Lifeboat Foundation

A team of researchers at the National Institute of Health Doutor Ricardo Jorge in Portugal, working with a colleague at Lusófona University, also in Portugal, has found that the monkeypox virus has been evolving at a faster rate than expected. In their paper published in the journal Nature Medicine, the researchers describe their genetic study of the virus collected from 15 samples.

Monkeypox is a double-stranded DNA virus from the same genus as smallpox, and it mostly infects people in Africa. Scientist have known of its existence since the 1950s. Despite its name, the virus is more commonly found in rodents than monkeys. Prior research has shown that there are two main varieties of monkeypox: West African and Congo Basin—the former is far less deadly and is the clade that has infected several thousand people outside Africa. Prior research has also shown that viruses like monkeypox typically only mutate once or twice in a given year.

In this new effort, the researchers collected samples from 15 patients and subjected them to genetic analysis to learn more about how quickly the virus is evolving. They found the virus has mutated at a rate six to 12 times as high as was expected. The researchers suggest the sudden accelerated rate of mutation in the virus may be a sign that the virus has developed a new way to infect people—currently, it is believed to move from person to person through close contact with open lesions, through body fluids or by airborne droplets.

New research suggests that Darwinian evolution could be happening up to four times faster than previously thought, based on an analysis of genetic variation.

The more genetic differences there are in a species, the faster evolution can happen, as certain traits die off and stronger ones get established. The team behind this latest study calls it the “fuel of evolution”, and they looked at data on 19 different wild animal groups around the world.

That data analysis revealed this raw material for evolution is more abundant than earlier estimates, and as a result we may have to adjust our expectations for how quickly animals evolve – a pertinent question in our age of climate change.

Circa 2021 First breakthrough in immortality of the eyes of rats using the inducing of pluripotent stem cells in the eye. Which will eventually lead to immortality of the human eye.

The retina is neural tissue located in the posterior part of the eye and is an extension of the central nervous system (CNS), which has limited regenerative potential once damaged¹. Therefore, to maintain homeostasis of the retinal microenvironment and protect itself from harmful stimuli, the retina has a unique structure consisting of inner and outer blood-retinal barriers (BRBs)^2,3,4. The outer BRB is mainly composed of retinal pigment epithelial (RPE) cells, which support photoreceptor cells, the primary neurons in the retina, and play a significant role in the pathogenesis of retinal degenerative disorders, such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP)^5,6,7,8,9. These disorders are commonly characterized by the irreversible loss of photoreceptor cells and RPE cells, and the only fundamental treatment for these retinal degenerative disorders is replacement of damaged or atrophied cells^10,11,12. Thus, regenerative treatments, such as stem cell transplantation, are emerging as attractive options for targeting retinal degeneration that was previously considered untreatable¹³.

RP refers to a set of hereditary retinal degenerative disorders that initially involve photoreceptors and leads to subsequent RPE cell damage; it affects 1 in 4,000 individuals worldwide⁹. Due to its inherent nature, extensive genetic studies are ongoing, and more than 50 causal genes have been identified¹⁴. Among the causal genes, PDE6B is a gene that encodes rod cGMP-phosphodiesterase, which is a critical component of the biochemical light transduction pathway⁹. Although various molecular and genetic studies have identified the pathomechanisms of RP, attempts to restore vision in patients with RP have failed. To overcome this issue, preclinical stem cell-based studies involving transient dosing or permanent implantation of pluripotent stem cells are being conducted^10,11,15,16.

Continue reading “Long-term effects of human induced pluripotent stem cell-derived retinal cell transplantation in Pde6b knockout rats” »

Our bodies can’t plug-and-play organs like replacement computer parts. The first rule of organ transplant is that the donor organs need to “match” with the host to avoid rejection. That is, the protein molecules that help the body discriminate between self and other need to be similar—a trait common (but not guaranteed) among members of the same family.

The key for getting an organ to “take” is reducing destructive immune attacks—the holy grail in transplantation. One idea is to genetically engineer the transplanted organ so that it immunologically “fits” better with the recipient. Another idea is to look beyond the organ itself to the source of rejection: haemopoietic stem cells, nestled inside the bone marrow, that produce blood and immune cells.

DISOT’s theory is simple but clever: swap out the recipient’s immune system with the donor’s, then transplant the organ. The recipient’s bone marrow is destroyed, but quickly repopulates with the donor’s stem cells. Once the new immune system takes over, the organ goes in.

Yet when faced with enormous protein complexes, AI faltered. Until now. In a mind-bending feat, a new algorithm deciphered the structure at the heart of inheritance—a massive complex of roughly 1,000 proteins that helps channel DNA instructions to the rest of the cell. The AI model is built on AlphaFold by DeepMind and RoseTTAfold from Dr. David Baker’s lab at the University of Washington, which were both released to the public to further experiment on.

Our genes are housed in a planet-like structure, dubbed the nucleus, for protection. The nucleus is a high-security castle: only specific molecules are allowed in and out to deliver DNA instructions to the outside world—for example, to protein-making factories in the cell that translate genetic instructions into proteins.

Continue reading “In Its Greatest Biology Feat Yet, AI Unlocks the Complex Proteins Guarding Our DNA” »

The gene-editing technology has led to innovations in medicine, evolution and agriculture — and raised profound ethical questions about altering human DNA.

When something goes wrong in mitochondria, the tiny organelles that power cells, it can cause a bewildering variety of symptoms such as poor growth, fatigue and weakness, seizures, developmental and cognitive disabilities, and vision problems. The culprit could be a defect in any of the 1,300 or so proteins that make up mitochondria, but scientists have very little idea what many of those proteins do, making it difficult to identify the faulty protein and treat the condition.

Researchers at Washington University School of Medicine in St. Louis and the University of Wisconsin–Madison systematically analyzed dozens of mitochondrial proteins of unknown function and suggested functions for many of them. Using these data as a starting point, they identified the genetic causes of three mitochondrial diseases and proposed another 20 possibilities for further investigation. The findings, published May 25 in Nature, indicate that understanding how mitochondria’s hundreds of proteins work together to generate power and perform the organelles’ other functions could be a promising path to finding better ways to diagnose and treat such conditions.

“We have a parts list for mitochondria, but we don’t know what many of the parts do,” said co-senior author David J. Pagliarini, Ph.D., the Hugo F. and Ina C. Urbauer Professor and a BJC Investigator at Washington University. “It’s similar to if you had a problem with your car, and you brought it to a mechanic, and upon opening the hood they said, ‘We’ve never seen half of these parts before.’ They wouldn’t know how to fix it. This study is an attempt to define the functions of as many of those mitochondrial parts as we can so we have a better understanding of what happens when they don’t work and, ultimately, a better chance at devising therapeutics to rectify those problems.”

Just a quick update in the E5 experiment all control rats have died and 3 treated rats remain.

Does the survival curve reflect the epigenetic age reduction seen in previous experiment? Blog post from the Live Forever Club.

Continue reading “Harold Katcher’s E5/Elixir (Young Plasma) Rat Trial Results” »

As they grow, solid tumors surround themselves with a thick, hard-to-penetrate wall of molecular defenses. Getting drugs past that barricade is notoriously difficult. Now, scientists at UT Southwestern have developed nanoparticles that can break down the physical barriers around tumors to reach cancer cells. Once inside, the nanoparticles release their payload: a gene editing system that alters DNA inside the tumor, blocking its growth and activating the immune system.

The new nanoparticles, described in Nature Nanotechnology, effectively stopped the growth and spread of ovarian and liver tumors in mice. The system offers a new path forward for the use of the gene editing tool known as CRISPR-Cas9 in cancer treatment, said study leader Daniel Siegwart, Ph.D., Associate Professor of Biochemistry at UT Southwestern.

“Although CRISPR offers a new approach for treating cancer, the technology has been severely hindered by the low efficiency of delivering payloads into tumors,” said Dr. Siegwart, a member of the Harold C. Simmons Comprehensive Cancer Center.