A subset of dendritic cells orchestrates the formation of tertiary lymphoid structures in tumor tissues
The fact that you, or I, or any living creature, is here at all is a series of astonishing strokes of luck stretching back more than 4 billion years.
One of the biggest hurdles was the very first one: How did life emerge from a primordial soup of stuff that very much wasn’t alive?
A radical new study, published in Science Advances, suggests that this unlikely threshold may actually have been crossed not once, but twice.
GLP-1 drugs such as Ozempic have transformed healthcare in recent years, dramatically altering how we treat conditions like type 2 diabetes and obesity.
But while the medications are primarily used to help lower blood sugar and reduce appetite, scientists keep finding GLP-1 effects appear to extend much further, affecting our health in ways we never expected.
Now, a new study has uncovered another unintended effect, and it shows we’re still only scratching the surface of fully understanding how GLP-1 receptor agonists impact the body.
Spinal cord injuries affect an estimated 15 to 20 million people worldwide, often causing lasting impairments in movement, sensation and independence. Such injuries can be especially devastating when they occur at the level of the neck, where damaged spinal circuits disrupt signals that control the diaphragm, the main muscle used for breathing.
Despite advances in emergency care and rehabilitation, no approved therapies exist to rebuild the neurons and connections lost after a spinal cord injury. But new research from scientists at Gladstone Institutes offers hope for a regenerative treatment in the future.
The study, published in Science Translational Medicine, shows that human stem cell-derived spinal interneurons—cells that are critical for breathing and movement— can survive after being transplanted in injured rats, connect with the animals’ own neural circuits and improve breathing-related motor function.
It can be done again…
No one can predict with any confidence how long it will be before it may be possible to repair and revive patients in biostasis. It is plausible that it will take a century. It could be decades less – especially if artificial intelligence accelerates biomedical advances – or it could be decades longer. But one century gives us something to work with. It is a long time in terms of changes in the world.
This raises an obvious question: How can a biostasis organization survive for a century or more until its patients can be returned to life?
Telomere shortening is associated with increased risk of disease and decreased lifespan. Various nutrients have been shown to support the length and health of telomeres in clinical and preclinical studies.
Scientifically reviewed by: Gary Gonzalez, MD, in May 2026. Written by: Richard Ross.