Credits: Wikimedia Commons
Nine-time Grand Slam champion Monica Seles is using her popularity and platform to shed light on a rare chronic neuromuscular condition that has changed her life. Myasthenia Gravis.
In an interview with Good Morning America on Tuesday, the former World No. 1 revealed for the first time that she was diagnosed three years ago with myasthenia gravis, or MG, an autoimmune disease that causes muscle weakness.
"It was 30 years ago that I came back to the [U.S.] Open ... It was like a reset, and this was one of the reasons I decided to go public with my myasthenia gravis," Seles said. "It’s been a huge reset not just in my professional life as a tennis player, but also in my personal life."
Seles, who last played professionally in 2003 and officially retired in 2008, said she hopes her story will help others who may be struggling with unexplained symptoms.
The 51-year-old said her training as a professional athlete helped her notice early changes in her body.
"I started experiencing these symptoms of extreme leg weakness, arm weakness, double vision. So I realized, ‘This is very unusual,’" she explained. "Once I was diagnosed, it was like a relief, but also it was a challenge."
Travel, once routine during her tennis career, has become more complicated. "Even coming here today, in the old days, traveling would be a no-brainer. Now I had to get packing tips. I had to learn a new way to live with MG," she said.
Seles admitted she had never heard of myasthenia gravis before her diagnosis. "I had no clue what it was. I had a hard time pronouncing it," she said with a smile.
She hopes that talking about her experience will encourage people to seek medical advice if they notice changes in their health.
"It’s been a very challenging time dealing with it," she added. "But knowing there’s hope out there and a great community has helped me tremendously."
Her message to others: "Advocate for yourself and know your symptoms."
Also Read: Tennis Player Monica Seles Opens Up About Her Myasthenia Gravis Diagnosis
According to the U.S. National Institute of Neurological Disorders and Stroke (NINDS), myasthenia gravis is a chronic neuromuscular disease that causes weakness in voluntary muscles, the muscles responsible for movements like walking, swallowing, breathing, and facial expressions.
MG occurs when the immune system mistakenly attacks healthy muscle receptors, disrupting the signals needed for muscle contraction. Johns Hopkins Medicine notes that the condition is not inherited or contagious and often develops later in life.
The disease can affect anyone, but it most commonly impacts women under 40 and men over 60. Symptoms may include:
Symptoms can vary widely between individuals. In rare situations, a myasthenic crisis may occur, affecting breathing muscles and requiring emergency medical care.
Because the symptoms of MG can resemble other health conditions, diagnosis involves a combination of physical and neurological exams, blood tests, and nerve stimulation studies.
There is currently no cure, but treatments can help manage symptoms and improve quality of life. These may include medications that enhance communication between nerves and muscles, immunosuppressive drugs, and in some cases, surgery to remove the thymus gland.
Temporary forms of MG can occur in newborns if a mother has the disease, but these cases usually resolve within two to three months.
While managing myasthenia gravis has brought challenges, Seles continues to find joy in life and in the sport she loves. She still follows tennis closely and is excited about the current generation of players.
"I wish I had a crystal ball," she said. "I love Coco Gauff, the electricity she brought to the U.S. Open. As a tennis fan, we just want great matches and the excitement of the fans."
By sharing her personal journey, Seles hopes to break the silence around MG and help others feel less alone. "When I got diagnosed, I wished I had heard someone talk about it. Now, I hope my story can be that for someone else."
Credits: Reddit
Parts of the US, particularly Fort Collins, Colorado, are currently playing host to rabbits with black tentacles that are definitely not pleasing to look at. They have got black, spike-like growths sprouting from their faces, resembling something between sea anemone tentacles and mediaeval torture devices. And officials say you should absolutely avoid touching them.
The unsettling appearance is caused by the cottontail papilloma virus (CRPV), also known as the Shope papilloma virus. This rare condition causes wart-like tumours to erupt on or around the head of a rabbit, eventually hardening into horn-like growths made of keratin, the same stuff your fingernails are made of.
Colorado Parks and Wildlife (CPW) officials say they do not believe the virus can spread to humans or pets, but the advice is still clear: do not attempt to handle, rescue, or play with these unfortunate creatures.
CRPV is mostly spread via blood-sucking insects like mosquitoes and ticks. Once they bite an infected rabbit, they can pass the virus to the next one they feed on. The good news is that scientists say it is almost never transmitted by direct rabbit-to-rabbit contact and there is no evidence of insect bites passing the virus to humans.
First signs include small red bumps that eventually morph into grotesque growths. In extreme cases, these tumours can get so large they block the rabbit’s vision, hearing, or even ability to eat, leading to slow starvation.
On social media, the debate is heating up over whether it is more humane to euthanise severely infected wild rabbits to prevent suffering.
Animal control officials have not endorsed any such measures. Their position is simple: the virus does not pose a public health threat, and interfering with wildlife generally causes more harm than good. The standing advice is to leave the animals undisturbed and let nature take its course, however grim it might seem.
For those with pet rabbits, the threat is real but manageable. Since the virus spreads via insects, the best prevention is pest control, keeping rabbits indoors during peak mosquito activity and using protective enclosures. If a pet does become infected, veterinarians can surgically remove the growths before they become malignant. Occasionally, tumours shrink on their own, but in wild rabbits, they often grow bigger year after year.
There is no cure for CRPV in wild rabbits, and the prognosis is rarely good once the growths interfere with basic functions like eating. Wildlife officials stress that the best way to help is to keep your distance, avoid feeding or attempting to “save” them, and report sightings if local authorities request it.
These infected rabbits are a reminder of how viruses can warp the natural world in unsettling ways.
Credits: Health and me
Millions of people worldwide continue to experience symptoms weeks, months, or even years after an initial SARS-CoV-2 infection. For more than four years, long COVID has remained one of the pandemic’s most perplexing mysteries. Yet, despite the global scale of the problem, there has been no objective way to confirm a diagnosis. Doctors have relied almost entirely on patient-reported symptoms and a process of elimination to rule out other causes.
That may be about to change. A team of researchers from the Translational Genomics Research Institute (TGen), part of City of Hope, and the Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center has identified a potential biomarker that could offer the first measurable, laboratory-based confirmation of long COVID. Their findings, published in the journal Infection, point to a new way of detecting the lingering footprint of the virus in the body — and with it, the possibility of changing how long COVID is diagnosed, studied, and treated.
Long COVID is not a single, uniform illness. It’s a complex, post-viral condition with more than 200 possible symptoms, ranging from crushing fatigue and brain fog to shortness of breath, chest pain, and neurological changes. According to estimates, anywhere from 15% to over 40% of people infected with COVID-19 may experience lingering symptoms, depending on which definition is used.
That lack of standardization is a huge problem. A recent study analyzing definitions from five countries — the US, UK, Netherlands, Sweden, and Puerto Rico — found wildly different prevalence rates when the same patient dataset was assessed. Without an objective test, researchers struggle to identify who truly has long COVID, making large-scale studies inconsistent and slowing the development of targeted treatments.
William Stringer, M.D., a senior author of the new study and a Lundquist Institute investigator, explains the gap: “If a patient arrives in clinic and describes the persistence of typical signs and symptoms of long COVID, 12 weeks or more after COVID-19 infection, I give them a presumptive diagnosis. But I don’t have any blood tests or biomarkers to confirm this diagnosis.”
Also Read: Is 'Stratus' COVID Variant The Pandemic’s Next Chapter In 2025 With New Symptoms?
The new research zeroes in on extracellular vesicles (EVs) — microscopic packages released by cells to transport proteins, metabolites, and other materials throughout the body. These vesicles act like biological couriers, shuttling information from cell to cell.
Researchers collected and analyzed 56 blood samples from 14 long COVID patients over 12 weeks of aerobic exercise training, as part of an ongoing clinical trial. What they found was striking- 65 distinct protein fragments from SARS-CoV-2 inside the EVs, all originating from the virus’s Pp1ab protein.
This protein is an RNA replicase enzyme — crucial to the virus’s ability to copy itself and produce new viral particles — and is unique to SARS-CoV-2. It does not occur in uninfected human cells. “We thought that maybe if the virus is circulating or moving in the body, we should try to see if EVs are carrying those viral fragments,” says lead author Asghar Abbasi, Ph.D., of the Lundquist Institute.
Importantly, these viral peptides were detected in every patient, though not in every individual blood draw, and were absent in a separate control group using pre-pandemic EV samples. That suggests the biomarker may be specific to long COVID.
One of the most debated questions in long COVID research is whether the virus — or pieces of it — persist in the body long after the initial infection. Evidence has been mounting that SARS-CoV-2 may remain in certain tissues, creating “viral reservoirs” that could contribute to ongoing symptoms.
The new study supports this theory. The detection of Pp1ab fragments inside EVs hints that remnants of the virus might be traveling through the body, possibly reaching tissues without typical viral entry points, such as the brain. How this happens remains unknown. EVs may play a role in delivering these viral remnants to distant sites, potentially influencing symptoms.
Still, co-senior author Patrick Pirrotte, Ph.D., of TGen urges caution. “The molecular signal of the viral peptides was subtle and not consistently detected at every time point,” he notes. “We don’t yet know if exercise triggers the release of these proteins, if they come from a permanent reservoir, or if they’re simply leftover molecular ‘trash’ from past viral replication.”
If validated by further studies, this biomarker could be a game-changer for both clinical care and research.
For patients- An objective blood test could confirm a diagnosis and give legitimacy to those whose symptoms have been dismissed or attributed to other causes. It could also guide treatment decisions, help monitor disease progression, and potentially measure response to therapy.
For researchers- A biomarker could bring much-needed consistency to clinical trials. Right now, varying definitions and diagnostic criteria make it difficult to compare studies or determine which interventions truly work. With a measurable indicator, scientists could better select participants, study the underlying mechanisms, and test targeted treatments more effectively.
The study leaves several unanswered questions. For one, it’s not yet clear whether these viral fragments are present in people who had COVID-19 but recovered without long-term symptoms. Without that comparison, it’s hard to know if the biomarker is unique to long COVID or simply a lingering byproduct of infection.
The mechanism is also murky, are these proteins signs of ongoing viral replication somewhere in the body, or are they debris being cleared out over time? And if they are part of an active process, could targeting them improve patient outcomes?
Until these issues are resolved, the biomarker is more of a promising lead than a definitive diagnostic tool.
Long COVID remains an evolving medical challenge. Despite years of research, we still don’t fully know what causes it, why it affects some people and not others, or how to predict recovery. Without a standardized definition, prevalence estimates vary widely, and with more than 800 million COVID cases worldwide, the potential number of patients is staggering.
The National Academies of Sciences, Engineering, and Medicine in the US has proposed a definition that includes up to 200 symptoms and states that no single symptom can confirm or rule out a diagnosis. While comprehensive, some experts argue that narrowing the symptom list could make diagnosis more specific and practical for research and clinical use.
The researchers behind the new study are already planning follow-up work to test whether the biomarker appears in people who had COVID-19 without developing long COVID. They also aim to investigate whether its presence changes over time or in response to treatments.
If their findings hold, this biomarker could mark the start of a new chapter in the fight against long COVID — one where diagnosis is not just about listening to symptoms, but also about identifying a clear, measurable biological signal.
As Dr. Stringer puts it, “This raises the question: is this just continuing to take out the trash from the COVID-infected cell, or is this really ongoing replication someplace? That’s the mechanistic issue that needs to be resolved in future studies.”
A new study from scientists in Miami has raised a big red flag saying that heavy alcohol consumption does not just damage your liver; it could also be quietly harming your pancreas and paving the way to one of the most lethal cancers in the world. While nobody talks much about this organ, it keeps your show running. Sitting behind the stomach, the pancreas organ produces the digestive enzymes that help you break down food, as well as the hormones that regulate your blood sugar.
The fresh study, published in Cellular and Molecular Gastroenterology and Hepatology, sheds new light on how alcohol-induced inflammation accelerates the development of the deadly disease.
The Miami researchers discovered that alcohol, in high quantities, can damage the very pancreatic cells that make those enzymes. This injury sparks inflammation that can smoulder away until it creates precancerous lesions. Left unchecked, these can evolve into pancreatic cancer, a disease with a grim reputation.
Not everyone who enjoys a tipple is destined for cancer. For the disease to develop, researchers found that a mutation in a gene called Ras, which controls cell growth, must also be present. But when alcohol was paired with a pro-inflammatory molecule in experiments, the effects mimicked alcohol-induced pancreatitis, complete with inflammation, lesions, and cancer.
The breakthrough? By disabling a gene called CREB, the scientists stopped both precancerous and cancerous lesions from forming. In other words, CREB seems to hold the keys to either the safe or self-destruct modes for your pancreas.
Pancreatic cancer kills over 9,000 people in the UK and more than 52,000 in the US every year. The five-year survival rate? About 10 to 12 per cent, among the lowest of any cancer. To make matters worse, cases are rising among younger people, though deaths have not yet spiked.
What makes this cancer so deadly is its silence. Symptoms rarely appear until it has already spread, and by then, treatment options are limited.
By the time these appear, the disease is often in an advanced stage, which is why prevention is key.
The study defined heavy alcohol use as eight or more drinks per week for women and 15 or more for men. Over months and years, that adds up to a consistent assault on your pancreas.
Pancreatic cancer isn’t just fatal; it can also cause a series of painful, exhausting complications:
Reportedly, managing these often requires procedures like stent placements or even nerve-block injections, adding more physical and emotional strain to an already heavy burden.
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