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Beautiful new paper: methods for getting stem-cell derived retinal ganglion cells to integrate into the retina (mouse). Cells were capable of migrating & surviving. #NEIfunded Baranov Lab Levi Todd Mass Eye and Ear Harvard Ophthalmology PNASNews paper:

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Michael F. Chiang, MD

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14,508 次观看 • 2 年前 •via X (Twitter)

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🚨 SCIENTISTS JUST BUILT AN ARTIFICIAL RETINA THAT RESTORES VISION AND ADDS INFRARED SIGHT. Researchers at Yonsei University in South Korea have developed a flexible, three-layer implant that bypasses dead photoreceptors and directly stimulates healthy retinal ganglion cells. The device not only helps restore vision in cases of retinal degeneration (like retinitis pigmentosa) but also gives the eye the ability to detect near-infrared light that humans normally cannot see. The key innovation is a soft 3D array of liquid metal micropillars (gallium-indium alloy) that gently conform to the curved retina without causing damage or inflammation a major improvement over rigid electrodes used in earlier implants. Why this matters: • Retinal diseases destroy light-sensing cells, but the neurons deeper in the eye often remain healthy and capable of sending signals to the brain • The implant uses an ultrathin filter + phototransistor array to convert near-infrared light into electrical signals the ganglion cells can understand • In mouse tests, blind animals regained visual responses, while healthy mice gained infrared sensitivity on top of their normal vision • The liquid metal electrodes are soft and biocompatible, dramatically reducing the risk of scarring or tissue damage The deeper implication: This isn’t just about restoring lost vision it’s about augmenting human sight. If it reaches human trials and proves safe long-term, people with partial vision loss could keep their remaining natural sight while gaining an entirely new sensory channel (infrared). The biggest open question is how the human brain would interpret this new stream of information whether it would feel like a new color, an overlay, or something else entirely. We’re moving from “fixing blindness” to “expanding what it means to see.” How do you think gaining the ability to see infrared light would change daily life or human perception? Follow for more frontier neurotechnology and bionic vision breakthroughs.
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🚨 SCIENTISTS JUST BUILT AN ARTIFICIAL RETINA THAT RESTORES VISION AND ADDS INFRARED SIGHT. Researchers at Yonsei University in South Korea have developed a flexible, three-layer implant that bypasses dead photoreceptors and directly stimulates healthy retinal ganglion cells. The device not only helps restore vision in cases of retinal degeneration (like retinitis pigmentosa) but also gives the eye the ability to detect near-infrared light that humans normally cannot see. The key innovation is a soft 3D array of liquid metal micropillars (gallium-indium alloy) that gently conform to the curved retina without causing damage or inflammation a major improvement over rigid electrodes used in earlier implants. Why this matters: • Retinal diseases destroy light-sensing cells, but the neurons deeper in the eye often remain healthy and capable of sending signals to the brain • The implant uses an ultrathin filter + phototransistor array to convert near-infrared light into electrical signals the ganglion cells can understand • In mouse tests, blind animals regained visual responses, while healthy mice gained infrared sensitivity on top of their normal vision • The liquid metal electrodes are soft and biocompatible, dramatically reducing the risk of scarring or tissue damage The deeper implication: This isn’t just about restoring lost vision it’s about augmenting human sight. If it reaches human trials and proves safe long-term, people with partial vision loss could keep their remaining natural sight while gaining an entirely new sensory channel (infrared). The biggest open question is how the human brain would interpret this new stream of information whether it would feel like a new color, an overlay, or something else entirely. We’re moving from “fixing blindness” to “expanding what it means to see.” How do you think gaining the ability to see infrared light would change daily life or human perception? Follow for more frontier neurotechnology and bionic vision breakthroughs.

TheNewPhysics

34,362 次观看 • 2 个月前

🚨 Scientists discover wisdom teeth contain stem cells capable of repairing the heart, brain, and bones. Wisdom teeth contain dental pulp, a soft connective tissue threaded with blood vessels and nerves. Inside that pulp lives a dense population of mesenchymal stem cells, a class of undifferentiated cells that researchers classify as among the most therapeutically valuable biological material a human body produces. These are not ordinary cells maintaining routine tissue. They are blueprint cells, capable of receiving chemical signals from damaged environments and reshaping themselves into whatever the body needs most, neurons, cardiomyocytes, osteoblasts, even hepatic cells under the right conditions. The brain operates under a brutal rule: most of its neurons do not regenerate after damage. A stroke, a traumatic injury, a neurodegenerative disease removes cells the brain cannot replace through normal biological processes. Researchers have spent decades attempting to solve this through synthetic means, engineered cell therapies, growth factor injections, gene editing approaches that cost extraordinary resources and produce inconsistent results. What dental pulp stem cells demonstrated in laboratory conditions is that they can migrate toward neural damage sites, integrate with existing tissue architecture, and begin producing neurons and glial support cells. The mechanism involves neurotrophic factor secretion, essentially the cells releasing signaling proteins that stimulate the surrounding neural environment to repair itself from within. Cardiac muscle operates under a similarly unforgiving rule. After a heart attack, the dead muscle tissue becomes fibrotic scar material. The heart compensates by making surviving muscle work harder, a process that gradually leads to enlargement, weakening, and eventual failure. Dental pulp stem cells introduced into cardiac tissue in multiple studies produced measurable reductions in scar formation and demonstrated the ability to differentiate into functional cardiomyocytes, beating in synchrony with native heart cells. Some studies recorded improved ejection fraction in animal models, the core measurement of how effectively the heart pumps blood. Bone regeneration represents the most clinically advanced application already moving toward human trials. Dental pulp stem cells express high levels of osteogenic markers and respond rapidly to bone morphogenetic proteins, the chemical messengers that trigger skeletal repair. Their application in craniofacial reconstruction, spinal fusion, and long bone defect repair is being studied across multiple institutions simultaneously. What separates these cells from other stem cell sources is the combination of accessibility and biological youth. Bone marrow aspiration requires sedation and produces significant post procedure pain. Umbilical cord blood requires planning around birth. Wisdom teeth emerge between 17 and 25, during peak cellular vitality, and come out during a procedure most people already schedule. The extraction window is permanent. Once the teeth are gone and the pulp degrades, that specific population of young, highly potent cells is irretrievable from that individual. Cryogenic preservation protocols now exist that maintain dental pulp stem cell viability for over two decades. Several countries have commercial dental stem cell banks operating with the same institutional model as cord blood banking, long term frozen storage, indexed against future therapeutic need. The science supporting the value of preservation is no longer speculative. What lags behind is public awareness and clinical infrastructure in markets where this remains obscure. The wider pattern is worth recognizing. Medicine has repeatedly discovered that profound biological tools were present in tissues it previously categorized as vestigial, unnecessary, or inconvenient. The appendix was considered evolutionary junk for over a century before researchers identified its role in gut microbiome preservation. Wisdom teeth carried the same dismissal, a developmental relic from ancestors who needed extra molars for coarse diets, relevant only in their capacity to cause orthodontic problems. The pulp inside them was never junk. It was a repair system the body built during youth and stored in one of the most protected anatomical locations, surrounded by enamel, the hardest substance the human body produces. Evolution rarely wastes that kind of architecture.
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🚨 Scientists discover wisdom teeth contain stem cells capable of repairing the heart, brain, and bones. Wisdom teeth contain dental pulp, a soft connective tissue threaded with blood vessels and nerves. Inside that pulp lives a dense population of mesenchymal stem cells, a class of undifferentiated cells that researchers classify as among the most therapeutically valuable biological material a human body produces. These are not ordinary cells maintaining routine tissue. They are blueprint cells, capable of receiving chemical signals from damaged environments and reshaping themselves into whatever the body needs most, neurons, cardiomyocytes, osteoblasts, even hepatic cells under the right conditions. The brain operates under a brutal rule: most of its neurons do not regenerate after damage. A stroke, a traumatic injury, a neurodegenerative disease removes cells the brain cannot replace through normal biological processes. Researchers have spent decades attempting to solve this through synthetic means, engineered cell therapies, growth factor injections, gene editing approaches that cost extraordinary resources and produce inconsistent results. What dental pulp stem cells demonstrated in laboratory conditions is that they can migrate toward neural damage sites, integrate with existing tissue architecture, and begin producing neurons and glial support cells. The mechanism involves neurotrophic factor secretion, essentially the cells releasing signaling proteins that stimulate the surrounding neural environment to repair itself from within. Cardiac muscle operates under a similarly unforgiving rule. After a heart attack, the dead muscle tissue becomes fibrotic scar material. The heart compensates by making surviving muscle work harder, a process that gradually leads to enlargement, weakening, and eventual failure. Dental pulp stem cells introduced into cardiac tissue in multiple studies produced measurable reductions in scar formation and demonstrated the ability to differentiate into functional cardiomyocytes, beating in synchrony with native heart cells. Some studies recorded improved ejection fraction in animal models, the core measurement of how effectively the heart pumps blood. Bone regeneration represents the most clinically advanced application already moving toward human trials. Dental pulp stem cells express high levels of osteogenic markers and respond rapidly to bone morphogenetic proteins, the chemical messengers that trigger skeletal repair. Their application in craniofacial reconstruction, spinal fusion, and long bone defect repair is being studied across multiple institutions simultaneously. What separates these cells from other stem cell sources is the combination of accessibility and biological youth. Bone marrow aspiration requires sedation and produces significant post procedure pain. Umbilical cord blood requires planning around birth. Wisdom teeth emerge between 17 and 25, during peak cellular vitality, and come out during a procedure most people already schedule. The extraction window is permanent. Once the teeth are gone and the pulp degrades, that specific population of young, highly potent cells is irretrievable from that individual. Cryogenic preservation protocols now exist that maintain dental pulp stem cell viability for over two decades. Several countries have commercial dental stem cell banks operating with the same institutional model as cord blood banking, long term frozen storage, indexed against future therapeutic need. The science supporting the value of preservation is no longer speculative. What lags behind is public awareness and clinical infrastructure in markets where this remains obscure. The wider pattern is worth recognizing. Medicine has repeatedly discovered that profound biological tools were present in tissues it previously categorized as vestigial, unnecessary, or inconvenient. The appendix was considered evolutionary junk for over a century before researchers identified its role in gut microbiome preservation. Wisdom teeth carried the same dismissal, a developmental relic from ancestors who needed extra molars for coarse diets, relevant only in their capacity to cause orthodontic problems. The pulp inside them was never junk. It was a repair system the body built during youth and stored in one of the most protected anatomical locations, surrounded by enamel, the hardest substance the human body produces. Evolution rarely wastes that kind of architecture.

The Curious Tales

24,267 次观看 • 5 个月前

A single E. coli cell, placed on a dish, will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.
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A single E. coli cell, placed on a dish, will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.

Niko McCarty.

58,047 次观看 • 1 年前

💪 Muscle cells merging in real time You’re watching one of [in my opinion] the coolest things your body does without you ever noticing (muscle precursor cells literally fusing into one long, powerful fiber). 🔵 Alignment: individual myoblasts migrate and line up like they’re preparing for formation 🟢 Recognition: cells “sense” compatible neighbors through surface proteins 🟡 Contact: membranes begin to thin and synchronize their signaling 🟠 Fusion: boundaries dissolve and nuclei gather inside a shared cytoplasm 🔴 Strengthening: the new multinucleated fiber becomes the machinery that lets you lift, run, and repair The glowing green nuclei are each a tiny command center contributed by a merging cell. The red signal traces the membranes as they stretch, touch, and finally blend into a unified structure. This is how muscles grow and regenerate - i.e. this is "strength" engineerednat the cellular level Credit: Yue Lu, Elizabeth Chen Lab
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💪 Muscle cells merging in real time You’re watching one of [in my opinion] the coolest things your body does without you ever noticing (muscle precursor cells literally fusing into one long, powerful fiber). 🔵 Alignment: individual myoblasts migrate and line up like they’re preparing for formation 🟢 Recognition: cells “sense” compatible neighbors through surface proteins 🟡 Contact: membranes begin to thin and synchronize their signaling 🟠 Fusion: boundaries dissolve and nuclei gather inside a shared cytoplasm 🔴 Strengthening: the new multinucleated fiber becomes the machinery that lets you lift, run, and repair The glowing green nuclei are each a tiny command center contributed by a merging cell. The red signal traces the membranes as they stretch, touch, and finally blend into a unified structure. This is how muscles grow and regenerate - i.e. this is "strength" engineerednat the cellular level Credit: Yue Lu, Elizabeth Chen Lab

William A. Wallace, Ph.D.

40,417 次观看 • 8 个月前

🚨 SCIENTISTS MAY HAVE FOUND A WAY TO STOP BLINDNESS BEFORE VISION IS LOST. Researchers have developed a new laser-based treatment that gently heats the back of the eye not to destroy tissue, but to activate the eye’s own repair systems. The target is dry age-related macular degeneration (AMD) one of the leading causes of blindness worldwide. Around one in three people over 80 develop it, and until now there have been almost no ways to stop it early. Why this matters: Instead of waiting for vision loss and then trying to replace damaged cells, this treatment uses precisely controlled near-infrared laser pulses to raise retinal temperature by just a few degrees. That tiny heat signal triggers: • heat shock proteins • cellular repair mechanisms • autophagy (the cell’s own waste-removal process) In simple terms: the laser may help aging eye cells clean and repair themselves before permanent damage occurs. The deeper implication is enormous: Future medicine may not always work by replacing broken parts. It may work by reactivating the repair systems evolution already built into us. What if many age-related diseases, including blindness, begin when our cells simply lose the ability to clean up after themselves? Follow for more frontier medicine and future science.
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🚨 SCIENTISTS MAY HAVE FOUND A WAY TO STOP BLINDNESS BEFORE VISION IS LOST. Researchers have developed a new laser-based treatment that gently heats the back of the eye not to destroy tissue, but to activate the eye’s own repair systems. The target is dry age-related macular degeneration (AMD) one of the leading causes of blindness worldwide. Around one in three people over 80 develop it, and until now there have been almost no ways to stop it early. Why this matters: Instead of waiting for vision loss and then trying to replace damaged cells, this treatment uses precisely controlled near-infrared laser pulses to raise retinal temperature by just a few degrees. That tiny heat signal triggers: • heat shock proteins • cellular repair mechanisms • autophagy (the cell’s own waste-removal process) In simple terms: the laser may help aging eye cells clean and repair themselves before permanent damage occurs. The deeper implication is enormous: Future medicine may not always work by replacing broken parts. It may work by reactivating the repair systems evolution already built into us. What if many age-related diseases, including blindness, begin when our cells simply lose the ability to clean up after themselves? Follow for more frontier medicine and future science.

TheNewPhysics

43,943 次观看 • 3 个月前

Some microbes carry a protein, called SNIPE, that "chops up" phage DNA as it's being injected into the cell. This is a new mechanism for phage defense! CRISPR–Cas and restriction enzymes also evolved to fight against phages, but they work by recognizing sequences. SNIPE works, instead, by sensing "touch." SNIPE is a protein with about 500 amino acids. After it's made by the ribosome, it latches onto ManYZ, two proteins which sit on the cell's inner membrane. (ManYZ is an importer; it brings mannose and other sugars into the cell.) Once attached to ManYZ, SNIPE sits and waits for an invading phage. Some phages, including lambda, actually infect cells by pushing their DNA through this ManYZ channel. Lambda uses its "tail" to reach inside the protein channel, basically, and inject its DNA. When this physical touch happens, though, SNIPE is waiting. As soon as the phage DNA starts entering the cell, and passes through ManYZ and SNIPE, it gets immediately destroyed. This means that SNIPE is the first phage defense system discovered, so far, that uses spatial positioning at the injection site to destroy invaders. But there are caveats, of course. If you untether SNIPE from ManYZ, such that it can freely diffuse through the cell, it will chew up the bacterium's genome. It is not a highly discerning nuclease! Also, SNIPE is not found in most bacteria. A prior pangenome study, which sequenced lots of different microbes, found that roughly a third of well-studied bacterial lineages had at least one member with a SNIPE-like protein. (For this paper, they just ported one of those homologs into an E. coli laboratory strain.) And finally, because SNIPE's mechanism is tightly tied to ManYZ, it cannot be used to defend against phages that enter the cell through different routes. T4 phages, for example, inject their DNA straight through the cell membrane and into the cytoplasm, without interacting with ManYZ. This is a nice basic science paper. Applications TBD. (Just remember that scientists figured out that bacteria had a phage defense system, called CRISPR-Cas, many years before it was repurposed into a gene-editing tool.) P.S. The video below shows how cells with the SNIPE gene (middle row) kill invading phages, and thus continue growing and dividing. Empty vector (top row) refers to bacteria carrying a plasmid with no SNIPE gene; this is a control group. And SNIPE E414A refers to cells which received a mutated SNIPE gene, where the glutamate at position 414 has been changed to an alanine, thus destroying the protein's nuclease activity. These cells also die when they get infected with a phage.
0:10

Some microbes carry a protein, called SNIPE, that "chops up" phage DNA as it's being injected into the cell. This is a new mechanism for phage defense! CRISPR–Cas and restriction enzymes also evolved to fight against phages, but they work by recognizing sequences. SNIPE works, instead, by sensing "touch." SNIPE is a protein with about 500 amino acids. After it's made by the ribosome, it latches onto ManYZ, two proteins which sit on the cell's inner membrane. (ManYZ is an importer; it brings mannose and other sugars into the cell.) Once attached to ManYZ, SNIPE sits and waits for an invading phage. Some phages, including lambda, actually infect cells by pushing their DNA through this ManYZ channel. Lambda uses its "tail" to reach inside the protein channel, basically, and inject its DNA. When this physical touch happens, though, SNIPE is waiting. As soon as the phage DNA starts entering the cell, and passes through ManYZ and SNIPE, it gets immediately destroyed. This means that SNIPE is the first phage defense system discovered, so far, that uses spatial positioning at the injection site to destroy invaders. But there are caveats, of course. If you untether SNIPE from ManYZ, such that it can freely diffuse through the cell, it will chew up the bacterium's genome. It is not a highly discerning nuclease! Also, SNIPE is not found in most bacteria. A prior pangenome study, which sequenced lots of different microbes, found that roughly a third of well-studied bacterial lineages had at least one member with a SNIPE-like protein. (For this paper, they just ported one of those homologs into an E. coli laboratory strain.) And finally, because SNIPE's mechanism is tightly tied to ManYZ, it cannot be used to defend against phages that enter the cell through different routes. T4 phages, for example, inject their DNA straight through the cell membrane and into the cytoplasm, without interacting with ManYZ. This is a nice basic science paper. Applications TBD. (Just remember that scientists figured out that bacteria had a phage defense system, called CRISPR-Cas, many years before it was repurposed into a gene-editing tool.) P.S. The video below shows how cells with the SNIPE gene (middle row) kill invading phages, and thus continue growing and dividing. Empty vector (top row) refers to bacteria carrying a plasmid with no SNIPE gene; this is a control group. And SNIPE E414A refers to cells which received a mutated SNIPE gene, where the glutamate at position 414 has been changed to an alanine, thus destroying the protein's nuclease activity. These cells also die when they get infected with a phage.

Niko McCarty.

20,536 次观看 • 6 个月前

New Cell paper from Bergles lab at Johns Hopkins just built the most comprehensive map of brain myelin ever made — every oligodendrocyte, across the entire mouse brain, across the lifespan. The scale: >10 million cells per brain, terabyte-scale 3D lightsheet volumes, registered to the Allen Brain Atlas across 417 regions from 2 months to 2+ years of age. The technical stack: Custom tissue clearing (CUBIC-L + SHIELD + uRIMS with 40% urea) to preserve endogenous fluorescence. 3D Mask R-CNN for instance segmentation — not just semantic, instance — so it can distinguish individual cells within dense clusters at scale via overlapping sliding windows. Vision Transformer to classify newly-formed vs. mature oligodendrocytes using soma morphology. All cross-referenced against Allen ISH transcriptomics and MICrONS serial EM. What they found: Oligodendrocyte density varies 10,000-fold across brain regions. Left-right hemispheres: r=0.99. Sex: no significant difference. Strain: matters. The brain never stops myelinating. New oligodendrocytes are still being generated in 2-year-old mice. Prefrontal cortex L6 shows the fastest rates of new myelination into old age — the circuits for executive function keep rewiring throughout life. After demyelination, L4 sensory cortex is the most resilient — oligodendrocytes survive at higher rates. The hippocampus loses nearly everything and barely recovers. Degree of injury doesn't predict rate of recovery. These are independent axes. The Alzheimer's result is the most surprising: Dense-core plaques dominate in cortex and hippocampus. Diffuse/small-core plaques dominate in white matter fiber tracts. Old assumption: diffuse plaques are "less toxic." The data says the opposite — small plaques in fiber tracts cause more myelin loss per plaque than dense-core plaques in gray matter. Plaque load and oligodendrocyte loss are essentially uncorrelated (ρ=0.22). The damage is plaque-type and location specific, not load-dependent. For MS and AD research: you can't read off white matter injury from gray matter plaque burden. The pathology in fiber tracts is running on different rules. Data: Paper:
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New Cell paper from Bergles lab at Johns Hopkins just built the most comprehensive map of brain myelin ever made — every oligodendrocyte, across the entire mouse brain, across the lifespan. The scale: >10 million cells per brain, terabyte-scale 3D lightsheet volumes, registered to the Allen Brain Atlas across 417 regions from 2 months to 2+ years of age. The technical stack: Custom tissue clearing (CUBIC-L + SHIELD + uRIMS with 40% urea) to preserve endogenous fluorescence. 3D Mask R-CNN for instance segmentation — not just semantic, instance — so it can distinguish individual cells within dense clusters at scale via overlapping sliding windows. Vision Transformer to classify newly-formed vs. mature oligodendrocytes using soma morphology. All cross-referenced against Allen ISH transcriptomics and MICrONS serial EM. What they found: Oligodendrocyte density varies 10,000-fold across brain regions. Left-right hemispheres: r=0.99. Sex: no significant difference. Strain: matters. The brain never stops myelinating. New oligodendrocytes are still being generated in 2-year-old mice. Prefrontal cortex L6 shows the fastest rates of new myelination into old age — the circuits for executive function keep rewiring throughout life. After demyelination, L4 sensory cortex is the most resilient — oligodendrocytes survive at higher rates. The hippocampus loses nearly everything and barely recovers. Degree of injury doesn't predict rate of recovery. These are independent axes. The Alzheimer's result is the most surprising: Dense-core plaques dominate in cortex and hippocampus. Diffuse/small-core plaques dominate in white matter fiber tracts. Old assumption: diffuse plaques are "less toxic." The data says the opposite — small plaques in fiber tracts cause more myelin loss per plaque than dense-core plaques in gray matter. Plaque load and oligodendrocyte loss are essentially uncorrelated (ρ=0.22). The damage is plaque-type and location specific, not load-dependent. For MS and AD research: you can't read off white matter injury from gray matter plaque burden. The pathology in fiber tracts is running on different rules. Data: Paper:

Bo Wang

24,777 次观看 • 6 个月前

Neuralink Integration with ANKTIVA for Revolutionary Immunotherapy Elon Musk, a visionary collaboration opportunity by Dr. Sarabi and Grok. Dear Mr Musk: Good morning sir! I would like to bring to your attention the remarkable work of Dr. Patrick Soon-Shiong, who has developed a groundbreaking therapy, Anktiva, capable of supercharging key immune molecules to combat cancer and COVID-19. In a recent discussion with Tucker Carlson, Dr. Soon-Shiong described this advance as akin to the “E=mc²” of medicine—the discovery of “God’s equation,” a biological key that has eluded us for half a century until now. Just as Tesla has revolutionized the automotive and environmental industries, and SpaceX has advanced the expansion of humanity into a multi-planetary species to ensure our long-term survival, Anktiva represents a comparable paradigm shift in medicine, safeguarding human health and endurance. Given your shared commitment to advancing humanity, I respectfully inquire whether you might consider extending your support to Dr. Soon-Shiong in this critical pursuit. Moreover, I propose exploring the integration of Neuralink, employing the stepwise protocol outlined below, in collaboration with Dr. Soon-Shiong. Such a partnership could propel an unprecedented advancement in medicine and the future of humankind. Grok has developed a preliminary conceptual integration of Neuralink to enhance and supercharge IL-15 production 1/7: Identify Target Neural Circuits • Map the hypothalamic paraventricular nucleus (PVN) and dorsal motor nucleus of the vagus • Trace efferent projections from the PVN to the intermediolateral cell column (IML) in the spinal cord. • Identify sympathetic nerve fibers innervating the spleen and lymph nodes. • Map vagus nerve branches terminating in gut-associated lymphoid tissue and the hepatic portal system. 2/7: Implant Neuralink and Integrate with Neural Pathways • Place Neuralink electrodes in the PVN and dorsal motor nucleus of the vagus, using extended threads for subcortical/brainstem access. • Configure for recording/stimulation to modulate autonomic outflow to the IML at thoracic spinal levels. • Establish central control over peripheral pathways (e.g., splenic/vagus nerves) via targeted brain stimulation. 3/7: Develop Stimulation Protocols • Program Neuralink for high-frequency stimulation to the PVN for sympathetic activation. • Apply low-frequency patterned stimulation to the dorsal motor nucleus to engage feedback loops. • Modulate splenic/vagal pathways with phase-locked cycles through central interfaces. 4/7: Initiate Immune Cell Activation • Stimulate pathways to induce IFN-γ and TNF-α release in spleen/lymph nodes. • Trigger IL-15 transcription/translation in dendritic cells, monocytes, and epithelial cells. • Monitor for increased membrane-bound IL-15/IL-15Rα complex formation. 5/7: Enhance Local IL-15 Presentation • Concentrate stimulation at tumor/inflammation sites. • Promote immune cell clustering via chemokine/adhesion molecule induction. • Sustain localized IL-15/IL-15Rα trans-presentation to NK and CD8+ T cells. 6/7: Implement Real-Time Monitoring and Feedback • Record neural/immune biomarkers continuously via Neuralink telemetry. • Adjust stimulation based on IL-15 levels and NK/T cell activity. • Set safety thresholds to avoid excessive immune activation. 7/7: Synchronize with Immunotherapy • Time stimulation with IL-15 superagonists or adoptive therapies. • Evaluate synergies using immune monitoring/imaging. • Optimize based on patient responses. Thank you! #Neuralink #ANKTIVA #Grok #trendingvideo #cancer #medicalnews #health #trendingnow
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Neuralink Integration with ANKTIVA for Revolutionary Immunotherapy Elon Musk, a visionary collaboration opportunity by Dr. Sarabi and Grok. Dear Mr Musk: Good morning sir! I would like to bring to your attention the remarkable work of Dr. Patrick Soon-Shiong, who has developed a groundbreaking therapy, Anktiva, capable of supercharging key immune molecules to combat cancer and COVID-19. In a recent discussion with Tucker Carlson, Dr. Soon-Shiong described this advance as akin to the “E=mc²” of medicine—the discovery of “God’s equation,” a biological key that has eluded us for half a century until now. Just as Tesla has revolutionized the automotive and environmental industries, and SpaceX has advanced the expansion of humanity into a multi-planetary species to ensure our long-term survival, Anktiva represents a comparable paradigm shift in medicine, safeguarding human health and endurance. Given your shared commitment to advancing humanity, I respectfully inquire whether you might consider extending your support to Dr. Soon-Shiong in this critical pursuit. Moreover, I propose exploring the integration of Neuralink, employing the stepwise protocol outlined below, in collaboration with Dr. Soon-Shiong. Such a partnership could propel an unprecedented advancement in medicine and the future of humankind. Grok has developed a preliminary conceptual integration of Neuralink to enhance and supercharge IL-15 production 1/7: Identify Target Neural Circuits • Map the hypothalamic paraventricular nucleus (PVN) and dorsal motor nucleus of the vagus • Trace efferent projections from the PVN to the intermediolateral cell column (IML) in the spinal cord. • Identify sympathetic nerve fibers innervating the spleen and lymph nodes. • Map vagus nerve branches terminating in gut-associated lymphoid tissue and the hepatic portal system. 2/7: Implant Neuralink and Integrate with Neural Pathways • Place Neuralink electrodes in the PVN and dorsal motor nucleus of the vagus, using extended threads for subcortical/brainstem access. • Configure for recording/stimulation to modulate autonomic outflow to the IML at thoracic spinal levels. • Establish central control over peripheral pathways (e.g., splenic/vagus nerves) via targeted brain stimulation. 3/7: Develop Stimulation Protocols • Program Neuralink for high-frequency stimulation to the PVN for sympathetic activation. • Apply low-frequency patterned stimulation to the dorsal motor nucleus to engage feedback loops. • Modulate splenic/vagal pathways with phase-locked cycles through central interfaces. 4/7: Initiate Immune Cell Activation • Stimulate pathways to induce IFN-γ and TNF-α release in spleen/lymph nodes. • Trigger IL-15 transcription/translation in dendritic cells, monocytes, and epithelial cells. • Monitor for increased membrane-bound IL-15/IL-15Rα complex formation. 5/7: Enhance Local IL-15 Presentation • Concentrate stimulation at tumor/inflammation sites. • Promote immune cell clustering via chemokine/adhesion molecule induction. • Sustain localized IL-15/IL-15Rα trans-presentation to NK and CD8+ T cells. 6/7: Implement Real-Time Monitoring and Feedback • Record neural/immune biomarkers continuously via Neuralink telemetry. • Adjust stimulation based on IL-15 levels and NK/T cell activity. • Set safety thresholds to avoid excessive immune activation. 7/7: Synchronize with Immunotherapy • Time stimulation with IL-15 superagonists or adoptive therapies. • Evaluate synergies using immune monitoring/imaging. • Optimize based on patient responses. Thank you! #Neuralink #ANKTIVA #Grok #trendingvideo #cancer #medicalnews #health #trendingnow

Dr. Kash Sarabi

16,057 次观看 • 1 年前

The bacterial flagellum looks like a simple tail, or whip. But it’s actually a rotating motor, and perhaps the most sophisticated protein complex nature has ever evolved. In e. coli, these motors are capable of astonishing speeds; about 15,000 rpm. (The world record, according to one study, is for a Vibrio cell that was “clocked at 100,000 rpm by laser microscopy.) The flagellum propels the cell forward at speeds of 20-30 microns per second, or roughly 15 body lengths per second. If scaled up to the size of a cheetah, E. coli would *nearly* be the fastest land organism. The darting movements of a microbe were first observed in 1676 by Antony van Leeuwenhoek, a Dutch cloth merchant. Antony was delighted by the motion of his “animalcules,” writing: “I must say, for my part, that no more pleasant sight has ever yet come before my eye than these many thousands of living creatures, seen all alive in a little drop of water, moving among one another, each several creature having its own proper motion.” But Leeuwenhoek did not see flagella. He assumed, rather, that these animalcules must be “furnished with paws” instead. Christian Ehrenberg would not properly describe flagella until 1836. But amazingly, all the way up until the 1970s, nobody actually knew how the flagellum spun! In 1973, there were two competing models people argued over: the helical-wave (bending) model and the rotating (corkscrew) model. The first model suggested that the flagellum whipped back and forth, side-to-side, to propel the cell like paddle. The corkscrew model suggested that the whole flagellum instead spins around like a screw. In 1974, the corkscrew model finally won out. For two separate studies, scientists affixed flagella to glass slides using antibodies, and watched as the cells spun around and around like corkscrews. And finally, in just the last year, high-resolution structures of the flagellum have revealed a LOT more about its intricate assembly. The tail is made from ~20,000 self-assembling copies of a single protein, called flagellin. A “driveshaft,” or rod, spins the tail and is itself made of 26 protein subunits. Each “motor” in E. coli consists of 11 stators, each of which is made from 7 proteins.(Other types of cells have even more stators, and swim with much higher torques.) The flagellum spins when protons flow into the cell through tiny channels in these stators; akin to water running through a turbine. Each proton makes a small part of the stator change shape and push against the rotor, nudging it forward one step. With dozens of stators working at once, these nudges quickly spin the propeller. I'm writing an essay for Asimov Press about this now, and am really enjoying learning about the flagellum and its history. It's an extraordinarily complicated structure, though, and has been a challenge to understand!
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The bacterial flagellum looks like a simple tail, or whip. But it’s actually a rotating motor, and perhaps the most sophisticated protein complex nature has ever evolved. In e. coli, these motors are capable of astonishing speeds; about 15,000 rpm. (The world record, according to one study, is for a Vibrio cell that was “clocked at 100,000 rpm by laser microscopy.) The flagellum propels the cell forward at speeds of 20-30 microns per second, or roughly 15 body lengths per second. If scaled up to the size of a cheetah, E. coli would *nearly* be the fastest land organism. The darting movements of a microbe were first observed in 1676 by Antony van Leeuwenhoek, a Dutch cloth merchant. Antony was delighted by the motion of his “animalcules,” writing: “I must say, for my part, that no more pleasant sight has ever yet come before my eye than these many thousands of living creatures, seen all alive in a little drop of water, moving among one another, each several creature having its own proper motion.” But Leeuwenhoek did not see flagella. He assumed, rather, that these animalcules must be “furnished with paws” instead. Christian Ehrenberg would not properly describe flagella until 1836. But amazingly, all the way up until the 1970s, nobody actually knew how the flagellum spun! In 1973, there were two competing models people argued over: the helical-wave (bending) model and the rotating (corkscrew) model. The first model suggested that the flagellum whipped back and forth, side-to-side, to propel the cell like paddle. The corkscrew model suggested that the whole flagellum instead spins around like a screw. In 1974, the corkscrew model finally won out. For two separate studies, scientists affixed flagella to glass slides using antibodies, and watched as the cells spun around and around like corkscrews. And finally, in just the last year, high-resolution structures of the flagellum have revealed a LOT more about its intricate assembly. The tail is made from ~20,000 self-assembling copies of a single protein, called flagellin. A “driveshaft,” or rod, spins the tail and is itself made of 26 protein subunits. Each “motor” in E. coli consists of 11 stators, each of which is made from 7 proteins.(Other types of cells have even more stators, and swim with much higher torques.) The flagellum spins when protons flow into the cell through tiny channels in these stators; akin to water running through a turbine. Each proton makes a small part of the stator change shape and push against the rotor, nudging it forward one step. With dozens of stators working at once, these nudges quickly spin the propeller. I'm writing an essay for Asimov Press about this now, and am really enjoying learning about the flagellum and its history. It's an extraordinarily complicated structure, though, and has been a challenge to understand!

Niko McCarty.

51,913 次观看 • 1 年前

RULE #6 OF THE PRIMAL DIET Do not eat rock salt. Salt is a rock, and our body cannot process rocks. It has a toxic effect, different from the sodium found as a nutrient in plant or animal foods. Water dissolves rocks, and plants eat rocks, then animals eat plants, and we eat the plants or animals. This for us is food, the minerals are made into nutrients, becoming bio-available. Rock salt is very different from the sodium found in food. According to Aajonus, rock salt is an explosive: "I just want to make sure that you understand salt is dangerous. Salt is an explosive. It is more volatile than nitroglycerin. If you had a pure cake of sodium as big as a football it would take out all of New York City. Just like a 200 ton hydrogen bomb could take out New York City and all of its buildings. So [...] the government, the military gave General Electric 2 billion dollars to make a weapon, out of salt. My father worked on the project for 6 years. It was so untenable they could not make it into a bomb, thank God. Because one and a half degree temperature change a completely isolated sodium could set it off. So they could never temper it, never break it down and ulitize it." — Aajonus Rock salt is a mineral formed from sodium chloride (NaCl). When eating rock salt, during digestion, the sodium is separated from the chloride, so the sodium ion becomes isolated. Isolated sodium is more volatile than nitroglycerin, this is when it becomes an explosive. So during digestion and after, this isolated sodium creates micro-explosions in the blood, destroying other nutrients and killing cells. Aajonus describes in detail what is happening on a cellular level: "When the cell eats normally, there’s a whole network – smorgasbord of nutrients – anywhere from 97 to 117 nutrients…all your vitamins…all your minerals, fats …all the 60 varieties of cholesterol that can be formed …all the different proteins – pyruvates – all 22 amino acids. Everything is in this smorgasbord. When a cell eats, it gets the whole dose and it’s completely nutrified. When salt is eaten, it causes explosions of these nutrients so you may only get 27 or 57 of these nutrients into a cell at once. So every cell becomes deficient any time you use salt with a meal. Not only that, it dehydrates cells." Additionally, when the isolated sodium doesn't explode right away, it can draw other isolated sodium ions to itself, creating sodium clusters, and the magnetism of them can rip off the guts of cells. This makes using rock salt the second worst thing next to cooking in standard diet practices. "One million red blood cells are destroyed by one little grain of salt.", claims Aajonus. Of course, this is not noticeable right away, but long term, it creates significant damage. When part of raw foods, even during digestion, sodium is always bound to other nutrients, they are always connected on a chemical level, it doesn't get isolated and therefore doesn't have this damaging effect. This is why it is key to get sodium from food only. The body detoxifies the unusable, isolated, form of sodium by sweating it out when possible (the body is throwing it off, don't put it back in). Salt also ends up getting stored like most toxins that the body cannot process because they are in excess, which can lead to headaches when it finally gets detoxified. People who have been eating raw and salt-free for many years will often have an immediate reaction when eating salt: Aajonus explains that is what a healthy body does, it has the resources to immediately repeal a toxin instead of "giving up" and storing it somewhere in its tissues, getting more damaged from it. Rock salt also starts tasting too strong, which people report when eating salted cheese after having only eaten raw unsalted cheese for a while. What about salt licks? First of all, herbivores do this, not carnivores. What about sodium needs, and salt cravings? Needs are not the same with raw and cooked foods, but in either case, you get enough sodium from eating raw foods, there is plenty in raw milk, raw celery juice, raw tomatoes, and raw oysters. At least one or two of these foods can easily be added daily to anyone's diet. "Celery contains lots of sodium. The blood is very high like the ocean in sodium, Celery meets that almost perfectly without causing the clumping of the sodium molecules that rock salt does. Salt will destroy red blood cells very quickly, numbs nerves, burns them, ages prematurely inside even without noticing it, until it hits all of a sudden." — Aajonus Note: This is about eating salt. When used in bath, salt doesn't penetrate through the skin, and draws toxins out. It can still be drying and people without moisturized skin could get skin irritation from it.
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RULE #6 OF THE PRIMAL DIET Do not eat rock salt. Salt is a rock, and our body cannot process rocks. It has a toxic effect, different from the sodium found as a nutrient in plant or animal foods. Water dissolves rocks, and plants eat rocks, then animals eat plants, and we eat the plants or animals. This for us is food, the minerals are made into nutrients, becoming bio-available. Rock salt is very different from the sodium found in food. According to Aajonus, rock salt is an explosive: "I just want to make sure that you understand salt is dangerous. Salt is an explosive. It is more volatile than nitroglycerin. If you had a pure cake of sodium as big as a football it would take out all of New York City. Just like a 200 ton hydrogen bomb could take out New York City and all of its buildings. So [...] the government, the military gave General Electric 2 billion dollars to make a weapon, out of salt. My father worked on the project for 6 years. It was so untenable they could not make it into a bomb, thank God. Because one and a half degree temperature change a completely isolated sodium could set it off. So they could never temper it, never break it down and ulitize it." — Aajonus Rock salt is a mineral formed from sodium chloride (NaCl). When eating rock salt, during digestion, the sodium is separated from the chloride, so the sodium ion becomes isolated. Isolated sodium is more volatile than nitroglycerin, this is when it becomes an explosive. So during digestion and after, this isolated sodium creates micro-explosions in the blood, destroying other nutrients and killing cells. Aajonus describes in detail what is happening on a cellular level: "When the cell eats normally, there’s a whole network – smorgasbord of nutrients – anywhere from 97 to 117 nutrients…all your vitamins…all your minerals, fats …all the 60 varieties of cholesterol that can be formed …all the different proteins – pyruvates – all 22 amino acids. Everything is in this smorgasbord. When a cell eats, it gets the whole dose and it’s completely nutrified. When salt is eaten, it causes explosions of these nutrients so you may only get 27 or 57 of these nutrients into a cell at once. So every cell becomes deficient any time you use salt with a meal. Not only that, it dehydrates cells." Additionally, when the isolated sodium doesn't explode right away, it can draw other isolated sodium ions to itself, creating sodium clusters, and the magnetism of them can rip off the guts of cells. This makes using rock salt the second worst thing next to cooking in standard diet practices. "One million red blood cells are destroyed by one little grain of salt.", claims Aajonus. Of course, this is not noticeable right away, but long term, it creates significant damage. When part of raw foods, even during digestion, sodium is always bound to other nutrients, they are always connected on a chemical level, it doesn't get isolated and therefore doesn't have this damaging effect. This is why it is key to get sodium from food only. The body detoxifies the unusable, isolated, form of sodium by sweating it out when possible (the body is throwing it off, don't put it back in). Salt also ends up getting stored like most toxins that the body cannot process because they are in excess, which can lead to headaches when it finally gets detoxified. People who have been eating raw and salt-free for many years will often have an immediate reaction when eating salt: Aajonus explains that is what a healthy body does, it has the resources to immediately repeal a toxin instead of "giving up" and storing it somewhere in its tissues, getting more damaged from it. Rock salt also starts tasting too strong, which people report when eating salted cheese after having only eaten raw unsalted cheese for a while. What about salt licks? First of all, herbivores do this, not carnivores. What about sodium needs, and salt cravings? Needs are not the same with raw and cooked foods, but in either case, you get enough sodium from eating raw foods, there is plenty in raw milk, raw celery juice, raw tomatoes, and raw oysters. At least one or two of these foods can easily be added daily to anyone's diet. "Celery contains lots of sodium. The blood is very high like the ocean in sodium, Celery meets that almost perfectly without causing the clumping of the sodium molecules that rock salt does. Salt will destroy red blood cells very quickly, numbs nerves, burns them, ages prematurely inside even without noticing it, until it hits all of a sudden." — Aajonus Note: This is about eating salt. When used in bath, salt doesn't penetrate through the skin, and draws toxins out. It can still be drying and people without moisturized skin could get skin irritation from it.

The Primal Diet by Aajonus Vonderplanitz

18,211 次观看 • 2 年前

She Lived to 117. Scientists Studied Her for Months. Her Secret Cost $2. Maria Branyas Morera ate three yogurts a day. Every single day, for as long as anyone could remember. She mentioned this to anyone who asked about her longevity, which was often, and it was the kind of advice people receive with a warm smile and then immediately discard, because we prefer our longevity secrets to involve something more exotic than a supermarket dairy aisle. Maria died in Barcelona in 2024. She was 117. Then scientists actually looked inside her, and the smiling stopped. Her gut was packed with Bifidobacterium, a bacterium almost never found in people past 110, and far more commonly associated with infants. Her body had, in the most literal biological sense, not been informed of her actual age. It was operating on entirely different assumptions. Her DNA suggested she was somewhere between 100 and 110. She was 117. Seven years younger on the inside than the calendar insisted, which at 117 is not a rounding error. That is a extraordinary number. But to appreciate why any of this matters, you need to understand what kind of person we are talking about. Maria was born in San Francisco in 1907, the year before the Model T Ford, when Theodore Roosevelt was still in the White House and most of humanity died of things we now treat with a Tuesday afternoon at the pharmacy. Her Catalan father had come to America to make something of himself, and for a while it worked beautifully. He founded a Spanish-language magazine in New Orleans, one of the most chaotic, beautiful, swampy, and gastronomically unhinged cities on the continent, a place that has always operated on the reasonable philosophy that life is uncertain and the gumbo is excellent. Then the family got on a boat back to Spain. Maria fell on deck and permanently lost the hearing in one ear. Her father died of tuberculosis before the coast of Catalonia came into view. He was 37. She was eight. Her mother arrived in Europe with five children, no husband, and presumably very little appetite for what came next. Maria managed. She nursed soldiers in the Spanish Civil War. She outlived Franco, which required considerable patience. She raised three children. She played piano until she was 108. At 113 she caught COVID-19 and dispatched it, which at that point resembles less a medical event than a statement of intent. Then she joined Twitter. Her bio read: “I am old, very old, but not an idiot.” Her last request, before she died peacefully in her sleep, was three words: “Please study me.” The geneticists obliged with considerable enthusiasm, and their subsequent paper in Cell Reports Medicine runs to forty pages of scientists explaining, in the careful and hedged language that science requires, that this woman was remarkable in ways they had not previously encountered and were not entirely sure how to explain. The yogurt, it turns out, had been doing quiet and serious work for over a century. Nomadic peoples of Central Asia were fermenting milk 8,000 years ago, long before germ theory, before microscopes, before anyone had the faintest idea what a bacterium was. They didn’t need to understand it. Their guts understood it. The knowledge was older than writing. Maria understood it too. She didn’t publish a paper. She didn’t launch a wellness brand. She just ate her yogurt every morning and got on with the extraordinary business of being alive. Gandalv / Gandalv ✦ AI-generated image. Not the actual person. Full story:
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She Lived to 117. Scientists Studied Her for Months. Her Secret Cost $2. Maria Branyas Morera ate three yogurts a day. Every single day, for as long as anyone could remember. She mentioned this to anyone who asked about her longevity, which was often, and it was the kind of advice people receive with a warm smile and then immediately discard, because we prefer our longevity secrets to involve something more exotic than a supermarket dairy aisle. Maria died in Barcelona in 2024. She was 117. Then scientists actually looked inside her, and the smiling stopped. Her gut was packed with Bifidobacterium, a bacterium almost never found in people past 110, and far more commonly associated with infants. Her body had, in the most literal biological sense, not been informed of her actual age. It was operating on entirely different assumptions. Her DNA suggested she was somewhere between 100 and 110. She was 117. Seven years younger on the inside than the calendar insisted, which at 117 is not a rounding error. That is a extraordinary number. But to appreciate why any of this matters, you need to understand what kind of person we are talking about. Maria was born in San Francisco in 1907, the year before the Model T Ford, when Theodore Roosevelt was still in the White House and most of humanity died of things we now treat with a Tuesday afternoon at the pharmacy. Her Catalan father had come to America to make something of himself, and for a while it worked beautifully. He founded a Spanish-language magazine in New Orleans, one of the most chaotic, beautiful, swampy, and gastronomically unhinged cities on the continent, a place that has always operated on the reasonable philosophy that life is uncertain and the gumbo is excellent. Then the family got on a boat back to Spain. Maria fell on deck and permanently lost the hearing in one ear. Her father died of tuberculosis before the coast of Catalonia came into view. He was 37. She was eight. Her mother arrived in Europe with five children, no husband, and presumably very little appetite for what came next. Maria managed. She nursed soldiers in the Spanish Civil War. She outlived Franco, which required considerable patience. She raised three children. She played piano until she was 108. At 113 she caught COVID-19 and dispatched it, which at that point resembles less a medical event than a statement of intent. Then she joined Twitter. Her bio read: “I am old, very old, but not an idiot.” Her last request, before she died peacefully in her sleep, was three words: “Please study me.” The geneticists obliged with considerable enthusiasm, and their subsequent paper in Cell Reports Medicine runs to forty pages of scientists explaining, in the careful and hedged language that science requires, that this woman was remarkable in ways they had not previously encountered and were not entirely sure how to explain. The yogurt, it turns out, had been doing quiet and serious work for over a century. Nomadic peoples of Central Asia were fermenting milk 8,000 years ago, long before germ theory, before microscopes, before anyone had the faintest idea what a bacterium was. They didn’t need to understand it. Their guts understood it. The knowledge was older than writing. Maria understood it too. She didn’t publish a paper. She didn’t launch a wellness brand. She just ate her yogurt every morning and got on with the extraordinary business of being alive. Gandalv / Gandalv ✦ AI-generated image. Not the actual person. Full story:

Gandalv

16,674 次观看 • 5 个月前

~Hail Mary for the Vaccine-Injured: Hope for Nurse Lyndsey, RN 💜🐭 in Japan with Kevin W. McCairn PhD~ via: Mary Talley Bowden MD Nurse Lyndsey suffered severe post-vaccine injury in late 2020, with a Pfizer booster triggering persistent symptoms, including high cytokine levels & spike protein damage Neuroscientist Kevin McCairn theorizes that vaccine injuries stem from amyloid-like spike protein accumulation, similar to prion diseases He has developed a dual filtration plasma apheresis (DFPP) & stem cell therapy in Japan showing promise in reducing amyloid & symptoms in patients Though costly & not FDA-approved, the treatment offers hope for those like Lyndsey, urging wider adoption & research in the U.S In the shadow of the pandemic, stories like Lyndseys reveal a devastating undercurrent of injury & resilience As a dedicated nurse, Lindsey received her first two Moderna doses in late 2020, experiencing typical side effects like body aches, fever, & fainting Pressured by her workplace, she got a Pfizer booster, & tragically, this third shot triggered a cascade of unrelenting symptoms, marking her four-year “anniversary” of injury on the day of the interview Lyndseys ordeal began subtly, mirroring her prior reactions, but escalated on day 10 into a full cytokine storm Her interleukin-6 levels spiked to 48.8 (normal: 1-3), activating 11 out of 14 cytokines & exhausting her immune system She describes a life of constant pain, diminished quality of life, & unyielding spike protein production, confirmed by years of labs, videos, & panels “I’m dying every day,” she laments, highlighting the frustration of being dismissed by a system that mandated these shots Divorced & childless at 40, her dreams of family were shattered, underscoring the personal devastation amid a broader crisis affecting millions Enter Kevin McCairn, a neuroscientist displaced from academia by COVID controversies, who attributes such injuries to the spike protein’s amyloidogenic properties—inducing protein misfolding akin to prions in diseases like Parkinson’s or mad cow Drawing from biowarfare research suspicions, he argues the virus & vaccines exploit fibrin to form persistent clots, evading standard treatments like ivermectin, nattokinase, or EBOO apheresis His lab tests on over 100 patients, including embalmer clots, confirm amyloid signatures in blood, resistant to conventional protocols Hope emerges from McCairn’s innovative therapy in Japan: dual filtration plasma apheresis (DFPP) combined with stem cell growth factors. DFPP, a closed-circuit blood filtration via jugular catheter, scrubs amyloids & cytokines without donor plasma risks, while growth factors—derived from dental pulp stem cells—inhibit clot formation in vitro Early results are striking: a severe long-COVID patient reported brain fog lifting within hours; a vaccine-injured teen’s amyloid signals dropped significantly post-treatment Two sessions, plus daily IV infusions over two weeks, cost around $20,000-25,000—cheaper than U.S. equivalents but still burdensome This protocol, not FDA-approved yet common in Asia for autoimmune conditions, represents a “Hail Mary” for Lyndsey Crowdfunded efforts aim to cover her costs, emphasizing community over corporate accountability As McCairn notes, pharmaceutical giants like Pfizer should fund such recoveries, but delays could prove fatal Lyndseys story isn’t isolated; it’s a call to action against censorship, fraud, & neglect With data showing cytokine normalization & symptom relief, this treatment offers tangible hope, urging trials in the U.S. to restore lives ravaged by an experimental rollout In the end, healing demands not just science, but solidarity—proving that even in darkness, innovation & empathy can prevail - Mary Talley Bowden, MD Mary Talley Bowden MD
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~Hail Mary for the Vaccine-Injured: Hope for Nurse Lyndsey, RN 💜🐭 in Japan with Kevin W. McCairn PhD~ via: Mary Talley Bowden MD Nurse Lyndsey suffered severe post-vaccine injury in late 2020, with a Pfizer booster triggering persistent symptoms, including high cytokine levels & spike protein damage Neuroscientist Kevin McCairn theorizes that vaccine injuries stem from amyloid-like spike protein accumulation, similar to prion diseases He has developed a dual filtration plasma apheresis (DFPP) & stem cell therapy in Japan showing promise in reducing amyloid & symptoms in patients Though costly & not FDA-approved, the treatment offers hope for those like Lyndsey, urging wider adoption & research in the U.S In the shadow of the pandemic, stories like Lyndseys reveal a devastating undercurrent of injury & resilience As a dedicated nurse, Lindsey received her first two Moderna doses in late 2020, experiencing typical side effects like body aches, fever, & fainting Pressured by her workplace, she got a Pfizer booster, & tragically, this third shot triggered a cascade of unrelenting symptoms, marking her four-year “anniversary” of injury on the day of the interview Lyndseys ordeal began subtly, mirroring her prior reactions, but escalated on day 10 into a full cytokine storm Her interleukin-6 levels spiked to 48.8 (normal: 1-3), activating 11 out of 14 cytokines & exhausting her immune system She describes a life of constant pain, diminished quality of life, & unyielding spike protein production, confirmed by years of labs, videos, & panels “I’m dying every day,” she laments, highlighting the frustration of being dismissed by a system that mandated these shots Divorced & childless at 40, her dreams of family were shattered, underscoring the personal devastation amid a broader crisis affecting millions Enter Kevin McCairn, a neuroscientist displaced from academia by COVID controversies, who attributes such injuries to the spike protein’s amyloidogenic properties—inducing protein misfolding akin to prions in diseases like Parkinson’s or mad cow Drawing from biowarfare research suspicions, he argues the virus & vaccines exploit fibrin to form persistent clots, evading standard treatments like ivermectin, nattokinase, or EBOO apheresis His lab tests on over 100 patients, including embalmer clots, confirm amyloid signatures in blood, resistant to conventional protocols Hope emerges from McCairn’s innovative therapy in Japan: dual filtration plasma apheresis (DFPP) combined with stem cell growth factors. DFPP, a closed-circuit blood filtration via jugular catheter, scrubs amyloids & cytokines without donor plasma risks, while growth factors—derived from dental pulp stem cells—inhibit clot formation in vitro Early results are striking: a severe long-COVID patient reported brain fog lifting within hours; a vaccine-injured teen’s amyloid signals dropped significantly post-treatment Two sessions, plus daily IV infusions over two weeks, cost around $20,000-25,000—cheaper than U.S. equivalents but still burdensome This protocol, not FDA-approved yet common in Asia for autoimmune conditions, represents a “Hail Mary” for Lyndsey Crowdfunded efforts aim to cover her costs, emphasizing community over corporate accountability As McCairn notes, pharmaceutical giants like Pfizer should fund such recoveries, but delays could prove fatal Lyndseys story isn’t isolated; it’s a call to action against censorship, fraud, & neglect With data showing cytokine normalization & symptom relief, this treatment offers tangible hope, urging trials in the U.S. to restore lives ravaged by an experimental rollout In the end, healing demands not just science, but solidarity—proving that even in darkness, innovation & empathy can prevail - Mary Talley Bowden, MD Mary Talley Bowden MD

Lyndsey, RN 💜🐭

10,798 次观看 • 6 个月前

Never Knew This 🇺🇸🙏🇺🇸 The teenager working as a theater usher wasn't supposed to amount to much. He'd already dropped out of high school. He was sweeping up popcorn and tearing tickets when the news broke over the radio on December 7, 1941. Japan had bombed Pearl Harbor. Within weeks, he walked into a Marine Corps recruitment office and enlisted. Boot camp at New River, North Carolina broke him down and rebuilt him from scratch. He came out the other side leaner, harder, and assigned to the 2nd Marine Division — one of the most battle-tested units in the entire Pacific Theater. By mid-1942, his unit was training in Samoa. Everyone knew what was coming. On August 7, 1942, American forces launched their first major offensive against Japan — storming the beaches of a remote jungle island in the Solomon Islands called Guadalcanal. Military planners expected a quick victory. Instead, they walked into six months of savage, suffocating combat. Japanese forces counterattacked. A severe, life-threatening complication of malaria, blackwater fever causes red blood cells to rupture inside the body. Victims develop violent chills, raging fever, jaundice, and eventually kidney failure. The urine turns dark — almost black — as the body begins destroying itself from within. In the 1940s, without modern treatment, surviving it was considered extraordinary. Donald should not have made it. He was evacuated to a Navy hospital in Wellington, New Zealand, where he spent over a year fighting to live. There were days he couldn't stand. Days he couldn't eat. Days when the line between alive and gone felt impossibly thin. Against every expectation, he recovered. He returned to duty, was promoted to Corporal, and spent the remainder of the war as a Marine Drill Instructor — shaping the next generation of Marines with the same precision that had once been drilled into him. He was an expert marksman. He was honorably discharged in 1945. He'd married a nightclub singer named Adelaide Adams. They had daughters to feed and bills to pay and a future that wasn't at all guaranteed. He started doing stand-up. Then, to get called earlier at alphabetical auditions, he adopted his wife's last name professionally. Donald Yarmy became Don Adams. In 1954, he won on Arthur Godfrey's Talent Scouts, cracking open the door to television. Through the late 1950s and early 1960s, he appeared on The Ed Sullivan Show, The Steve Allen Show, and developed a lovably incompetent detective character that kept making audiences roar. Then in 1965, producers Mel Brooks and Buck Henry came calling. They were creating a spy spoof for NBC — a comedic takedown of Cold War paranoia and James Bond glamour. They needed someone to play Maxwell Smart, Agent 86, a bumbling secret agent who somehow always saved the day despite himself. Don Adams was born for the role. Get Smart premiered September 18, 1965, and became a cultural phenomenon almost overnight. Three Emmy Awards followed - 1967, 1968, 1969 — for Outstanding Performance. Later, a whole new generation of children would fall in love with his voice as the accident-prone Inspector Gadget, the bumbling cartoon detective who somehow always triumphed. They laughed without knowing anything about Guadalcanal. They just knew the voice made them happy. He never made his military service the centerpiece of his identity. Don Adams passed away on September 25, 2005, at age 82, from a lung infection. He was buried at Hollywood Forever Cemetery in Los Angeles, surrounded by the legends of an industry he'd helped define. It's in every person who still smiles when they hear "Would you believe..?" It's in every child who grew up watching Inspector Gadget and had no idea they were laughing at a warrior. It's in the quiet dignity of a man who faced death in a jungle at 18, came home with nothing, and built something beautiful anyway. Private Donald Yarmy survived when he shouldn't have. Don Adams made sure it meant something beautiful.
0:18

Never Knew This 🇺🇸🙏🇺🇸 The teenager working as a theater usher wasn't supposed to amount to much. He'd already dropped out of high school. He was sweeping up popcorn and tearing tickets when the news broke over the radio on December 7, 1941. Japan had bombed Pearl Harbor. Within weeks, he walked into a Marine Corps recruitment office and enlisted. Boot camp at New River, North Carolina broke him down and rebuilt him from scratch. He came out the other side leaner, harder, and assigned to the 2nd Marine Division — one of the most battle-tested units in the entire Pacific Theater. By mid-1942, his unit was training in Samoa. Everyone knew what was coming. On August 7, 1942, American forces launched their first major offensive against Japan — storming the beaches of a remote jungle island in the Solomon Islands called Guadalcanal. Military planners expected a quick victory. Instead, they walked into six months of savage, suffocating combat. Japanese forces counterattacked. A severe, life-threatening complication of malaria, blackwater fever causes red blood cells to rupture inside the body. Victims develop violent chills, raging fever, jaundice, and eventually kidney failure. The urine turns dark — almost black — as the body begins destroying itself from within. In the 1940s, without modern treatment, surviving it was considered extraordinary. Donald should not have made it. He was evacuated to a Navy hospital in Wellington, New Zealand, where he spent over a year fighting to live. There were days he couldn't stand. Days he couldn't eat. Days when the line between alive and gone felt impossibly thin. Against every expectation, he recovered. He returned to duty, was promoted to Corporal, and spent the remainder of the war as a Marine Drill Instructor — shaping the next generation of Marines with the same precision that had once been drilled into him. He was an expert marksman. He was honorably discharged in 1945. He'd married a nightclub singer named Adelaide Adams. They had daughters to feed and bills to pay and a future that wasn't at all guaranteed. He started doing stand-up. Then, to get called earlier at alphabetical auditions, he adopted his wife's last name professionally. Donald Yarmy became Don Adams. In 1954, he won on Arthur Godfrey's Talent Scouts, cracking open the door to television. Through the late 1950s and early 1960s, he appeared on The Ed Sullivan Show, The Steve Allen Show, and developed a lovably incompetent detective character that kept making audiences roar. Then in 1965, producers Mel Brooks and Buck Henry came calling. They were creating a spy spoof for NBC — a comedic takedown of Cold War paranoia and James Bond glamour. They needed someone to play Maxwell Smart, Agent 86, a bumbling secret agent who somehow always saved the day despite himself. Don Adams was born for the role. Get Smart premiered September 18, 1965, and became a cultural phenomenon almost overnight. Three Emmy Awards followed - 1967, 1968, 1969 — for Outstanding Performance. Later, a whole new generation of children would fall in love with his voice as the accident-prone Inspector Gadget, the bumbling cartoon detective who somehow always triumphed. They laughed without knowing anything about Guadalcanal. They just knew the voice made them happy. He never made his military service the centerpiece of his identity. Don Adams passed away on September 25, 2005, at age 82, from a lung infection. He was buried at Hollywood Forever Cemetery in Los Angeles, surrounded by the legends of an industry he'd helped define. It's in every person who still smiles when they hear "Would you believe..?" It's in every child who grew up watching Inspector Gadget and had no idea they were laughing at a warrior. It's in the quiet dignity of a man who faced death in a jungle at 18, came home with nothing, and built something beautiful anyway. Private Donald Yarmy survived when he shouldn't have. Don Adams made sure it meant something beautiful.

G-PA

70,214 次观看 • 6 个月前

The Chickenpox Virus Never Left. It May Have Been Slowly Rewiring Your Brain. There is a virus living inside you right now. It has been there since you were small, since the week you were covered in spots and your mother dabbed you with calamine lotion and told you not to scratch, which you did anyway. When the illness passed and you got on with the business of growing up, the virus did not leave. It retreated into your nerve cells, pulled the blanket over its head, and settled in for a very long stay indeed. That virus is varicella-zoster. And it is beginning to look like it may have a considerably larger amount to answer for than one miserable itchy week in childhood. The discovery came about in the way so many important ones do: almost entirely by accident, and in Wales. When health authorities rolled out their shingles vaccine program, they had to draw an eligibility line somewhere. People born before September 2, 1933 were out. People born on or after that date were in. A perfectly arbitrary cutoff, the kind bureaucracies produce routinely, without anyone imagining it might one day illuminate the workings of the aging human brain. And yet. Stanford researchers examined Welsh health records and found that those who received the shingles vaccine were 20 percent less likely to develop dementia over the following seven years. The two groups were otherwise essentially the same people: same education levels, same rates of diabetes and heart disease, same general relationship with healthcare. The only meaningful difference was a notable drop in dementia diagnoses among the vaccinated. They checked Australia. Same pattern. Then England, New Zealand, Canada. Dataset after dataset produced the same strong protective signal. At a certain point, when you keep seeing the same result everywhere you look, it stops resembling coincidence. A follow-up study in Cell found that the vaccine does not merely help prevent dementia in healthy people. Among those who already have it, the vaccinated were nearly 30 percent less likely to die from the disease over nine years, suggesting something closer to a therapeutic effect than a preventive one. Remarkable, for a vaccine designed to prevent a rash. The leading theory is not especially comforting. Varicella-zoster can reactivate quietly, below the threshold of obvious symptoms, causing slow cumulative damage through inflammation, abnormal protein accumulation, and changes to the small blood vessels supplying neural tissue. Those mechanisms overlap uncomfortably with the ones already implicated in Alzheimer’s disease. “In some ways,” one Harvard epidemiologist noted, “we are being lucky.” Lucky is putting it mildly. Dementia affects more than 55 million people worldwide, with no reliable treatment and no clear prevention strategy beyond the familiar advice about sleep and vegetables. And here, sitting on pharmacy shelves across the developed world, is a vaccine that has apparently been handing out significant neurological protection to everyone who rolled up their sleeve for it, without anyone fully realizing it was doing so. If you are over fifty and have not had your shingles vaccine, that is worth raising with your doctor. If you have, you may have done your brain a rather larger favour than you knew. Stay connected. Follow Gandalv Gandalv
0:10

The Chickenpox Virus Never Left. It May Have Been Slowly Rewiring Your Brain. There is a virus living inside you right now. It has been there since you were small, since the week you were covered in spots and your mother dabbed you with calamine lotion and told you not to scratch, which you did anyway. When the illness passed and you got on with the business of growing up, the virus did not leave. It retreated into your nerve cells, pulled the blanket over its head, and settled in for a very long stay indeed. That virus is varicella-zoster. And it is beginning to look like it may have a considerably larger amount to answer for than one miserable itchy week in childhood. The discovery came about in the way so many important ones do: almost entirely by accident, and in Wales. When health authorities rolled out their shingles vaccine program, they had to draw an eligibility line somewhere. People born before September 2, 1933 were out. People born on or after that date were in. A perfectly arbitrary cutoff, the kind bureaucracies produce routinely, without anyone imagining it might one day illuminate the workings of the aging human brain. And yet. Stanford researchers examined Welsh health records and found that those who received the shingles vaccine were 20 percent less likely to develop dementia over the following seven years. The two groups were otherwise essentially the same people: same education levels, same rates of diabetes and heart disease, same general relationship with healthcare. The only meaningful difference was a notable drop in dementia diagnoses among the vaccinated. They checked Australia. Same pattern. Then England, New Zealand, Canada. Dataset after dataset produced the same strong protective signal. At a certain point, when you keep seeing the same result everywhere you look, it stops resembling coincidence. A follow-up study in Cell found that the vaccine does not merely help prevent dementia in healthy people. Among those who already have it, the vaccinated were nearly 30 percent less likely to die from the disease over nine years, suggesting something closer to a therapeutic effect than a preventive one. Remarkable, for a vaccine designed to prevent a rash. The leading theory is not especially comforting. Varicella-zoster can reactivate quietly, below the threshold of obvious symptoms, causing slow cumulative damage through inflammation, abnormal protein accumulation, and changes to the small blood vessels supplying neural tissue. Those mechanisms overlap uncomfortably with the ones already implicated in Alzheimer’s disease. “In some ways,” one Harvard epidemiologist noted, “we are being lucky.” Lucky is putting it mildly. Dementia affects more than 55 million people worldwide, with no reliable treatment and no clear prevention strategy beyond the familiar advice about sleep and vegetables. And here, sitting on pharmacy shelves across the developed world, is a vaccine that has apparently been handing out significant neurological protection to everyone who rolled up their sleeve for it, without anyone fully realizing it was doing so. If you are over fifty and have not had your shingles vaccine, that is worth raising with your doctor. If you have, you may have done your brain a rather larger favour than you knew. Stay connected. Follow Gandalv Gandalv

Gandalv

42,699 次观看 • 4 个月前

What if any preparations have you seen Iran make ahead of the war? Can you discuss It’s missile capabilities? Any intelligence capabilities? Any surprises it might happen in store? When the 12-day war ended, I estimated that Iran would need about six months to recover, including its nuclear program. Contrary to popular belief, Iran did not lose its entire long-range or medium-range air defense network; while some launchers were damaged, the primary targets of the Israeli strikes were the radar systems. Once the radars were neutralized, Iran successfully hid the bulk of its remaining batteries, leaving much of its arsenal intact. In contrast, short-range systems like the Tor-M1 and domestic variants were heavily engaged against cruise missiles, often being lost or damaged only after their ammunition was completely exhausted. Since then, Iran has worked to rebuild its destroyed radar network and, above all, to implement a genuine counterintelligence doctrine. The Mossad operations against Iranian radars and air defense systems have shaped new perimeter defense and counterintelligence doctrines not only in Iran but in other countries as well. If we look at the quantity of weapons and the organization of armed groups during Iran’s most recent protests, I would say the problem of foreign intelligence operations inside the country remains severe. This seriously threatens much of Iran’s capabilities, and I foresee a wave of sabotage operations as a new war draws closer. Iran has begun receiving collaboration from China across multiple areas,from satellites to internal counterintelligence, but it may still take some time for this to produce tangible results. During the last years, the Mossad relied heavily on cell phones, using SMS for recruitment and accessing device GPS for target location. Iran has since focused intensely on preventing any repetition of this, and on this specific issue, the Chinese appear to have provided support. Although foreign intelligence services have operated extensively inside Iran, the scale of any armed opposition groups is negligible compared to the Iranian armed forces, which could still draw on allied paramilitaries and militias in neighboring countries, including the Houthis. Iran has become a missile power with a stockpile far larger than Western estimates suggest. As early as 1998, Iran was already producing missiles with ranges exceeding 1,000 km, and it has continued doing so ever since, developing 12 to 15 different models in that range - meaning all are capable of reaching Israel. That is nearly 30 years of continuous missile production, resulting in a stockpile of several thousands. Another area where Iran has emerged as a global power is drones, including underwater ones. Iran’s UUVs have evolved rapidly into mass-produced models with integrated AI, and I believe they hold some major surprises in reserve. A key point today is that the AN/TPY-2 radars, which played a critical role in tracking Iranian missiles, would be among the first targets to be engaged. These high-powered X-band radars are the backbone of regional missile defense, providing essential data to THAAD and Patriot batteries. However, because they are large, stationary, and emit high-energy signals, they are highly vulnerable to a first-strike or saturation attack, which would effectively 'blind' the entire defensive network. Obviously, a defense budget of nearly one trillion dollars cannot be compared to Iran’s, but the real question is whether the cost and effort are worth the potential casualties. Even without Israel, the Americans maintain an immense advantage in aerial operations over Iran; however, as I have stated before, this superiority does not translate to the maritime theater.
0:18

What if any preparations have you seen Iran make ahead of the war? Can you discuss It’s missile capabilities? Any intelligence capabilities? Any surprises it might happen in store? When the 12-day war ended, I estimated that Iran would need about six months to recover, including its nuclear program. Contrary to popular belief, Iran did not lose its entire long-range or medium-range air defense network; while some launchers were damaged, the primary targets of the Israeli strikes were the radar systems. Once the radars were neutralized, Iran successfully hid the bulk of its remaining batteries, leaving much of its arsenal intact. In contrast, short-range systems like the Tor-M1 and domestic variants were heavily engaged against cruise missiles, often being lost or damaged only after their ammunition was completely exhausted. Since then, Iran has worked to rebuild its destroyed radar network and, above all, to implement a genuine counterintelligence doctrine. The Mossad operations against Iranian radars and air defense systems have shaped new perimeter defense and counterintelligence doctrines not only in Iran but in other countries as well. If we look at the quantity of weapons and the organization of armed groups during Iran’s most recent protests, I would say the problem of foreign intelligence operations inside the country remains severe. This seriously threatens much of Iran’s capabilities, and I foresee a wave of sabotage operations as a new war draws closer. Iran has begun receiving collaboration from China across multiple areas,from satellites to internal counterintelligence, but it may still take some time for this to produce tangible results. During the last years, the Mossad relied heavily on cell phones, using SMS for recruitment and accessing device GPS for target location. Iran has since focused intensely on preventing any repetition of this, and on this specific issue, the Chinese appear to have provided support. Although foreign intelligence services have operated extensively inside Iran, the scale of any armed opposition groups is negligible compared to the Iranian armed forces, which could still draw on allied paramilitaries and militias in neighboring countries, including the Houthis. Iran has become a missile power with a stockpile far larger than Western estimates suggest. As early as 1998, Iran was already producing missiles with ranges exceeding 1,000 km, and it has continued doing so ever since, developing 12 to 15 different models in that range - meaning all are capable of reaching Israel. That is nearly 30 years of continuous missile production, resulting in a stockpile of several thousands. Another area where Iran has emerged as a global power is drones, including underwater ones. Iran’s UUVs have evolved rapidly into mass-produced models with integrated AI, and I believe they hold some major surprises in reserve. A key point today is that the AN/TPY-2 radars, which played a critical role in tracking Iranian missiles, would be among the first targets to be engaged. These high-powered X-band radars are the backbone of regional missile defense, providing essential data to THAAD and Patriot batteries. However, because they are large, stationary, and emit high-energy signals, they are highly vulnerable to a first-strike or saturation attack, which would effectively 'blind' the entire defensive network. Obviously, a defense budget of nearly one trillion dollars cannot be compared to Iran’s, but the real question is whether the cost and effort are worth the potential casualties. Even without Israel, the Americans maintain an immense advantage in aerial operations over Iran; however, as I have stated before, this superiority does not translate to the maritime theater.

Patricia Marins

21,142 次观看 • 6 个月前

🚨 ATLANTIS WAS NEVER ON EARTH. It is the exact topological blueprint of the Solar System, and its secret code is hidden in your DNA! For 2,000 years, humanity has scoured the ocean floor looking for a sunken city. We failed. We failed because we took an advanced astrophysical blueprint of the Universe and mistook it for a map of a Mediterranean resort. I have spent my life meticulously studying ancient legends, myths, and sacred texts from all over the world. I was looking for a pattern. I saw that the "Atlantis" structure repeats itself in the deepest esoteric traditions. But the final, world-shattering piece of the puzzle didn't come from archaeology—it came from human genetics and the world's largest astrophysical database. 🧬 THE NOBEL PRIZE SHOCKWAVE To understand the stars, we had to look inside the human cell. My co-author in this research is Dr. Jean-Claude Perez jean-claude perez , a brilliant interdisciplinary biomathematician who worked for years alongside Nobel Laureate Dr. Luc Montagnier (who won the Nobel Prize in Medicine). Together, they mathematically decoded the standing waves, the golden ratio proportions, and the fractal harmonies hidden deep within the 64 codons of human DNA. They found the biological source code of life. What we did next was considered absolute heresy by mainstream physics. We took this exact mathematical DNA operator and we projected it outward into the macroscopic vacuum of outer space. We were crossing the ultimate boundary between biology and astrophysics. Nobody knew if it would work. We established a direct uplink to the Harvard-Smithsonian Minor Planet Center (MPCORB) catalog. We fed the live orbital data of 1,553,229 real celestial bodies into the algorithm. We held our breath. And when the render finished, our jaws dropped. The chaos of the Solar System vanished. The planets and asteroids did not float randomly. They snapped into a rigid, quantized, crystalline "House" strictly governed by the Logvinovich Field: K = ℚ(√2, √3, √5). We call this 3D vacuum structure the Perez Hourglass. And when I looked at the top-down (XY) projection of this cosmic Hourglass... I realized it PERFECTLY repeats the exact layout of Plato's Atlantis. Plato didn't invent this. The ancient Greeks or the Egyptian priests before them did not build a city. They likely found surviving manuscripts or structural blueprints from a highly advanced, lost civilization. They didn't understand the astrophysics of the macroscopic atom, so they preserved the geometry by describing it as a "sunken city." That is all the Atlantis myth is! A misunderstood schematic of the Cosmos! Watch the live Python execution in the attached video. 📜 THE EGYPTIAN MISUNDERSTANDING: How an Astrophysical Blueprint Became a MythHistory itself proves this. Plato did not invent the story; he recorded that it was handed down from the Greek lawmaker Solon. Around 600 BC, Solon traveled to Egypt, where the high priests of Sais mocked him, saying: "O Solon, Solon, you Hellenes are never anything but children... you have no knowledge hoary with age." What was this ancient, "hoary" knowledge? It was the immutable source code of the Universe itself, hardwired into the quantum vacuum. The priests brought out their oldest, most sacred temple registers and showed him the blueprint of a supreme structure. Solon saw precise mathematical proportions—such as a central core measuring exactly 5 stades, surrounded by strictly quantified concentric rings. These numbers were not the random fantasies of an ancient city planner. They are the exact, unyielding geometric constants that our Python algorithms are spitting out today when running topological operators across 1.55 million asteroids! But Solon didn't understand what he was looking at. He was staring at the surviving astrophysical schematics of a highly advanced, lost civilization. Lacking the vocabulary of spectral geometry and quantum mechanics, Solon—and later Plato in his Critias—suffered a catastrophic translation error. They took the terrifying cosmic "Vacuum Shear" (the impassable topological voids where matter cannot exist) and translated it into the only word they knew: "Water." They took the "Stable Quantum Orbits" (the rigid Diophantine nodes where mass crystallizes) and called it "Earth." They looked at the discrete architectural blueprint of the Solar System's phase space, and they mistook it for a sunken island! Here is the ancient myth translated into raw, empirical astrophysics: 🌊 The Belts of Water (The Mass Gap): The forbidden zones. These are the topological voids where vacuum shear forces prevent stable orbits. You cannot "stand" here. 🌍 The Belts of Earth (The Diophantine Floors):The allowed quantum orbits. Planets and asteroids are the inhabitants standing on these belts. They scale by a rigorous discrete rule: R_n = 27(√3)ⁿ⁻¹. 🏛️ The Royal Island (5 stades): The narrow neck of the Hourglass (Sn=0). Look at the GOLD CLOUD in the video. Our Harvard database audit proves that 1,546,364 out of 1,553,229 objects (99.56% of all tracked mass!) are geometrically locked inside this exact isthmus. 🧱 The Outer Wall: The strict Valence Shell (Sn=2). Plato placed the great wall exactly 50 stades beyond the harbor. In the cosmos, this is the Kuiper Cliff at exactly 46.77 AU (the TEAL RING in the video), where the macroscopic atom sharply terminates. 🚢 The Canal from the Ocean:The single entry vector for free interstellar comets coming from the continuous spectrum outside the House. Plato was not a historian; he was blindly preserving the mathematical architecture of the quantized vacuum. We do not live "on a planet in an empty void." We live on an inner earth ring of a macroscopic topological hourglass, trapped inside the valence wall. Atlantis is the XY-icon of the house we live in. The continuous universe (ℝ⁴) is a mathematical illusion. Space is a discrete, pulsing machine. The code inside your DNA is the exact same code that spins the stars, and the ancient builders knew it. 📐🌌 Audit the Harvard MPCORB proofs and watch the House unfold: 🔗 🔗 #Astrophysics #Plato #Atlantis #DNA #NobelPrize #QuantumTopology #Cosmology
0:17

🚨 ATLANTIS WAS NEVER ON EARTH. It is the exact topological blueprint of the Solar System, and its secret code is hidden in your DNA! For 2,000 years, humanity has scoured the ocean floor looking for a sunken city. We failed. We failed because we took an advanced astrophysical blueprint of the Universe and mistook it for a map of a Mediterranean resort. I have spent my life meticulously studying ancient legends, myths, and sacred texts from all over the world. I was looking for a pattern. I saw that the "Atlantis" structure repeats itself in the deepest esoteric traditions. But the final, world-shattering piece of the puzzle didn't come from archaeology—it came from human genetics and the world's largest astrophysical database. 🧬 THE NOBEL PRIZE SHOCKWAVE To understand the stars, we had to look inside the human cell. My co-author in this research is Dr. Jean-Claude Perez jean-claude perez , a brilliant interdisciplinary biomathematician who worked for years alongside Nobel Laureate Dr. Luc Montagnier (who won the Nobel Prize in Medicine). Together, they mathematically decoded the standing waves, the golden ratio proportions, and the fractal harmonies hidden deep within the 64 codons of human DNA. They found the biological source code of life. What we did next was considered absolute heresy by mainstream physics. We took this exact mathematical DNA operator and we projected it outward into the macroscopic vacuum of outer space. We were crossing the ultimate boundary between biology and astrophysics. Nobody knew if it would work. We established a direct uplink to the Harvard-Smithsonian Minor Planet Center (MPCORB) catalog. We fed the live orbital data of 1,553,229 real celestial bodies into the algorithm. We held our breath. And when the render finished, our jaws dropped. The chaos of the Solar System vanished. The planets and asteroids did not float randomly. They snapped into a rigid, quantized, crystalline "House" strictly governed by the Logvinovich Field: K = ℚ(√2, √3, √5). We call this 3D vacuum structure the Perez Hourglass. And when I looked at the top-down (XY) projection of this cosmic Hourglass... I realized it PERFECTLY repeats the exact layout of Plato's Atlantis. Plato didn't invent this. The ancient Greeks or the Egyptian priests before them did not build a city. They likely found surviving manuscripts or structural blueprints from a highly advanced, lost civilization. They didn't understand the astrophysics of the macroscopic atom, so they preserved the geometry by describing it as a "sunken city." That is all the Atlantis myth is! A misunderstood schematic of the Cosmos! Watch the live Python execution in the attached video. 📜 THE EGYPTIAN MISUNDERSTANDING: How an Astrophysical Blueprint Became a MythHistory itself proves this. Plato did not invent the story; he recorded that it was handed down from the Greek lawmaker Solon. Around 600 BC, Solon traveled to Egypt, where the high priests of Sais mocked him, saying: "O Solon, Solon, you Hellenes are never anything but children... you have no knowledge hoary with age." What was this ancient, "hoary" knowledge? It was the immutable source code of the Universe itself, hardwired into the quantum vacuum. The priests brought out their oldest, most sacred temple registers and showed him the blueprint of a supreme structure. Solon saw precise mathematical proportions—such as a central core measuring exactly 5 stades, surrounded by strictly quantified concentric rings. These numbers were not the random fantasies of an ancient city planner. They are the exact, unyielding geometric constants that our Python algorithms are spitting out today when running topological operators across 1.55 million asteroids! But Solon didn't understand what he was looking at. He was staring at the surviving astrophysical schematics of a highly advanced, lost civilization. Lacking the vocabulary of spectral geometry and quantum mechanics, Solon—and later Plato in his Critias—suffered a catastrophic translation error. They took the terrifying cosmic "Vacuum Shear" (the impassable topological voids where matter cannot exist) and translated it into the only word they knew: "Water." They took the "Stable Quantum Orbits" (the rigid Diophantine nodes where mass crystallizes) and called it "Earth." They looked at the discrete architectural blueprint of the Solar System's phase space, and they mistook it for a sunken island! Here is the ancient myth translated into raw, empirical astrophysics: 🌊 The Belts of Water (The Mass Gap): The forbidden zones. These are the topological voids where vacuum shear forces prevent stable orbits. You cannot "stand" here. 🌍 The Belts of Earth (The Diophantine Floors):The allowed quantum orbits. Planets and asteroids are the inhabitants standing on these belts. They scale by a rigorous discrete rule: R_n = 27(√3)ⁿ⁻¹. 🏛️ The Royal Island (5 stades): The narrow neck of the Hourglass (Sn=0). Look at the GOLD CLOUD in the video. Our Harvard database audit proves that 1,546,364 out of 1,553,229 objects (99.56% of all tracked mass!) are geometrically locked inside this exact isthmus. 🧱 The Outer Wall: The strict Valence Shell (Sn=2). Plato placed the great wall exactly 50 stades beyond the harbor. In the cosmos, this is the Kuiper Cliff at exactly 46.77 AU (the TEAL RING in the video), where the macroscopic atom sharply terminates. 🚢 The Canal from the Ocean:The single entry vector for free interstellar comets coming from the continuous spectrum outside the House. Plato was not a historian; he was blindly preserving the mathematical architecture of the quantized vacuum. We do not live "on a planet in an empty void." We live on an inner earth ring of a macroscopic topological hourglass, trapped inside the valence wall. Atlantis is the XY-icon of the house we live in. The continuous universe (ℝ⁴) is a mathematical illusion. Space is a discrete, pulsing machine. The code inside your DNA is the exact same code that spins the stars, and the ancient builders knew it. 📐🌌 Audit the Harvard MPCORB proofs and watch the House unfold: 🔗 🔗 #Astrophysics #Plato #Atlantis #DNA #NobelPrize #QuantumTopology #Cosmology

Dr. Logvinovich

160,003 次观看 • 4 天前

Blog 265 Diamondbacks first pitch ◦6-9: Gym, called parents, posted walking videos ◦10: Reunited with MikeyBets and felt complete ◦10:45: Arrived at Chase Stadium and was welcomed by the awesome Diamondbacks staff (shoutout Casey Wilcox) and walked right through the dugout and onto the field ◦Also huge thank you to Mike Dellosa (VP of ticket sales) who answered my LinkedIn dm and helped get set this all up ◦10:55: MikeyBets setup his camera in the Diamondbacks dugout which was hilarious to watch (he was viciously hungover) ◦11: Met with lots of the Diamondbacks and A’s players and coaches while they warmed up on Chase Field. Frank was in his element cracking jokes and talking baseball with the fellas ◦Everyone was incredibly welcoming, humble, and fun. The Diamondbacks manager, Torey Lovullo, called Frank a fucking legend ◦We crushed walk 277 circling the field pregame as Frank tracked the Mets game ◦11:30: Practiced the first pitch. We needed to loosen up the cannon more than we did in Milwaukee ◦12: Took a little break behind the dugout for Frank to mentally prepare for pitch ◦12:40: Mets tied it up ◦12:43: Frank broke into a dance-off with the mascots ◦12:45: Frank walked out for yet another Ceremonial First Pitch at an MLB game. Solid pitch, not quite a strike but we are getting there. These moments are always surreal for all of Fleming Enterprises ◦To Frank’s surprise, Paul Sewald, a former Met who Frank regularly eviscerated caught the first pitch. Paul is clearly a great person with a tremendous sense of humor and he gave Frank a customized autograph saying “fuck your computer” 🐐 ◦Frank is living his dream for the world to see ◦1:06: National Anthem, they had Frank and me stand in line with the Diamondbacks which was insane ◦1:10: Game started and we were brought into a beautiful suite ◦1:20: Frank did a food review in the suite and everyone fell dead silent watching in amazement ◦1:45: Got full stadium tour which concluded with Frank watching some baseball from the pool in centerfield. Of course, MikeyBets jumped right in full body ◦2:22: Frank raw dogged in the stadium and mentioned the Mets were tied in a rain delay in the 9th ◦2:45: Settled into our seats and watched the Diamondbacks take the lead in the 7th ◦3:15: Finished filming with Bets behind the sticks ◦3:30: The game was an elite experience via the Diamondbacks red carpet treatment. We can’t thank you all enough and congrats on the win ◦3:45: Drove to raw dog in Phoenix laughing about the absurdly fun day ◦3:47: Mets game resumed and car got real tense real quick ◦4: Raw dogged in a small place with a loud strikeout, not awkward at all ◦4:16: Mets gave up three runs and died, as did the vibes. Frank lost it and the great day had turned ◦4:28: Connected with Notre Dame football 👀 #FrankWalks ◦4:45: Frank declared the Arizona state flag as the 🐐 ◦5: Said goodbye to MikeyBets (always hurts) who had a later flight and wanted to hit the casino. HIM ◦5:10: Went to Scottsdale Fashion Center to pad step count before the red eye home Walking now. After we hit 15K steps we’ll pop over to the airport for our red eye back to New Jersey. Thank you so much to Casey, Mike, and the Diamondbacks for welcoming Frank and delivering an unforgettable day. Weigh in 9 tomorrow morning after we land and go directly to Belleville HQ around 5-6 am. We are nervous. I already miss MikeyBets severely. Anudder adventure almost in the books
0:04

Blog 265 Diamondbacks first pitch ◦6-9: Gym, called parents, posted walking videos ◦10: Reunited with MikeyBets and felt complete ◦10:45: Arrived at Chase Stadium and was welcomed by the awesome Diamondbacks staff (shoutout Casey Wilcox) and walked right through the dugout and onto the field ◦Also huge thank you to Mike Dellosa (VP of ticket sales) who answered my LinkedIn dm and helped get set this all up ◦10:55: MikeyBets setup his camera in the Diamondbacks dugout which was hilarious to watch (he was viciously hungover) ◦11: Met with lots of the Diamondbacks and A’s players and coaches while they warmed up on Chase Field. Frank was in his element cracking jokes and talking baseball with the fellas ◦Everyone was incredibly welcoming, humble, and fun. The Diamondbacks manager, Torey Lovullo, called Frank a fucking legend ◦We crushed walk 277 circling the field pregame as Frank tracked the Mets game ◦11:30: Practiced the first pitch. We needed to loosen up the cannon more than we did in Milwaukee ◦12: Took a little break behind the dugout for Frank to mentally prepare for pitch ◦12:40: Mets tied it up ◦12:43: Frank broke into a dance-off with the mascots ◦12:45: Frank walked out for yet another Ceremonial First Pitch at an MLB game. Solid pitch, not quite a strike but we are getting there. These moments are always surreal for all of Fleming Enterprises ◦To Frank’s surprise, Paul Sewald, a former Met who Frank regularly eviscerated caught the first pitch. Paul is clearly a great person with a tremendous sense of humor and he gave Frank a customized autograph saying “fuck your computer” 🐐 ◦Frank is living his dream for the world to see ◦1:06: National Anthem, they had Frank and me stand in line with the Diamondbacks which was insane ◦1:10: Game started and we were brought into a beautiful suite ◦1:20: Frank did a food review in the suite and everyone fell dead silent watching in amazement ◦1:45: Got full stadium tour which concluded with Frank watching some baseball from the pool in centerfield. Of course, MikeyBets jumped right in full body ◦2:22: Frank raw dogged in the stadium and mentioned the Mets were tied in a rain delay in the 9th ◦2:45: Settled into our seats and watched the Diamondbacks take the lead in the 7th ◦3:15: Finished filming with Bets behind the sticks ◦3:30: The game was an elite experience via the Diamondbacks red carpet treatment. We can’t thank you all enough and congrats on the win ◦3:45: Drove to raw dog in Phoenix laughing about the absurdly fun day ◦3:47: Mets game resumed and car got real tense real quick ◦4: Raw dogged in a small place with a loud strikeout, not awkward at all ◦4:16: Mets gave up three runs and died, as did the vibes. Frank lost it and the great day had turned ◦4:28: Connected with Notre Dame football 👀 #FrankWalks ◦4:45: Frank declared the Arizona state flag as the 🐐 ◦5: Said goodbye to MikeyBets (always hurts) who had a later flight and wanted to hit the casino. HIM ◦5:10: Went to Scottsdale Fashion Center to pad step count before the red eye home Walking now. After we hit 15K steps we’ll pop over to the airport for our red eye back to New Jersey. Thank you so much to Casey, Mike, and the Diamondbacks for welcoming Frank and delivering an unforgettable day. Weigh in 9 tomorrow morning after we land and go directly to Belleville HQ around 5-6 am. We are nervous. I already miss MikeyBets severely. Anudder adventure almost in the books

Matteo Piper Jenks 🧲 🇮🇹

133,039 次观看 • 2 年前

As we prepare to launch several projects, we're eager to provide a general update to our community. We are steadily approaching our end goal, thanks to the daily progress we're making toward our vision. Achieving our objectives will bring about a significant transformation in cross-chain interoperability and the flow of liquidity within protocols. This will address crucial challenges and drive mass adoption. Our future-focused approach and effective team collaboration keep us moving forward in an organized manner. Let’s delve deeper into the state of development of our current products and upcoming projects. Tao Bridge Starting with the Tao Bridge, which enables the #Bittensor community to unlock DeFi opportunities with their $TAO via a highly efficient blockchain like #MultiversX, known for its security, speed, and affordability. We deeply admire #Bittensor and believe a project like that is crucial for the future of not just the crypto space but also humanity, as it addresses the major challenges AI faces today: centralization, siloed and isolated work, which pose risks and hinder the technology's potential. We are committed to the vision of subnets and dynamic $TAO, convinced that this ecosystem is as groundbreaking as #Ethereum or #Bitcoin. We will continue to support #Bittensor wherever possible, and our bridge will also expand to other chains with Hatom V2. The TAO Bridge, deployed on and accessible through will launch on the Mainnet in 14 days, on March 27th. You can follow the countdown on the lending page at Given that our main priorities are security and stability, this period will be primarily focused on quality assurance to ensure a flawless Mainnet launch. The launch will also introduce TAO Liquid Staking at along with the integration of both $wTAO and $swTAO on the lending page. This allows #Bittensor users to leverage liquid stake, employ short or long strategies, among other DeFi strategies, or simply access stablecoin liquidity while maintaining exposure to their $TAO. Up to $1M will be distributed as additional incentives on top of the supply APYs at the launch of the $wTAO and $swTAO money markets, with $200K allocated for the first month specifically for bootstrapping. Initially, 70% of rewards will go to liquidity providers, and 30% to those using $HTM to boost their lending positions. This changes to a 50-50 split in the second month, and by the third month, all incentives are directed through the Booster. This approach encourages early participation and sustained engagement with $HTM. Introducing $TAO to #MultiversX will result in the creation of Liquidity Pools (LPs) on both AshSwap 🔥 and xExchange ⚡. These LPs will be incentivized by both entities, and Hatom will distribute extra rewards at launch. The goal is to make #MultiversX a one-stop hub for $TAO holders. Upon stabilizing the volumes, there will also be plans to integrate it on AshPerp 🔥. Furthermore, with the release of $USH, users will have the ability to mint it while retaining exposure to their $TAO. The TAO Bridge and TAO Liquid Staking smart contracts have been audited by Runtime Vеrification and @arda_project, while penetration testing and DevSecOps have been performed on our infrastructure by CertiK. We're excited to announce our exclusive partnership with TAONEW one of the top 5 validators on #Bittensor. TAONEW has been extremely helpful and supportive from day one. By sharing 50% of its service fee with its stakers, TAONEW enables Hatom to offer an optimized Staking APY to its users. Since our initial reference, #Bittensor has grown sevenfold, becoming the largest AI project in the crypto sphere. We reiterate our commitment to contribute to such technology and hope to address some of its current DeFi challenges. Syfy Moving forward, today marks a significant milestone, not only for our decentralized protocols but also for our development companies, which currently stand as the sole and primary contributors to the Hatom Labs and Soul Labs. We’re excited to unveil Syfy, the evolved identity of Hatom Labs and Soul Labs, now serving as the parent entity for our burgeoning development companies. Organization is crucial for scalability, which is why Syfy was established to cultivate an environment where our teams can collaborate more seamlessly, enhancing our effectiveness and efficiency. At the same time, we remain committed to upholding the financial independence of each project, supported by its own community of funding contributors. Feel free to explore our website at for more information! Additionally, don't forget to follow Syfy and explore their Genesis article highlighted in their initial post: Booster V2 The Booster V2 will introduce a range of new features and opportunities for $HTM holders: Optimized Position Boosting: Previously, boosting was done individually for each money market, necessitating $HTM token distribution and periodic rebalancing due to price fluctuations. With Booster V2, the system now considers the overall position, eliminating the need for manual rebalancing. Gas Fee Reduction: Booster V2 implements optimizations that result in reduced gas fees, making transactions more cost-effective for users. Incorporation of Governance: Users staking $HTM tokens gain voting rights directly within the Booster, allowing them to participate in governance decisions while maintaining their staked positions. (Note: Only $HTM tokens are considered for governance; LP tokens are not included.) Enhanced Boosting Mechanism: The Booster V2 enables LP Tokens to boost positions within the Booster, leveraging trading fees from swaps and farm incentives while boosting lending positions. Smart Contract Completion: The Booster smart contract has been completed and audited by @arda_project, ensuring security and reliability. Frontend Implementation: The frontend design for Booster V2 has been successfully implemented, providing users with an intuitive interface. Collaboration with xExchange: Exploration is ongoing for collaboration with xExchange ⚡ to enable LP creation, farming, and meta-staking within the Booster. Upon finalization of testing, we will launch the Booster V2 on the devnet to gather community feedback and begin preparations for the mainnet release. Soul Before delving into Soul Labs's developments, it's essential to summarize its core functionality briefly: Soul Labs seamlessly connects different lending protocols and blockchains, facilitating lending and borrowing across platforms like Aave, Compound Labs, and Hatom Labs, consolidating liquidity and users' borrowing capabilities. Utilizing LayerZero Labs and other messaging layers for cross-chain communication, Soul Labs bypasses asset bridging or synthetics, unlocking novel DeFi strategies and solidifying its position as the ultimate solution for cross-lending dilemmas. Soul V1 will be permissionless, holding censorship-resistant features, incorporating multiple redundancy mechanisms, and providing support for various DApps. We're thrilled to announce that, following the launch of the Tao Bridge in 2-3 weeks, we will introduce the Soul Labs website. This platform has been meticulously crafted over 250 days to not only provide a comprehensive overview of our vision but also to offer an engaging and captivating experience that promises to be memorable. Regarding the app, significant progress has been made on the V1 protocol, including: Smart Contract Development and Testing: • Completion of the initial phase of smart contract development. • Conducting advanced testing to ensure the system's robustness. • Establishment of a fully functional proof of concept. Successful deployment and testing on the #Goerli (#Ethereum Testnet) and #Mumbai (#Polygon Testnet), leveraging LayerZero Labs for seamless operation. Feature Enhancement and Protocol Optimization: • Enhanced testing procedures to bolster system resilience. • Integration of advanced features and significant code refactoring for optimization. • Incorporation of various communication methods, including LayerZero Labs, Formerly Axelar, now at @axelar, Chainlink CCIP), and wormholecrypto, into Soul Labs framework, enhancing its resilience and flexibility. This allows Soul Labs to maintain operation through alternative protocols if the primary one is temporarily paused. Website Development and Documentation: • Nearing the completion of the v1 app, with final touches being applied. • The preparation of comprehensive V1 documentation and the Yellow Paper, available upon Soul Labs's public launch, offering detailed insights into the platform's infrastructure and capabilities. USH Recognizing the critical need for stable liquidity within the ecosystem, we have positioned ourselves at the forefront of providing a solution by introducing $USH, the first native, decentralized, and over-collateralized stablecoin on #MultiversX. As market conditions have improved, we have observed a growing demand for stablecoins in the ecosystem, evidenced by the utilization rate in the Lending Protocol spiking to over 90% several times in recent months. Therefore, our goal is to tackle the current challenges faced by users by creating a robust product that will not only help them hedge against market volatility but also open up better opportunities to trade the markets and generate yield. We're happy to unveil the $USH website, now live with a sleek and intuitive user interface, designed for ease of use, which ensures that interacting with the protocol is straightforward and accessible for all. You can access it now through this link: For the technical side, we’re advancing steadily and we’ve accomplished the following milestones: Lending Protocol Facilitator: • Coded the first version to support multiple discount factors for different collaterals. • Implemented tracking of borrowing effectiveness to enable earnings forecasting for the module and support minting processes. Isolated Pools Facilitator: • Coded the first version of Isolated Pools Facilitator. • Use of $EGLD or $sEGLD as collateral, with positions stored always in $EGLD to benefit the protocol through Liquid Staking and lending interest. • Virtual account implementation for converting $sEGLD earnings into $USH, functioning like liquidation where users deposit $USH for a higher amount of $HsELGD. Staking Module • Coded the first version of the Staking Module that allows users to stake and unstake without any restrictions. We're currently focusing our efforts on the following tasks: • Implementation of HTM Booster in the discount model in the Lending Protocol. • Implementation of different depeg strategies and brainstorming further potential “soft” depeg mechanisms. • Research and implementation of rewards model for Staking Module. • Research and implementation of Boosted Vaults Facilitator. • Review and stress-test the first version of the code. Upon launch, $USH will be integrated into various protocols and AMMs across the ecosystem, further increasing both its utility and liquidity. The opportunities will be vast, enabling users to engage in a wide range of activities such as yield farming, staking, and arbitrage, all while leveraging a stable and reliable asset. Regarding the USH Airdrop campaign, it will continue until the official launch of $USH planned for late Q2-early Q3, rewarding all users who have actively participated in the initiative. Hatom V2 It is clear by now that we are driven to build a more robust, interoperable, and secure DeFi space, removing the current barriers that hinder users' capabilities to seamlessly interact with different blockchains. Through Hatom V2, we will introduce Hatom's cross-chain architecture, designed from the ground up for interoperability. This approach will elevate the protocol to unprecedented levels, enabling its deployment across various blockchains and facilitating seamless connections between them through Soul. By enhancing interoperability, Hatom V2 aims to foster a more inclusive and accessible ecosystem. This expansion will not only broaden the protocol's reach but also significantly increase its flexibility and utility, allowing users to interact with a diverse range of assets and products across different chains. We’re thrilled to share that we are currently crafting the V2 redesign of the Hatom webpage. Anticipate a jaw-dropping transformation that will truly astonish, blending cutting-edge design with an unparalleled user experience, elevating it to a dynamic, interactive hub, and making every interaction more engaging. Good things take time, but we are confident that the release of V2 website will take place in the second quarter of this year and will officially mark the start of our journey into the cross-chain landscape. We are excited about the future and we truly believe that this will mark the beginning of a new era for Hatom. It's crucial for us to develop rapidly without sacrificing the quality or the security of each product. We're strategically allocating resources to ensure smooth progress in every area of our work. As we push forward, we believe that the launch of Soul Labs will be the most important milestone due to its massive potential and disruptive technology. We would like to thank you all for the unwavering support you've shown over the past few months; it truly fuels our passion to push daily and make strides toward achieving our ambitious goals.
0:11

As we prepare to launch several projects, we're eager to provide a general update to our community. We are steadily approaching our end goal, thanks to the daily progress we're making toward our vision. Achieving our objectives will bring about a significant transformation in cross-chain interoperability and the flow of liquidity within protocols. This will address crucial challenges and drive mass adoption. Our future-focused approach and effective team collaboration keep us moving forward in an organized manner. Let’s delve deeper into the state of development of our current products and upcoming projects. Tao Bridge Starting with the Tao Bridge, which enables the #Bittensor community to unlock DeFi opportunities with their $TAO via a highly efficient blockchain like #MultiversX, known for its security, speed, and affordability. We deeply admire #Bittensor and believe a project like that is crucial for the future of not just the crypto space but also humanity, as it addresses the major challenges AI faces today: centralization, siloed and isolated work, which pose risks and hinder the technology's potential. We are committed to the vision of subnets and dynamic $TAO, convinced that this ecosystem is as groundbreaking as #Ethereum or #Bitcoin. We will continue to support #Bittensor wherever possible, and our bridge will also expand to other chains with Hatom V2. The TAO Bridge, deployed on and accessible through will launch on the Mainnet in 14 days, on March 27th. You can follow the countdown on the lending page at Given that our main priorities are security and stability, this period will be primarily focused on quality assurance to ensure a flawless Mainnet launch. The launch will also introduce TAO Liquid Staking at along with the integration of both $wTAO and $swTAO on the lending page. This allows #Bittensor users to leverage liquid stake, employ short or long strategies, among other DeFi strategies, or simply access stablecoin liquidity while maintaining exposure to their $TAO. Up to $1M will be distributed as additional incentives on top of the supply APYs at the launch of the $wTAO and $swTAO money markets, with $200K allocated for the first month specifically for bootstrapping. Initially, 70% of rewards will go to liquidity providers, and 30% to those using $HTM to boost their lending positions. This changes to a 50-50 split in the second month, and by the third month, all incentives are directed through the Booster. This approach encourages early participation and sustained engagement with $HTM. Introducing $TAO to #MultiversX will result in the creation of Liquidity Pools (LPs) on both AshSwap 🔥 and xExchange ⚡. These LPs will be incentivized by both entities, and Hatom will distribute extra rewards at launch. The goal is to make #MultiversX a one-stop hub for $TAO holders. Upon stabilizing the volumes, there will also be plans to integrate it on AshPerp 🔥. Furthermore, with the release of $USH, users will have the ability to mint it while retaining exposure to their $TAO. The TAO Bridge and TAO Liquid Staking smart contracts have been audited by Runtime Vеrification and @arda_project, while penetration testing and DevSecOps have been performed on our infrastructure by CertiK. We're excited to announce our exclusive partnership with TAONEW one of the top 5 validators on #Bittensor. TAONEW has been extremely helpful and supportive from day one. By sharing 50% of its service fee with its stakers, TAONEW enables Hatom to offer an optimized Staking APY to its users. Since our initial reference, #Bittensor has grown sevenfold, becoming the largest AI project in the crypto sphere. We reiterate our commitment to contribute to such technology and hope to address some of its current DeFi challenges. Syfy Moving forward, today marks a significant milestone, not only for our decentralized protocols but also for our development companies, which currently stand as the sole and primary contributors to the Hatom Labs and Soul Labs. We’re excited to unveil Syfy, the evolved identity of Hatom Labs and Soul Labs, now serving as the parent entity for our burgeoning development companies. Organization is crucial for scalability, which is why Syfy was established to cultivate an environment where our teams can collaborate more seamlessly, enhancing our effectiveness and efficiency. At the same time, we remain committed to upholding the financial independence of each project, supported by its own community of funding contributors. Feel free to explore our website at for more information! Additionally, don't forget to follow Syfy and explore their Genesis article highlighted in their initial post: Booster V2 The Booster V2 will introduce a range of new features and opportunities for $HTM holders: Optimized Position Boosting: Previously, boosting was done individually for each money market, necessitating $HTM token distribution and periodic rebalancing due to price fluctuations. With Booster V2, the system now considers the overall position, eliminating the need for manual rebalancing. Gas Fee Reduction: Booster V2 implements optimizations that result in reduced gas fees, making transactions more cost-effective for users. Incorporation of Governance: Users staking $HTM tokens gain voting rights directly within the Booster, allowing them to participate in governance decisions while maintaining their staked positions. (Note: Only $HTM tokens are considered for governance; LP tokens are not included.) Enhanced Boosting Mechanism: The Booster V2 enables LP Tokens to boost positions within the Booster, leveraging trading fees from swaps and farm incentives while boosting lending positions. Smart Contract Completion: The Booster smart contract has been completed and audited by @arda_project, ensuring security and reliability. Frontend Implementation: The frontend design for Booster V2 has been successfully implemented, providing users with an intuitive interface. Collaboration with xExchange: Exploration is ongoing for collaboration with xExchange ⚡ to enable LP creation, farming, and meta-staking within the Booster. Upon finalization of testing, we will launch the Booster V2 on the devnet to gather community feedback and begin preparations for the mainnet release. Soul Before delving into Soul Labs's developments, it's essential to summarize its core functionality briefly: Soul Labs seamlessly connects different lending protocols and blockchains, facilitating lending and borrowing across platforms like Aave, Compound Labs, and Hatom Labs, consolidating liquidity and users' borrowing capabilities. Utilizing LayerZero Labs and other messaging layers for cross-chain communication, Soul Labs bypasses asset bridging or synthetics, unlocking novel DeFi strategies and solidifying its position as the ultimate solution for cross-lending dilemmas. Soul V1 will be permissionless, holding censorship-resistant features, incorporating multiple redundancy mechanisms, and providing support for various DApps. We're thrilled to announce that, following the launch of the Tao Bridge in 2-3 weeks, we will introduce the Soul Labs website. This platform has been meticulously crafted over 250 days to not only provide a comprehensive overview of our vision but also to offer an engaging and captivating experience that promises to be memorable. Regarding the app, significant progress has been made on the V1 protocol, including: Smart Contract Development and Testing: • Completion of the initial phase of smart contract development. • Conducting advanced testing to ensure the system's robustness. • Establishment of a fully functional proof of concept. Successful deployment and testing on the #Goerli (#Ethereum Testnet) and #Mumbai (#Polygon Testnet), leveraging LayerZero Labs for seamless operation. Feature Enhancement and Protocol Optimization: • Enhanced testing procedures to bolster system resilience. • Integration of advanced features and significant code refactoring for optimization. • Incorporation of various communication methods, including LayerZero Labs, Formerly Axelar, now at @axelar, Chainlink CCIP), and wormholecrypto, into Soul Labs framework, enhancing its resilience and flexibility. This allows Soul Labs to maintain operation through alternative protocols if the primary one is temporarily paused. Website Development and Documentation: • Nearing the completion of the v1 app, with final touches being applied. • The preparation of comprehensive V1 documentation and the Yellow Paper, available upon Soul Labs's public launch, offering detailed insights into the platform's infrastructure and capabilities. USH Recognizing the critical need for stable liquidity within the ecosystem, we have positioned ourselves at the forefront of providing a solution by introducing $USH, the first native, decentralized, and over-collateralized stablecoin on #MultiversX. As market conditions have improved, we have observed a growing demand for stablecoins in the ecosystem, evidenced by the utilization rate in the Lending Protocol spiking to over 90% several times in recent months. Therefore, our goal is to tackle the current challenges faced by users by creating a robust product that will not only help them hedge against market volatility but also open up better opportunities to trade the markets and generate yield. We're happy to unveil the $USH website, now live with a sleek and intuitive user interface, designed for ease of use, which ensures that interacting with the protocol is straightforward and accessible for all. You can access it now through this link: For the technical side, we’re advancing steadily and we’ve accomplished the following milestones: Lending Protocol Facilitator: • Coded the first version to support multiple discount factors for different collaterals. • Implemented tracking of borrowing effectiveness to enable earnings forecasting for the module and support minting processes. Isolated Pools Facilitator: • Coded the first version of Isolated Pools Facilitator. • Use of $EGLD or $sEGLD as collateral, with positions stored always in $EGLD to benefit the protocol through Liquid Staking and lending interest. • Virtual account implementation for converting $sEGLD earnings into $USH, functioning like liquidation where users deposit $USH for a higher amount of $HsELGD. Staking Module • Coded the first version of the Staking Module that allows users to stake and unstake without any restrictions. We're currently focusing our efforts on the following tasks: • Implementation of HTM Booster in the discount model in the Lending Protocol. • Implementation of different depeg strategies and brainstorming further potential “soft” depeg mechanisms. • Research and implementation of rewards model for Staking Module. • Research and implementation of Boosted Vaults Facilitator. • Review and stress-test the first version of the code. Upon launch, $USH will be integrated into various protocols and AMMs across the ecosystem, further increasing both its utility and liquidity. The opportunities will be vast, enabling users to engage in a wide range of activities such as yield farming, staking, and arbitrage, all while leveraging a stable and reliable asset. Regarding the USH Airdrop campaign, it will continue until the official launch of $USH planned for late Q2-early Q3, rewarding all users who have actively participated in the initiative. Hatom V2 It is clear by now that we are driven to build a more robust, interoperable, and secure DeFi space, removing the current barriers that hinder users' capabilities to seamlessly interact with different blockchains. Through Hatom V2, we will introduce Hatom's cross-chain architecture, designed from the ground up for interoperability. This approach will elevate the protocol to unprecedented levels, enabling its deployment across various blockchains and facilitating seamless connections between them through Soul. By enhancing interoperability, Hatom V2 aims to foster a more inclusive and accessible ecosystem. This expansion will not only broaden the protocol's reach but also significantly increase its flexibility and utility, allowing users to interact with a diverse range of assets and products across different chains. We’re thrilled to share that we are currently crafting the V2 redesign of the Hatom webpage. Anticipate a jaw-dropping transformation that will truly astonish, blending cutting-edge design with an unparalleled user experience, elevating it to a dynamic, interactive hub, and making every interaction more engaging. Good things take time, but we are confident that the release of V2 website will take place in the second quarter of this year and will officially mark the start of our journey into the cross-chain landscape. We are excited about the future and we truly believe that this will mark the beginning of a new era for Hatom. It's crucial for us to develop rapidly without sacrificing the quality or the security of each product. We're strategically allocating resources to ensure smooth progress in every area of our work. As we push forward, we believe that the launch of Soul Labs will be the most important milestone due to its massive potential and disruptive technology. We would like to thank you all for the unwavering support you've shown over the past few months; it truly fuels our passion to push daily and make strides toward achieving our ambitious goals.

Hatom Labs

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