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Warp drive. Site-to-site transporter technology. A vast network of interstellar wormholes that take us to bountiful alien worlds. Beyond a hefty holiday wish-list, the ideas presented to us in sci-fi franchises like Gene Roddenberry’s “Star Trek” have inspired countless millions to dream of a time when humans have used technology to rise above the everyday limits of nature, and explore the universe.

But to guarantee the shortest path to turning at least some of these ideas into genuine scientific breakthroughs, we need to push ideas like general relativity to the breaking point. Tractor beams, one of the most exotic ideas proposed by the genre that involves manipulating space-time to pull or push objects at a distance, take us beyond the everyday paradigm of science, to the very edge of theoretical physics. And, a team of scientists examined how they might work in a recent study shared on a preprint server.

“In researching sci-fi ideas like tractor beams, the goal is to push and try to find a demarcation point where something more is needed, like quantum gravity,” said Sebastian Schuster, a scientist with a doctorate in mathematical physics from the Charles University of Prague, in an interview with IE. And, in finding out if tractor beams can work, we might also uncover even more exotic forces, like quantum gravity. So strap in.

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TABLE OF CONTENTS —————
0:00–21:02 : Introduction (Meaning of Life)
21:03–46:14 CHAPTER 1: Transhumanism and Life Extension.

TWITTER https://twitter.com/Transhumanian.
PATREON https://www.patreon.com/transhumania.
BITCOIN 14ZMLNppEdZCN4bu8FB1BwDaxbWteQKs8i.
ETHEREUM 0x1f89b261562C8D4C14aA01590EB42b2378572164
LITECOIN LdB94n8sTUXBto5ZKt82YhEsEmxomFGz3j.

#1 ) THE GENETIC PATHWAY

46:15–58:52 CHAPTER 2 : Biological Aging a. “Programmed Cell Death” Theory of Aging b. “Intercellular Competition” Theory of Aging c. “Antagonistic Pleiotropy” Theory of Aging.

#2 ) THE CYBERNETIC PATHWAY

58:53–1:12:26 CHAPTER 3 : Cyborgs.
1:12:27–1:24:35 CHAPTER 4 : Artiforgs.
1:24:36–1:41:10 CHAPTER 5 : Prosthetics.
1:41:11–2:00:44 CHAPTER 6 : Bionics.

The company is developing novel therapeutics targeting aging in humans and dogs by using genetically modified adeno-associated virus (AAV) vectors to deliver copies of the SIRT6 gene variant found in centenarians. SIRT6 has already been shown to have significant capabilities to repair DNA damage, and Genflow’s aim is to show that it can also improve healthspan and, potentially, increase lifespan. “Our business model is to develop our lead compound, GF-1002, that has already yielded encouraging pre-clinical results,” Leire told us. “We are currently undertaking pre-clinical trials which are expected to take approximately two years.


SIRT6 targeting longevity biotech announces intention to float on the London Stock Exchange, with IPO later this month.

𝙀𝙫𝙤𝙡𝙪𝙩𝙞𝙤𝙣𝙖𝙧𝙮 𝙗𝙞𝙤𝙡𝙤𝙜𝙞𝙨𝙩𝙨 𝙝𝙖𝙫𝙚 𝙩𝙧𝙤𝙪𝙗𝙡𝙚 𝙚𝙭𝙥𝙡𝙖𝙞𝙣𝙞𝙣𝙜 𝙬𝙝𝙮 𝙨𝙘𝙝𝙞𝙯𝙤𝙥𝙝𝙧𝙚𝙣𝙞𝙖 𝙖𝙣𝙙 𝙗𝙞𝙥𝙤𝙡𝙖𝙧 𝙙𝙞𝙨𝙤𝙧𝙙𝙚𝙧 — 𝙬𝙝𝙞𝙘𝙝 𝙖𝙧𝙚 𝙝𝙞𝙜𝙝𝙡𝙮 𝙝𝙚𝙧𝙞𝙩𝙖𝙗𝙡𝙚 𝙘𝙤𝙣𝙙𝙞𝙩𝙞𝙤𝙣𝙨 — 𝙥𝙚𝙧𝙨𝙞𝙨𝙩 𝙞𝙣 𝙥𝙤𝙥𝙪𝙡𝙖𝙩𝙞𝙤𝙣𝙨 𝙙𝙚𝙨𝙥𝙞𝙩𝙚 𝙝𝙖𝙧𝙢𝙞𝙣𝙜 𝙧𝙚𝙥𝙧𝙤𝙙𝙪𝙘𝙩𝙞𝙫𝙚 𝙛𝙞𝙩𝙣𝙚𝙨𝙨.

𝙍𝙚𝙨𝙚𝙖𝙧𝙘𝙝𝙚𝙧𝙨 𝙢𝙖𝙮 𝙝𝙖𝙫𝙚 𝙛𝙤𝙪𝙣𝙙 𝙖𝙣 𝙚𝙭𝙥𝙡𝙖𝙣𝙖𝙩𝙞𝙤𝙣 𝙞𝙣 𝙧𝙚𝙘𝙚𝙣𝙩𝙡𝙮 𝙚𝙫𝙤𝙡𝙫𝙚𝙙 𝙧𝙚𝙜𝙞𝙤𝙣𝙨 𝙤𝙛 𝙩𝙝𝙚 𝙝𝙪𝙢𝙖𝙣 𝙜𝙚𝙣𝙤𝙢𝙚 𝙩𝙝𝙖𝙩 𝙖𝙧𝙚 𝙣𝙤𝙩 𝙪𝙨𝙪𝙖𝙡𝙡𝙮 𝙧𝙚𝙘𝙤𝙜𝙣𝙞𝙯𝙚𝙙 𝙖𝙨 𝙜𝙚𝙣𝙚𝙨 𝙗𝙪𝙩 𝙘𝙖𝙣 𝙨𝙩𝙞𝙡𝙡 𝙘𝙤𝙙𝙚 𝙛𝙤𝙧 𝙥𝙧𝙤𝙩𝙚𝙞𝙣𝙨.

𝙏𝙝𝙞𝙨 “𝙙𝙖𝙧𝙠 𝙜𝙚𝙣𝙤𝙢𝙚” 𝙢𝙖𝙮 𝙜𝙚𝙣𝙚𝙧𝙖𝙩𝙚 𝙥𝙧𝙤𝙩𝙚𝙞𝙣𝙨 𝙩𝙝𝙖𝙩 𝙖𝙧𝙚 𝙫𝙞𝙩𝙖… See more.

The Neuro-Network.

𝐂𝐥𝐮𝐞𝐬 𝐭𝐨 𝐨𝐫𝐢𝐠𝐢𝐧𝐬 𝐨𝐟 𝐛𝐢𝐩𝐨𝐥𝐚𝐫 𝐚𝐧𝐝 𝐬𝐜𝐡𝐢𝐳𝐨𝐩𝐡𝐫𝐞𝐧𝐢𝐚 𝐟𝐨𝐮𝐧𝐝 𝐢𝐧 ‘𝐝𝐚𝐫𝐤 𝐠𝐞𝐧𝐨𝐦𝐞’


The authors of a recent study on the genetics of schizophrenia and bipolar disorder identify a potential role for the so-called dark genome.

Sinclair’s first episode. Enjoy.


In this episode, Dr. David Sinclair and co-host Matthew LaPlante discuss why we age. In doing so, they discuss organisms that have extreme longevity, the genes that control aging (mTOR, AMPK, Sirtuins), the role of sirtuin proteins as epigenetic regulators of aging, the process of “ex-differentiation” in which cells begin to lose their identity, and how all of this makes up the “Information Theory of Aging”, and the difference between “biological age” and “chronological age” and how we can measure biological age through DNA methylation clocks.

Thank you to our sponsors:
Athletic Greens — https://athleticgreens.com/sinclair.
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Levels — https://levels.link/sinclair.

Our Patreon page:
https://www.patreon.com/davidsinclair.

Lifespan book:
https://amzn.to/3sUqurT

Dr. David Sinclair Social:
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Twitter — https://twitter.com/davidasinclair.
Facebook — https://www.facebook.com/davidsinclairphd.

Matthew LaPlante’s Social:
Twitter — https://twitter.com/mdlaplante.

Timestamps:
00:00:00 Introduction.
00:03:14 Goal of the Lifespan Podcast.
00:07:11 Acknowledgement of Sponsors.
00:10:45 Aging is a Controllable Process that can be Slowed & Reversed.
00:16:42 Organisms with Extreme Longevity.
00:21:47 Genes that Regulate Aging: mTOR, AMPK, Sirtuins.
00:21:55 mTOR & Rapamycin.
00:24:33 AMP-activated protein kinase (AMPK) & Metformin.
00:30:57 Sirtuin Proteins as Epigenetic Regulators of Aging.
00:35:33 Ex-Differentiation.
00:43:30 Measuring Aging — Biological Age vs. Chronological Age.
00:49:30 “No Law That Says We Have To Age“
00:50:33 Episode Summary & Key Takeaways — Why Do We Age?
00:54:00 Information Theory of Aging.
00:57:59 Aging is a Medical Condition.
01:01:00 Aging Myths — Telomeres & Antioxidants.
01:01:55 Options for Subscription and Support.

DNA damage is constantly occurring in cells, either due to external sources or as a result of internal cellular metabolic reactions and physiological activities. Accurate repair of such DNA damages is critical to avoid mutations and chromosomal rearrangements linked to diseases including cancer, immunodeficiencies, neurodegeneration, and premature aging.

A team of researchers at Massachusetts General Hospital and the National Cancer Research Centre have identified a way to repair genetic damage and prevent DNA alterations using machine learning techniques.

The researchers state that it is possible to learn more about how cancer develops and how to fight it if we understand how DNA lesions originate and repair. Therefore, they hope that their discovery will help create better cancer treatments while also protecting our healthy cells.

The first humans emerged on Earth about 4 million years ago, but new evidence from the study of human evolution has revealed compelling evidence that a small group of these hominins was genetically modified by ancient alien visitors to create the first Homo sapiens.

Researcher and author Daniella Fenton has thoroughly analyzed humanity’s earliest origins and its sudden acceleration in brain development nearly 800,000 years ago, and this research has led to a major revelation.

“Homo sapiens is the creation of ancient astronauts who came through a wormhole in the Pleiades star cluster more than 780,000 years ago.”

The Australian researcher, an expert in equine lineages and gene expression, discovered numerous genetic changes that mark humans as abnormal when compared to modern primate species, some so extreme that they are best explained by advanced genetic engineering.

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“The potential to deliver ‘one shot cures’ is one of the most attractive aspects of gene therapy, genetically-engineered cell therapy and gene editing. However, such treatments offer a very different outlook with regard to recurring revenue versus chronic therapies,” analyst Salveen Richter wrote in the note to clients Tuesday. “While this proposition carries tremendous value for patients and society, it could represent a challenge for genome medicine developers looking for sustained cash flow.”

🤔


Goldman Sachs warns sales from the most successful disease treatments are difficult to maintain.

Down syndrome is the most common genetic disorder, impacting about 1 in 700 newborns around the world. At some point during their first hours and days of embryonic development, their dividing cells fail to properly wriggle a chromosome pair away from each other, leaving an extra copy where it shouldn’t be. Although scientists have known for more than six decades that this extra copy of chromosome 21 causes the cognitive impairment people with Down syndrome experience, exactly how it happens remains a matter of debate.


But in recent years, scientists using new RNA sequencing techniques to study cells from pairs of twins — one with Down syndrome and one without — have repeatedly turned up a curious pattern. It wasn’t just the genes on chromosome 21 that had been cranked way up in individuals with Down syndrome. Across every chromosome, gene expression had gone haywire. Something else was going on.

On Thursday, a team from the Massachusetts Institute of Technology reported in Cell Stem Cell that it may have found a surprising culprit: senescent cells, the same types implicated in many diseases of aging. The study was small and preliminary, and some experts want to see it replicated in samples from more individuals before buying into its interpretations. But they are nevertheless intriguing.

While doing their research, the teams had no knowledge of the other’s work, but after finding each other’s preprint proof-of-concept papers online, the two groups decided to submit their manuscripts for review together. “It’s insane that two groups did such similar studies in two places, but it’s also a very rare opportunity,” says Bohmann.

The fact the groups took different paths to find a similar result is particularly compelling, says Mark Johnson, who studies eDNA and Texas Tech University and was not involved in the work. “It’s really exciting looking at how both of these papers, done independently of each other, have produced, really, the same results,” says Johnson. “It adds that extra little bit of validation that what we’re seeing is real.” While hopeful about the future of airborne eDNA, Johnson notes huge leaps need to be made before the techniques used in the zoo can be applied in the field. Collecting eDNA in the wild adds a host of new variables, and enclosed spaces like caves may accumulate genetic material differently than open areas like grasslands. “The next step is to take it from the zoo into the natural environment and see what we find there,” says Johnson.

Clare and Bohmann anticipate that one of the best applications of airborne DNA could be to measure biodiversity in difficult-to-access places, such as burrows and caves. Fabian Roger, an eDNA researcher at ETH in Switzerland, is eager to see how the work could be applied to studying insects. “We have very little ways of monitoring them other than catching and killing them,” says Roger, who was not involved in the recent work. Using eDNA to detect insect species from a sample of air instead of trapping them could rapidly advance entomology research. The technique could also clue scientists into the presence or spread of an invasive species. Like Clare and Bohmann, Roger doesn’t see airborne eDNA as a replacement for traditional monitoring methods, but as another tool they can use. “Biodiversity science is sort of an all-hands-on-deck situation. It’s not one over the other, or one or the other,” says Roger.