Lifeboat Foundation

A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.

In a study, published in the journal eLife on Sept. 29, the researchers identified a factor that acts like a molecular switch in the skin of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goose bumps, an ability that is lost in adult human scars.

“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”

David Sinclair wants to slow down and ultimately reverse aging. Sinclair sees aging as a disease and he is convinced aging is caused by epigenetic changes, abnormalities that occur when the body’s cells process extra or missing pieces of DNA. This results in the loss of the information that keeps our cells healthy. This information also tells the cells which genes to read. David Sinclair’s book: “Lifespan, why we age and why we don’t have to”, he describes the results of his research, theories and scientific philosophy as well as the potential consequences of the significant progress in genetic technologies.

At present, researchers are only just beginning to understand the biological basis of aging even in relatively simple and short-lived organisms such as yeast. Sinclair however, makes a convincing argument for why the life-extension technologies will eventually offer possibilities of life prolongation using genetic engineering.

Continue reading “Harvard Professor Wants to Slow Down & Reverse Aging: David Sinclair’s Approach For a Longer Life” »

#DigitalTheology #TheologyofDigitalPhysics #PhenomenalConsciousness #CosmicSelf #HolographicPrinciple #DigitalPhysics #theology #pantheism #consciousness

Since we live in a world which isn’t random, but organized at every level, a role for consciousness seems unavoidable. The ‘digital theologian’ shows us compelling evidence from quantum mechanics, mathematics and computer sciences, which not only aligns with a philosophical worldview of the Primacy of Consciousness, but which also assigns a role to information as its modus operandi.

It is quantum mechanics which appears to connect the Universe as a whole to consciousness. A whole, which is more than the sum of its parts and irreducible to mere assumptions deriving from the anatomizing dissection into mental confabulations. Drawing from the holographic principle, perceptroniums and noocentrism, Alex provides crucial keys to unlock the mystery of consciousness to show us how our local consciousness can arise from a non-local cosmic consciousness network.

Continue reading “Theology of Digital Physics: The Universe of Conscious Minds” »

Summary: PLCG2-P522R, a genetic variant that protects against Alzheimer’s disease, enhances key functions of immune cells.

Source: University of Eastern Finland

A new study conducted by researchers at the University of Eastern Finland found that the PLCG2-P522R genetic variant, which protects against Alzheimer’s disease, enhances several key functions of immune cells. The results obtained in the study highlight the importance of immune cells as a target of future development of new therapies for Alzheimer’s disease.

11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.

Lil bits of info on DNA methylation, clocks.

Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7–8 million years ago when our ancestors branched away from the lineage of chimps.

Continue reading “Humans live much longer than chimps due to a slower epigenetic ‘clock’” »

Very interesting!

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“The plan was to scan patients’ genomes—in particular, a set of 13 genes involved in interferon immunity against influenza. In healthy people, interferon molecules act as the body’s security system. They detect invading viruses and bacteria and sound the alarm, which brings other immune defenders to the scene.

Continue reading “Some severe COVID-19 cases linked to genetic mutations or antibodies that attack the body” »

Toronto scientists have mapped the genes allowing cancer cells to avoid getting killed by the immune system in a finding that paves the way for the development of immunotherapies that would be effective for larger patient populations and across different tumour types.

“Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments but the reality is that they only generate durable responses in a fraction of patients and not for all tumour types,” says Jason Moffat, a professor of molecular genetics in the Donnelly Centre for Cellular and Biomolecular Research at the University of Toronto who led the work.

The study also revealed the need for new therapy to take into account the genetic composition of tumours because of mutations in the cancer cells that can potentially make the disease worse in response to treatment, often referred to as cancer resistance mutations.

Who are we? Where did we come from? How did we get here? Throughout the ages, humans have sought answers to these questions, pursuing wisdom through religion, philosophy, and eventually science. Evolutionary analyses published by Genome Biology and Evolution (GBE) allow us to peer into the mirror and better understand ourselves as a species, bringing us closer than ever to uncovering the answers to these long-held questions. GBE’s latest virtual issue on human genetics highlights some of the most exciting research published in the journal within the last year and a half, demonstrating the wide variety of evolutionary approaches to this avenue of research as well as a number of fascinating insights into our own biology.

Taking over a decade to complete, the original Human Genome Project cost nearly $3 billion and involved the collective effort of hundreds of scientists. Since then, advances in sequencing technology have resulted in an explosion in human genetics and genomics research, with an estimated one million human genomes sequenced to date. While this wealth of data has the potential to answer some of our most fundamental questions, unlocking its mysteries has necessitated the invention of new analytic and computational methods and the integration of techniques and ideas from diverse biological sciences, including physiology, anatomy, medicine, population genetics, bioinformatics, and computational, molecular, and evolutionary biology.

A key area of investigation involves identifying ways in which humans differ from other primates—in other words, what makes us human? Several studies published over the last 18 months suggest that part of the answer may be found in transcriptional regulation and changes in gene expression. Edsall et al. (2019) evaluated differences in chromatin accessibility, which impacts access of the transcriptional machinery to the DNA, across five primates including humans. They found high levels of differentiation across species, as well as classes of sites that differed based on selection, genomic location, and cell type specificity. More specifically, Swain-Lenz et al. (2019) found that differences in chromatin accessibility near genes involved in lipid metabolism may provide a mechanistic explanation for the higher levels of body fat observed in humans compared to other primates. Arakawa et al.