Lifeboat Foundation

Probiotics show a new to battle cancer and other diseases keeping the host body healthy with its anti inflammation abilities.

Gut microbiota is widely considered to be one of the most important components to maintain balanced homeostasis. Looking forward, probiotic bacteria have been shown to play a significant role in immunomodulation and display antitumour properties. Bacterial strains could be responsible for detection and degradation of potential carcinogens and production of short-chain fatty acids, which affect cell death and proliferation and are known as signaling molecules in the immune system. Lactic acid bacteria present in the gut has been shown to have a role in regression of carcinogenesis due to their influence on immunomodulation, which can stand as a proof of interaction between bacterial metabolites and immune and epithelial cells. Probiotic bacteria have the ability to both increase and decrease the production of anti-inflammatory cytokines which play an important role in prevention of carcinogenesis. They are also capable of activating phagocytes in order to eliminate early-stage cancer cells. Application of heat-killed probiotic bacteria coupled with radiation had a positive influence on enhancing immunological recognition of cancer cells. In the absence of active microbiota, murine immunity to carcinogens has been decreased. There are numerous cohort studies showing the correlation between ingestion of dairy products and the risk of colon and colorectal cancer. An idea of using probiotic bacteria as vectors to administer drugs has emerged lately as several papers presenting successful results have been revealed. Within the next few years, probiotic bacteria as well as gut microbiota are likely to become an important component in cancer prevention and treatment.

Cancer is considered as one of the most significant causes of death. The treatment of tumors has received much attention in the last years; however, the number of people suffering neoplastic syndrome is still increasing. Thus, researchers are trying to face this process searching for innovative therapies and prophylaxis. Despite the fact that cancer risk indisputably depends on genetic factors, immunological condition of the organism plays a considerable role in it, that being closely associated with probiotic bacteria and commensal bacterial flora presented mainly in the digestive tract. Probiotic strains, inter alia Bifidobacterium, or Lactobacillus, widely present in commonly consumed fermented milk products, are known to have various beneficial effects on health. To date, there is a plethora of studies investigating the correlation between intestinal microbiota and carcinogenesis which have been evaluated in this article.

Ever considered the notion that everything around you was cooked up by aliens in a lab? Theoretical physicist and former chair of Harvard’s astronomy department, Abraham ‘Avi’ Loeb, has proposed a wild – if unsettling – theory that our universe was intentionally created by a more advanced class of lifeform.

In an op-ed for Scientific American, “Was Our Universe Created In A Laboratory?”, Loeb suggested that aliens could have created a ‘baby universe’ using ‘quantum tunneling’, which would explain our universe’s ‘flat geometry’ with zero net energy. If this discovery were proven true, then the universe humans live in would be shown to be “like a biological system that maintains the longevity of its genetic material through multiple generations,” Loeb wrote.

Loeb put forward the idea of a scale of developed civilisations (A, B, etc.) and, due to that fact that on Earth we currently don’t have the ability to reproduce the astrophysical conditions that led to our existence, “we are a low-level technological civilisation, graded class C on the cosmic scale” (essentially: dumb). We would be higher up, he added, if we possessed the ability to recreate the habitable conditions on our planet for when the sun will die. But, due to our tendency to “carelessly destroy the natural habitat” on Earth through climate change, we should really be downgraded to class D.

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.”