The eye protein rhodopsin of the Greenland shark was found to have amino acid variations that made them more adept at processing blue-light wavelengths – a feature that is advantageous when living in the dim deep ocean waters.
“These genomic analyses offer new insights into the molecular basis of the exceptional longevity of the Greenland shark and highlight potential genetic mechanisms that could inform future research into longevity,” scientists wrote in the study.
In a trailblazing advancement in cancer therapy, researchers at Korea Advanced Institute of Science and Technology (KAIST) have developed a technology that transforms colon cancer cells into normal-like cells without destroying them.
This innovative approach, led by Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering, represents a significant departure from traditional cancer treatments that rely on killing cancer cells, often leading to severe side effects and risks of recurrence.
An expanded clinical trial that tested a groundbreaking, experimental stem cell treatment for blinding cornea injuries found the treatment was feasible and safe in 14 patients who were treated and followed for 18 months. In addition, there was a high proportion of complete or partial success.
The study developed a two-stage manufacturing process utilizing cultivated autologous limbal epithelial cells (CALEC), the first xenobiotic-free, serum-free, antibiotic-free protocol developed in the United States to treat blindness caused by unilateral limbal stem cell deficiency (LSCD).
The procedure consists of removing stem cells from a healthy eye with a biopsy, expanding them into a cellular tissue graft in a novel manufacturing process that takes two to three weeks, and then surgically transplanting the graft into the eye with a damaged cornea.
While his neighbors frantically fled from their oncoming doom, one man stayed in bed. For whatever reason, he didn’t join the other 2000 residents of Herculaneum—the ancient Roman city just north of Pompeii—as they ran from erupting Mount Vesuvius. The first scorching cloud of ash passed through the city so quickly, it turned his brain into black, glasslike shards. Now, a new analysis of these shards, published today in, offers clues about how the man and his neighbors perished in 79 C.E.
Until recently, scientists believed the people of Herculaneum were annihilated by Mount Vesuvius’s avalanche of hot rock, ash, and gas that buried their city, along with Pompeii. But when researchers announced the discovery of those black, glossy chips in 2020, a new culprit emerged: a swift ash cloud preceding this flood of debris. This rethink, however, hinged on whether the brain had indeed turned to glass.
For glass to form, a liquid needs to be cooled so rapidly that its molecules suddenly “freeze” into a rigid structure rather than forming crystals. For this reason, glass is sometimes referred to as a “liquid solid,” says Brian Wowk, a cryobiologist at 21st Century Medicine who was not involved with the work. Thick blankets of pyroclastic flow–the torrent of rocks, ash, and gas expelled by volcanos–cool off far too slowly for glass to form, says study co-author Guido Giordano, a volcanologist at the Roma Tre University. “Once they’re in place, they can take years to cool down.”
For decades, exercise was considered an optional part of cancer care—something beneficial for general health but not essential. The evidence is now overwhelming: exercise is not just supportive—it’s a therapeutic intervention that recalibrates tumor biology, enhances treatment tolerance, and improves survival outcomes.
With over 600 peer-reviewed studies, Dr. Kerry Courneya’s work has fundamentally reshaped our understanding of how structured exercise—whether aerobic, resistance training, or high-intensity intervals—can mitigate treatment side effects, enhance immune function, and directly influence cancer progression.
Train smarter with evidence-based strategies from top experts—get your free copy of “How to Train According to the Experts” at https://howtotrainguide.com/
CHAPTERS:
00:00:00 Introduction.
00:01:47 Why exercise should be effortful.
00:02:33 How to meaningfully reduce risk of cancer.
00:06:22 What type of exercise is best?
00:07:59 How exercise reduces risk—even for smokers and the obese.
00:10:48 Weekend-only exercise.
00:13:49 150 vs. 300 minutes per week (more is better—up to a point)
00:16:03 Why pre-diagnosis exercise matters.
00:19:09 Why resilience to cancer treatment starts with exercise.
00:21:01 Why low muscle mass drives cancer death.
00:23:58 Why BMI fails to measure true obesity.
00:27:51 Why daily activity isn’t enough (structured exercise matters)
00:29:34 Breaking up sedentary time—do ‘exercise snacks’ help?
00:31:50 Supplements vs. exercise.
00:32:32 Where exercise fits with chemo and immunotherapy.
00:35:30 Why rest is not the best medicine.
00:41:20 Aerobic vs. resistance.
00:42:11 How chemotherapy patients were able to put on over a kilogram of muscle.
00:42:13 How weight training improves ‘chemo completion’
00:44:41 Why exercise creates vulnerability in cancer cells (limitations do apply)
00:47:09 Why exercise might be crucial for tumor elimination.
00:53:03 Why cardio may be better at clearing tumor cells.
00:56:18 When cancer spreads quickly—and when it doesn’t.
00:57:43 Why liquid biopsies may prevent over-treatment.
01:02:56 Exercise-sensitive vs. exercise-resistant cancers.
01:06:06 Prostate cancer therapy—why strength training matters.
01:08:10 When exercise is the only therapy—does it work?
01:09:26 Why HIIT reduces PSA in prostate cancer.
01:11:40 Avoiding over-treatment—can exercise buy you time?
01:12:00 Why high-intensity exercise boosts anti-cancer biology.
01:13:11 Turning a diagnosis into a wake-up call.
01:16:11 Why oncologists are rethinking exercise.
01:18:50 Why exercise eases anxiety about cancer—proven psychological benefits.
01:25:00 Before, during, and after treatment.
01:27:02 Why exercise is unique among cancer therapies.
01:28:16 Why cancer patients stop exercising—the risky mistake almost everyone makes.
01:30:41 How to get sedentary cancer patients exercising (realistically)
01:33:15 The $1 million case for including exercise.
01:34:56 Why recurrence trials haven’t convinced doctors—yet.
01:37:36 The bottom-line message.
01:37:55 The myth of a cancer panacea (exercise included)
01:44:07 What’s the best $50 investment for staying active?
01:44:40 Only 15 minutes per day—what’s the best anti-cancer exercise?
A quick cautionary note: Always consult a qualified healthcare provider—presumably an oncologist if your questions involve cancer treatment—particularly if you’re considering actions based on or inspired by our conversation today. This episode should not be construed as a substitute for qualified medical advice.
*Kerry Courneya, PhD*
Researchers across 14 medical centers in China, including Peking University People’s Hospital, have found that an investigational drug, berberine ursodeoxycholate (HTD1801), significantly lowered blood sugar levels and improved metabolic and liver health in patients with type 2 diabetes (T2D). The findings and an invited commentary, both published in JAMA Network Open, suggest that HTD1801 could serve as a new oral treatment option for T2D and its related complications.
An arms race is unfolding in our cells: Transposons, also known as jumping genes or mobile genetic elements as they can replicate and reinsert themselves in the genome, threaten the cell’s genome integrity by triggering DNA rearrangements and causing mutations. Host cells, in turn, protect their genome using intricate defense mechanisms that stop transposons from jumping.
Now, for the first time, a retrotransposon has been caught in action inside a cell: Refining cryo-Electron Tomography (cryo-ET) techniques, scientists imaged the retrotransposon copia in the egg chambers of the fruitfly Drosophila melanogaster at sub-nanometer resolution. The paper is published in the journal Cell.
Among the international team of scientists achieving this detailed visualization are three scientists with Vienna BioCenter ties: Sven Klumpe, currently in the laboratory of Jürgen Plitzko at the Max Planck Institute of Biochemistry in Martinsried, will join IMBA and IMP to build a group as a Joint Fellow; Julius Brennecke, a Senior Group Leader at IMBA, the Institute of Molecular Biotechnology of the Austrian Academy of Sciences; and Kirsten Senti, staff scientist in the Brennecke group. Also involved in this collaboration is the group of Martin Beck at the Max Planck Institute of Biophysics in Frankfurt.
ETH researchers have developed a new gene switch that can be activated using a commercially available nitroglycerine patch applied to the skin. One day, researchers want to use switches of this kind to trigger cell therapies for various metabolic diseases.
The body regulates its metabolism precisely and continuously, with specialized cells in the pancreas constantly monitoring the amount of sugar in the blood, for example. When this blood sugar level increases after a meal, the body sets a signal cascade in motion in order to bring it back down.
In people suffering from diabetes, this regulatory mechanism no longer works exactly as it should. Those affected therefore have too much sugar in their blood and need to measure their blood sugar level and inject themselves with insulin in order to regulate it. This is a relatively imprecise approach compared to the body’s own mechanism.
The fields of regenerative medicine and cellular biology are advancing rapidly, demonstrating that some aging-related processes may be more reversible than previously thought.
Recent research has shown that it is possible to rejuvenate the skin cells of a 53-year-old woman by 30 years, a groundbreaking scientific achievement that could redefine modern approaches to treating age-related diseases.
Cellular aging is a complex process marked by gradual changes in cell structure and function. Over time, alterations in gene expression, DNA damage accumulation, and reduced tissue regeneration capacity occur.