Lifeboat Foundation

In my work, I build instruments to study and control the quantum properties of small things like electrons. In the same way that electrons have mass and charge, they also have a quantum property called spin. Spin defines how the electrons interact with a magnetic field, in the same way that charge defines how electrons interact with an electric field. The quantum experiments I have been building since graduate school, and now in my own lab, aim to apply tailored magnetic fields to change the spins of particular electrons.

Research has demonstrated that many physiological processes are influenced by weak magnetic fields. These processes include stem cell development and maturation, cell proliferation rates, genetic material repair, and countless others. These physiological responses to magnetic fields are consistent with chemical reactions that depend on the spin of particular electrons within molecules. Applying a weak magnetic field to change electron spins can thus effectively control a chemical reaction’s final products, with important physiological consequences.

Currently, a lack of understanding of how such processes work at the nanoscale level prevents researchers from determining exactly what strength and frequency of magnetic fields cause specific chemical reactions in cells. Current cell phone, wearable, and miniaturization technologies are already sufficient to produce tailored, weak magnetic fields that change physiology, both for good and for bad. The missing piece of the puzzle is, hence, a “deterministic codebook” of how to map quantum causes to physiological outcomes.

Ago when I was a kid in college my friend Eric got me into many things. We played music together and used a Kurzweil Keyboard, and a bunch of weird stuff. We had an ADAT hooked up to the Kurzweil with fiber optic cables. I had Roland keyboards & Drum machines but I loved the Kurzweil. He started teaching me many things because he was really smart. I was studying psychology so he loaned me his DSMIV and books on Industrial Organiza… See more.

A bit long, but a good read. About 20 years ago when I was a kid in college my friend Eric got me into many things. We played music together and used a Kurzweil Keyboard, and a bunch of weird stuff. We had an ADAT hooked up to the Kurzweil with fiber optic cables. I had Roland keyboards & Drum machines but I loved the Kurzweil. He started teaching me many things because he was really smart. I was studying psychology so he loaned me his DSMIV and books on Industrial Organizational Psychology. He then told me about other books like “Society of Mind”(Marvin Minsky), “Age of Intelligent Machine” (Ray Kurzweil), Engines of Creation (K Eric Drexler), of course Richard Feynman, and many more. I dreamed of that technology and kept reading more. In the 2000’s Drexler and Feynman’s visions became a paradign and applications started rolling out, and now nanotechnology is applied to most everything we know. We are now at the second paradigm where we see the visions of Minsky/McCarthy, Kurzweil and others becoming easily available applications. As a Child I watched the Jetsons & Srar Trek and now with flying cars it’s not if, but when. Space travel is already here. All these technologies will transform global societies, but we must all focus on investing more in the advancement of society than the destruction of it. Many of the things we now invision in our minds we may see in 10 years. People think saving your consciousness & longevity is impossible, but I don’t. Some even thought that regenerating tissue and organs is impossible, but we can do that now. Now people keep saying, “This ancient turtle died, this rhino died (I hear that all the time in Kenya), this elephant died, but I say okay it’s not cool, but what can we salvage from it to bring the species back with advances in technology later? Do we use cryogenics? How do we save the genetic material? Technology can be used in so many ways. Every Day Lifeboat posts feats many do not know. If more people on earth had such a focus, as opposed to dumbed down entertainment like The Kardashians for instance, we would be living in a much better world with more people proposing more ideas and collaborations. I always say we are moving in the wrong way in the evolutionary process, and it is a bit telling that some phones are smarter than many people. I you add ChatGPT. We have so much advanced technology and science, yet we can’t even fight cancer. It took decades for people to learn the importance of diet in HIV treatment. However, Ray Kurzweil has for decades talked about the importance of diet for longevity. Just the other day it was published that processed foods affect cognitive function. Before that it was released processed foods cause cancer. We must change, and go in the right way of evolution to the Singularity another paradigm shift and cooperarion, instead of backwards to a barbaric age of conflict and greed. Always share your knowledge and I thank all who do share in this group. More should share as well, and Lifeboat should use more platforms to reach more people.

Year 2015 face_with_colon_three

The genetically modified super-smart mice also proved to suffer less from anxiety, the scientists found.

For all that science has decoded the human genome, we don’t actually know what most of our DNA does, or even what a great many of our genes do. One way to elucidate what a gene does is to change it (mutate it) and see what happens.

Continue reading “Scientists create super-intelligent mice, discover they’re also very laid-back” »

Imagine using your cellphone to control the activity of your own cells to treat injuries and disease. It sounds like something from the imagination of an overly optimistic science fiction writer. But this may one day be a possibility through the emerging field of quantum biology.

Over the past few decades, scientists have made incredible progress in understanding and manipulating biological systems at increasingly small scales, from protein folding to genetic engineering. And yet, the extent to which quantum effects influence living systems remains barely understood.

Continue reading “Quantum physics proposes a new way to study biology—the results could revolutionize our understanding of how life works” »

As sponges and ctenophores are such disparate animals¹³, the nature of the first diverging animal lineage has implications for the evolution of fundamental animal characteristics. Adult sponges are generally sessile filter-feeding organisms with body plans organized into reticulated water-filtration channels, structures built out of silica or calcium carbonate, and specialized cell types and tissues used for feeding, reproduction and self-defence, but they lack neuronal and muscle cells¹⁵. By contrast, ctenophores are gelatinous marine predators that move using eight longitudinal ‘comb rows’ of ciliary bundles^16,17; they are superficially similar but unrelated to cnidarian medusae^13,18 and possess multiple nerve nets¹⁹. Thus, whereas the sponge-sister scenario suggests a single origin of neurons on the ctenophore–parahoxozoan stem, the ctenophore-sister scenario implies either that either ancestral metazoan neurons were lost in the sponge lineage, or that there was convergent evolution of neurons in the ctenophore and parahoxozoan lineages^3,6. Similar considerations apply to other metazoan cell types¹⁸, gene regulatory networks, animal development^13,18 and other uniquely metazoan features.

Despite its importance for understanding animal evolution, the relative branching order of sponges, ctenophores and other animals has proven to be difficult to resolve². The fossil record is largely silent on this issue as verified Precambrian sponge fossils are extremely rare²⁰ and putative fossils of the soft-bodied ctenophores are difficult to interpret²¹. Morphological characters of living groups (for example, choanocytes of sponges) are not sufficient to resolve the question because true homology is difficult to assign, and such characters are easily lost or can arise convergently^13,22. The ctenophore-sister hypothesis is supported by a pair of gene duplications shared by sponges, bilaterians, placozoans and cnidarians but not ctenophores²³. Although sophisticated methods for sequence-based phylogenomics have been developed and applied to increasingly large molecular datasets, there is still considerable debate about the relative position of sponges and ctenophores as results are sensitive to how sequence evolution is modelled¹¹, which taxa or sites are included^24,25, and the effects of long-branch artifacts and nucleotide compositional variation²⁶. New approaches are needed.

We reasoned that patterns of synteny, classically defined as chromosomal gene linkage without regard to gene order²⁷, could provide a powerful tool for resolving the ctenophore-sister versus sponge-sister debate. Chromosomal patterns of gene linkage evolve slowly in many lineages^12,28,29,30, probably because it is improbable for interchromosomal translocations to be fixed in populations with large effective population sizes^28,31,32. Notably, some changes in synteny are effectively irreversible. For example, when two distinct ancestral synteny groups are combined onto a single chromosome by translocation, and subsequent intrachromosomal rearrangements mix these two groups of genes, it is very unlikely that the ancestral separated pattern will be restored by further rearrangement and fission, in the same sense that spontaneous reduction in entropy is improbable¹². Such rare and irreversible changes are particularly useful for resolving challenging phylogenetic questions as they give rise to shared derived features that unambiguously unite all descendant lineages^33,34,35. Deeply conserved syntenies observed between animals and their closest unicellular relatives¹² suggest that outgroup comparisons could be used to infer ancestral metazoan states and polarize changes within animals to address the sponge-sister versus ctenophore-sister debate. Yet, chromosome-scale genome sequences of the unicellular or colonial eukaryotic outgroups closest to animals (choanoflagellates, filastereans and ichthyosporeans) have not been reported.

For more than a century, biologists have wondered what the earliest animals were like when they first arose in the ancient oceans more than half a billion years ago.

Searching among today’s most primitive-looking animals for the earliest branch of the animal tree of life, scientists gradually narrowed the possibilities down to two groups: sponges, which spend their entire adult lives in one spot, filtering food from seawater; and comb jellies, voracious predators that oar their way through the world’s oceans in search of food.

In a new study published this week in the journal Nature, researchers use a novel approach based on chromosome structure to come up with a definitive answer: Comb jellies, or ctenophores (pronounced teen’-a-fores), were the first lineage to branch off from the animal tree. Sponges were next, followed by the diversification of all other animals, including the lineage leading to humans.

A new study adds to an emerging, radically new picture of how bacterial cells continually repair faulty sections of their DNA.

Published online May 16 in the journal Cell, the report describes the molecular mechanism behind a DNA repair pathway that counters the mistaken inclusion of a certain type of molecular building block, ribonucleotides, into genetic codes. Such mistakes are frequent in code-copying process in bacteria and other organisms. Given that ribonucleotide misincorporation can result in detrimental DNA code changes (mutations) and DNA breaks, all organisms have evolved to have a DNA repair pathway called ribonucleotide excision repair (RER) that quickly fixes such errors.

Last year a team led by Evgeny Nudler, Ph.D., the Julie Wilson Anderson Professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone Health, published two analyses of DNA repair in living E. coli cells. They found that most of the repair of certain types of DNA damage (bulky lesions), such as those caused by UV irradiation, can occur because damaged code sections have first been identified by a protein machine called RNA polymerase. RNA polymerase motors down the DNA chain, reading the code of DNA “letters” as it transcribes instructions into RNA molecules, which then direct protein building.

NewLimit, a company working towards the radical extension of human healthspan using epigenetic reprogramming has announced it has secured $40 million in Series A funding from prominent investors including Dimension, Founders Fund, and Kleiner Perkins.

This investment further bolsters the company’s belief that therapies to delay, halt or even reverse aging can be found through the exploration of epigenetic reprogramming. With a strong belief that their innovative approach can also address various age-related diseases, NewLimit aims to revolutionize the field of aging biology and pave the way for transformative advancements in healthcare.

Longevity. Technology: Epigenetic reprogramming is an emerging but exciting field of geroscience. It involves the identification of specific sets of transcription factors that can induce changes in gene expression and cellular behavior, effectively reversing or modifying the epigenetic markers associated with aging. This approach offers a unique opportunity to rejuvenate cells and tissues, potentially slowing down or even reversing the effects of aging and its related diseases. NewLimit says that while its products are designed to treat aging itself, the company also believes “these products could treat or prevent many diseases associated with aging, including fibrosis, infectious disease, and neurodegenerative disease.”

Scientists with the Human Pangenome Reference Consortium have made groundbreaking progress in characterizing the fraction of human DNA that varies between individuals. They have assembled genomic sequences of 47 people from around the world into a so-called pangenome in which more than 99 percent of each sequence is rendered with high accuracy.

For two decades, scientists have relied on the human reference genome as a standard to compare against other genetic data. Thanks to this reference genome, it was possible to identify genes implicated in specific diseases and trace the evolution of human traits, among other things.

However, it has always been a flawed tool: 70% of its data came from a single man of predominantly African-European background whose DNA was sequenced during the Human Genome Project. Hence, it can reveal very little about individuals on this planet who are different from each other, creating an inherent bias in biomedical data believed to be responsible for some of the health disparities affecting patients today.