iteleshov

333 posts

iteleshov

iteleshov

@iteleshov

Programmist, transhumanist, traveler

Katılım Ağustos 2019
188 Takip Edilen15 Takipçiler
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Mikhail Batin
Mikhail Batin@MikhailBatin·
A few words about our experiment Two-headed planarians are not a recent sensation. They were first produced back in the 1920s (Rand & Ellis, 1926), when biologists discovered that the direction of regeneration in these simple organisms could be “knocked off course.” Nearly a century later, Michael Levin proposed that this phenomenon is driven by bioelectricity. In @drmichaellevin (2005) and Oviedo et al. (2010), researchers showed that temporarily blocking intercellular communication through gap junctions—and the resulting shift in membrane potentials (Vmem)—can reprogram the organism’s axial polarity. A planarian that would normally regrow a tail suddenly regenerates a second head—and keeps doing so after each subsequent amputation. This means the organism remembers its new form, rather than merely distorting it by chance. We’re dealing with something like a “memory of form”—a stable program encoded in the tissues, not in the DNA. Modern methods let us peer deeper into this phenomenon. Today we can map spatial Vmem gradients, track Wnt/Notum signaling activity, and run scRNA-seq on early blastemas to see how electrical signals control tissue self-organization. This is no longer an attempt to reproduce an old phenotype—it’s a step toward understanding the mechanism of morphogenetic memory. That’s exactly what we’re setting out to do. And we’ve already grown a two-headed planarian. Before Levin, double-headedness in planarians was usually induced mechanically or physiologically—by cutting, grafting, or using chemical inhibitors. As early as the beginning of the 20th century, Thomas Hunt Morgan and Child proposed the existence of “morphogenetic gradients”—factors that determine where the head and tail should form. But those ideas were vague. Levin was the first to show that the electrical potentials of cells and their gap-junction coupling form a language through which cells negotiate shape. Now we want to find out: is this bioelectricity truly the control code of form? Other people’s data are good—our own are better.
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First Approval
First Approval@FirstApproval·
🚨 Student Bio Data Competition 🚨 $7500 in prizes 💸 | Free submission | Publication with DOI 🧾 Open to undergrads, grads & PhDs 🧬 Deadline: Sept 15 🗓️ Submit 👉 firstapproval.io/contest 📢 Pls share with students & university departments! 🙏 #OpenScience #GoFair
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First Approval
First Approval@FirstApproval·
🚨 Student Bio Data Competition Alert! 🚨 Join the First Approval Contest — where students publish real scientific data & win big. 🧬 $7500 in prizes 📖 Free Open Access publication (with DOI!) 🧪 All kinds of data welcome — even negative results 🎓 Open to undergrads, grads, PhD
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Mikhail Batin
Mikhail Batin@MikhailBatin·
🔬 Calling all student biologists! This is your chance! 🔬 Announcing the First Approval Student Biological Data Competition! 🚀 Want to get your first publication with a DOI and compete for a $7500 prize pool? ✨ What we're looking for: High-quality scientific datasets (and their annotations) in biology, biotechnology, and biomedicine. Original, negative, or replicated data are all welcome! 🎓 Who can join: Undergraduate, Graduate, and PhD students. 🏆 What you'll get: * A chance to win a share of $7500 (32 prize winners!) * A guaranteed data publication (Open Access, DOI, first authorship) for EVERY participant! * Valuable publication experience and a contribution to Open Science. 🗓️ Submission Deadline: September 15, 2025 💰 Participation: FREE! Ready to share your data with the world? Learn more and submit your dataset! 👇 intro.dev.firstapproval.io/contest #FirstApproval #StudentCompetition #Biology #Biotechnology #Biomedicine #OpenData #OpenScience #ScienceCompetition #StudentResearch #Publication #ResearchGrant #OpenLongevity #AcademicTwitter #PhDLife #GradSchool
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ARPA-H
ARPA-H@ARPA_H·
Our streamlined awards process enables us to act quickly and catalyze cutting-edge biomedical and health research. arpa-h.gov/about/partneri…
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SpaceX
SpaceX@SpaceX·
Three launches from all three launch pads in California and Florida in ~36 hours
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SpaceX
SpaceX@SpaceX·
Two Falcon 9 boosters also returned to LZ-1 and LZ-2 after successfully launching our third Dragon mission of the year from pad 39A and our third Bandwagon rideshare mission from pad 40
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First Approval
First Approval@FirstApproval·
Hi Everyone! Tomorrow First Approval will participate in DeSci SF: Science x data x AI In Homebrew crypto club in SF. Reservation is here: lu.ma/4r67k5kl
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First Approval
First Approval@FirstApproval·
Today at 5PM! Join First Approval at Vitalist Bay in Berkeley for “Sharing Research Data: We Can Do Better.” 📍 2740 Telegraph Ave 🎤 Talk by Tim Glinin lu.ma/i61fbhyf
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Adam Gries
Adam Gries@adamgries·
Want to feel 30 when you hit 100? We can show you how! With Bryan Johnson, Kristen Fortney, Tim Urban & many more, we’ll spark an Apollo Program to solve aging. Upgrade your health & join the revolution in Berkeley, CA this Friday!
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Danila Immortalist
Danila Immortalist@DanilaImmortal·
The idea of a Longevity State is no longer just a utopian dream whispered in the corners of forums. It’s happening. The field is getting crowded, and that’s exactly what we need—more contenders, more strategies, more ambitious plans to tackle the ultimate enemy: death. Here’s a quick roundup of the big players: @InfinitaCity (formerly @VitaliaCity) The OG Longevity State. The pioneers. They’ve built the furthest along and made the idea of a longevity-first city something tangible. If you think the Caribbean is paradise, this one’s for you—it’s literal tropical immortality vibes. @CityOfViva The future looks promising here. They’re still building the foundation, but if they succeed, wherever this city appears, life expectancy in the region will skyrocket. @VitalismOrg On a quieter but no less strategic note, these folks are gaining influence fast. Our recent working group is scouting potential territories where a small, committed community of Vitalists could redirect resources toward the fight against aging and death. Plus, upcoming @VitalistBay gathering promises to be the largest assembly of like-minded individuals in one place—even if only for a couple of months. But those months will be time that changes everything. @JoinImmortalis Another project that, in my opinion, not many people have heard of. They tend to keep to themselves and interact very little with others. Then again, maybe that’s all part of their strategy. And now, officially, @bryan_johnson has entered this field and, predictably, outperformed everyone right from the start) Already over 5K participants, with a goal of 1 billion! To make it happen, just pledge to… "Rage, rage against the dying of the light. Become a practitioner of the don’t die ethos, caring for myself, others, and the planet, and honor existence as the highest virtue. Because we are… at war with death and its causes, building towards an infinite horizon, and fighting for the freedom to exist as long as one chooses. Why? Because we have things to do tomorrow.” The last couple of lines, in my opinion, are quite weak, but I suppose I agree. At least as long as our society considers it proper to have hotlines that brainwash and persuade people otherwise if someone wants to choose death. As for Why?—it’s quite a debatable question. Some people have things to do, while others don’t. Personally, after we solve the problem of aging, I’d gladly take a few days off for a change) I think life is valuable in and of itself and doesn’t need any further justification. Or rather, when it comes to the question of Why?, everyone can answer it for themselves—or not answer it at all, if that’s what they prefer. But the main and strongest line here is “we are at war with death” Nothing describes the situation more accurately than that. And yet, here we are: a few scrappy partisan groups with limited funding and no army, up against the industrial-scale death machine. They’ve got the numbers, the culture, and the centuries-old propaganda (“death gives life meaning,” anyone?) on their side. We’ve got… a handful of scientists, some Twitter accounts, and a growing—but still scattered—movement. Will Bryan be able to create an army? No one can say for sure, but everyone wishes him luck) Personally, I believe inaction is not an option, and we must IMMEDIATELY GET CITIZENSHIP on the don’t die website. But one thing is clear: if you want to build your own Longevity State, make sure you’ve got at least a million YouTube subscribers first.
Danila Immortalist@DanilaImmortal

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Mikhail Batin
Mikhail Batin@MikhailBatin·
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Memortalism
Memortalism@memortalism·
Longevity meme contest, sponsor—@strygah, prize—$140! • What to do? Publish a meme in the comments to this post, quoting it or tagging @memortalism in a tweet with your meme. • Deadlines Memes are accepted until the end of the week (January 26, 23:59:59 UTC). The results of the competition will be announced on Monday, January 27. • Prize The author of the best meme will receive $140 in USDT (TRC20) wallet. Meme topics: longevity, vitalism, immortality, longevity economics, aging, transhumanism. The meme must be original: not seen anywhere before. The winner will be determined subjectively. Judges @yangranat, @strygah, @MikhailBatin, @DanilaImmortal. But if your meme gets a lot of likes, views, comments, then this will be taken into account. Powered by @OpenLongevity. If you want to become a sponsor of the next contest, then write @MikhailBatin or @yangranat.
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Peter Fedichev
Peter Fedichev@fedichev·
me+@jangruber467+Kirill Denisov have just released a preprint that reveals a few novel insights into the mechanics of aging (there will be a separate post with the details and highlights; the ref to the preprint is in the first comment). One of these observations concerns the distribution of site-specific rates of methylation changes, a critical epigenetic modification where methyl groups are added to DNA, influencing gene expression without altering the genetic code. Over time, these methylation changes accumulate and collectively constitute the aging drift. A large fraction of methylation changes is reversible and orchestrate pathway activations. A lot more of them are individually rare. Picture each change as a small leak in a vast network. While a single leak may appear insignificant, our bodies contain approximately a trillion cells. This immense number means that even rare events can compound and collectively exert a significant force that propels the organism towards pathological states, contributing to aging and associated diseases. Why are these methylation changes so slow? It all comes down to protective free energy barriers. These barriers exceed the noise levels and act as high walls that separate different methylation states, making transitions between them infrequent and aiding in maintaining cellular stability. DNA methylation data convincingly shows that the distribution of methylation change rates are non-Gaussian— instead they follow exponential pattern. This indicates that while most changes occur at low rates, there are significantly more higher-rate events than one might anticipate. This exponential distribution suggests that the distribution of free energy barriers adheres to the Gumbel distribution, one of the three universal distributions in extreme value statistics. The Gumbel distribution arises, for instance, in hydrology where it helps to predict the probability of extreme flood events. A large river system may gather rains from vast areas. While the distribution of rainfall in each location may be unremarkable, the cumulative effect of such inputs on the river's level at river's mouth can occasionally lead to extreme values. This is why hydrologists use the Gumbel distribution to estimate the likelihood and scale of a 100-year flood. The link between exponential rates and the Gumbel distribution implies that in similar ways, when it comes to aging drift, most of damaging events are results of high energy transitions, each representing examples of those "100-years flood" level emergency - a perfect storm - most likely resulting from simultaneous failures across multiple highly redundant systems. Given that aging drift arises from these rare combined failures, reversing the aging process presents a monumental challenge. It would necessitate an impractical level of microscopic control to address and rectify each rare methylation event across trillions of cells. By revealing that the distribution of methylation change rates follows an exponential pattern and is connected to the Gumbel distribution, we develop a deeper understanding of how tiny, infrequent changes can collectively propel the aging process at the organism level. While reversing aging may seem increasingly elusive, attention should shift towards methods of reducing the rate of the aging drift as it drives the age-dependent functional decline. Stay tuned as we aim to showcase practical examples of this strategy. Please follow, like, and repost to see more of this.
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