Although we’ve been socialized to accept death as an inevitability, and live our lives knowing that its looming shadow will one day catch up with us, many of us might never really come to terms with it. Throughout our evolution, we’ve come up with ideas, beliefs and theories that attempt to shine a light deep into the cold, dark abyss of death to give ourselves a hope of continued living and everlasting existence. Could we really stop our cells from aging? If you could, would you want to be immortal?
Tardigrades have competition in the realm of microscopic and incredibly sturdy beasties. Like tardigrades, Bdelloid rotifers can also survive drying, freezing, starving, and even low-oxygen conditions. Now, scientists report that they revived some of these rotifers after having been frozen in Siberian permafrost for at least 24,000 years.
The incredible observations are reported in the journal Current Biology. The researchers took samples of permafrost about 3.5 meters (11.5 feet) deep and slowly warmed the sample, which led to the resurrection of several microscopic organisms including these tiny little animals.
“Our report is the hardest proof as of today that multicellular animals could withstand tens of thousands of years in cryptobiosis, the state of almost completely arrested metabolism,” co-author Stas Malavin of the Soil Cryology Laboratory at the Institute of Physicochemical and Biological Problems in Soil Science in Pushchino, Russia, said in a statement.
The whole interview is good and informative but starts with Sinclair commenting that at the moment he thinks living to 150 is possible in our lifetimes but not immortality. But given that, I’m 51. If I’m going to live potentially another century the technology will get better and better in that century and I would fully expect to life spans to become what we want rather than what we have to accept.
In this Ask Me Anything session, David and Peter discuss the latest age-reversal breakthroughs, getting approval from the FDA, and the possibility of living forever. David Sinclair is a biologist and academic known for his expertise in aging and epigenetics. Sinclair is a genetics professor and the Co-Director of Harvard Medical School’s Paul F. Glenn Center for Biology of Aging Research. He’s been included in Time100 as one of the 100 Most Influential People in the World, and his research has been featured all over the media. Besides writing a New York Times Best Seller, David has co-founded several biotech companies, a science publication called Aging, and is an inventor of 35 patents. Read David’s book, Lifespan: Why We Age-and Why We Don’t Have To: https://a.co/d/85H3Mll.
Leprosy is a chronic infectious disease caused by the bacterium Mycobacterium leprae. It affects the skin, nerves, and mucous membranes, and can lead to severe disfigurement and disability if left untreated.
Leprosy, a chronic infectious disease caused by the bacterium Mycobacterium leprae, is one of the oldest and most persistent diseases in the world. However, new surprising research suggests that the bacteria that cause leprosy may also have the ability to stimulate the growth and regeneration of the liver in adult animals without causing damage or scarring. Scientists have discovered that parasites associated with leprosy can reprogram cells to increase the size of the liver.
The findings suggest the potential to use this natural process to rejuvenate aging livers and extend the period of disease-free living in humans, known as healthspan. It may also be possible to use this process to regenerate damaged livers, potentially reducing the need for liver transplantation, which is currently the only effective treatment for individuals with severely scarred livers.
3D printers to create rapid on-demand objects have only been around for a short time. It’s a popular technique for making quick mock-ups or temporary solutions, but 3D-printing can also be used for more long-term applications. For example, some museums used it to create tactile models for interactive displays or even to create structural parts to support restoration projects. Either way, these are not temporary whimsical creations, but structures that they would likely still want to be in perfect shape several years down the line.
There are also other reasons to want to preserve 3D-printed materials for more than just a few years, but we haven’t had the technology for long enough to really know what will happen to these objects over time.
To find out, art conservation researchers at the Universidad Complutense de Madrid in Spain subjected two types of 3D printing materials to an artificial accelerated aging process. When plastics age, any damage such as loss of color or chemical changes in the materials are often caused either by UV radiation from exposure to light or by extreme temperature fluctuations. To simulate these extreme environments in a much faster scale than natural aging, the researchers put the 3D printed samples and the original filaments in two different chambers: One exposing the samples to UV light and the other subjecting them to a range of high temperatures.
At first, Professor Wolf Reik couldn’t quite believe the data. The experiment had involved an attempt to “rejuvenate” skin cells taken from a 53-year-old volunteer.
The results were better than anybody had expected: having been bathed in a cocktail of proteins, the cells now looked and behaved like those from somebody in their early twenties.
As different measurements of “biological age” confirmed the findings, the molecular biologist’s scepticism gave way to excitement. “I was falling off my chair three times over,” Reik said.
Anatomical decision-making by cellular collectives: Bioelectrical pattern memories, regeneration, and synthetic living organisms.
A key question for basic biology and regenerative medicine concerns the way in which evolution exploits physics toward adaptive form and function. While genomes specify the molecular hardware of cells, what algorithms enable cellular collectives to reliably build specific, complex, target morphologies? Our lab studies the way in which all cells, not just neurons, communicate as electrical networks that enable scaling of single-cell properties into collective intelligences that solve problems in anatomical feature space. By learning to read, interpret, and write bioelectrical information in vivo, we have identified some novel controls of growth and form that enable incredible plasticity and robustness in anatomical homeostasis. In this talk, I will describe the fundamental knowledge gaps with respect to anatomical plasticity and pattern control beyond emergence, and discuss our efforts to understand large-scale morphological control circuits. I will show examples in embryogenesis, regeneration, cancer, and synthetic living machines. I will also discuss the implications of this work for not only regenerative medicine, but also for fundamental understanding of the origin of bodyplans and the relationship between genomes and functional anatomy.
