopping here. They plan to expand MAARS to include other forms of arrhythmia-related heart diseases, such as cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy—conditions that also carry a high risk of sudden death but suffer from diagnostic ambiguity.

They’re also working to test the model in larger, more varied populations to move it closer to clinical adoption.

A New Era in Cardiology?

Artificial intelligence has long been hyped as the future of medicine. But MAARS is more than hype—it’s a working proof of concept that shows how deep learning can complement medical expertise, not replace it.

AI may soon become your cardiologist’s most powerful diagnostic tool—one that sees what even the best-trained human eyes might miss. And when lives are on the line, that kind of clarity could mean everything.