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Did a quick and dirty implementation of a spatial hash structure to speedup RTAO, ray results are stored in cells indexed by pos/normal/cell size and after storing a few rays occlusion can be queried from the cell instead of raytracing it. 3x faster RTAO with no denoising.

Kostas Anagnostou

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38,082 просмотров • 10 месяцев назад •via X (Twitter)

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If you have Cancer, this is your visualization. That is a cancerous cell reaching Apoptosis and Necrosis—they are gone. — Natural Killer (NK) cells play a the primary role in the immune system's defense against cancer. They induce cancer cell death primarily through two mechanisms: Apoptosis Necrosis Apoptosis is a programmed, non-inflammatory form of cell death, while necrosis is a more abrupt and inflammatory process. In many cases, NK cells can trigger a combination of both, leading to mixed forms of cell death. This dual capability allows NK cells to effectively target and destroy all tumor cells. Their ability to act without prior sensitization makes them vital for early cancer surveillance and curing existing cancer. One of the only ways cancer never starts or stops entirely is NK cells. They are the guerrilla warfare troops that never sleep. This is why it is vital for BioShield by to be approved, NOW for every cancer, not just a single cancer type. With the rest needing years and years of tests. Cancer is cancer, unregulated cell division and NK cells are NK cells. The ONLY thing that stops BioShield is government betrayal, and organized corruption disguised as following the “regulations” designed by the entrenched gatekeepers of corporate protection. Everyone knows it works that has even a molecule of biological understanding. Now you know.

If you have Cancer, this is your visualization. That is a cancerous cell reaching Apoptosis and Necrosis—they are gone. — Natural Killer (NK) cells play a the primary role in the immune system's defense against cancer. They induce cancer cell death primarily through two mechanisms: Apoptosis Necrosis Apoptosis is a programmed, non-inflammatory form of cell death, while necrosis is a more abrupt and inflammatory process. In many cases, NK cells can trigger a combination of both, leading to mixed forms of cell death. This dual capability allows NK cells to effectively target and destroy all tumor cells. Their ability to act without prior sensitization makes them vital for early cancer surveillance and curing existing cancer. One of the only ways cancer never starts or stops entirely is NK cells. They are the guerrilla warfare troops that never sleep. This is why it is vital for BioShield by to be approved, NOW for every cancer, not just a single cancer type. With the rest needing years and years of tests. Cancer is cancer, unregulated cell division and NK cells are NK cells. The ONLY thing that stops BioShield is government betrayal, and organized corruption disguised as following the “regulations” designed by the entrenched gatekeepers of corporate protection. Everyone knows it works that has even a molecule of biological understanding. Now you know.

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A video shows engineered heart muscle made up of allogeneic induced pluripotent stem-cell–derived cardiomyocytes and stromal cells for cardiac remuscularization in patients with heart failure. Read the full BioVAT-HF study results to learn more:

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Strands of DNA-like thread coil, loop, and spill upward, evoking the genome's dynamic three-dimensional architecture within the nucleus of a living cell. This special issue, with papers in Science and Science Advances, features single-cell and multiomic studies from the National Institutes of Health Common Fund's 4D Nucleome Program, which examines a fourth dimension of nuclear organization—how this folded structure shapes cell identity, shifts across development and aging, and goes awry in disease. Learn more:

Strands of DNA-like thread coil, loop, and spill upward, evoking the genome's dynamic three-dimensional architecture within the nucleus of a living cell. This special issue, with papers in Science and Science Advances, features single-cell and multiomic studies from the National Institutes of Health Common Fund's 4D Nucleome Program, which examines a fourth dimension of nuclear organization—how this folded structure shapes cell identity, shifts across development and aging, and goes awry in disease. Learn more:

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Since long time we tried to achieve “permanent” labelling of plasma membranes. Now it become possible with MemGraft probes, which exploit a new principle of lipid-directed covalent fluorescent labeling of membrane proteins. The MemGraft probes are compatible with fixation, permeabilization, trypsinization, presence of serum in the medium and enable long-term cell imaging, co-culture of cells and their imaging in multiple colors, cell barcoding and cell manipulation. Congrats and thanks to co-authors: Nathan Aknine Nathan Aknine & Remi Pelletier. - CNRS 🌍 CNRS 🌍_Alsace LBP UMR 7021 Just out in biorXiv:

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In Prisma Next, you can stream query results straight from the database, row by row and fully typed. That means exports, reports, and ETL jobs of any size run smoothly, with the same safety you get on a normal query.

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The Hamas cell mobilized, entered a Toyota vehicle, and began moving, only to be tracked and eliminated shortly after, highlighting the speed and precision of the operation by Israeli Defence Forces.

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The most detailed 3D reconstruction of a cell ever created. Blows my mind every time. But what exactly are we looking at here? The average human cell contains: ~ 15-20 total distinct organelle types, totalling between ~1-10 million working together per cell. All these nano-machines in the cell are made up of proteins. ~ 8,000-10,000 distinct types of unique proteins, adding up to between 40 million - 10 trillion total proteins making up all those cellular systems. ~ 10,000 - 15,000 distinct types of RNA shuttling information around the cell, totalling up to ~10 million RNA molecules moving around the cell simultaneously. ~ Billions of Lipid molecules packed together into the cell membrane, which is also packed tightly with millions more protein-based nano-machines. And let's not forget billions of lines of DNA information to build and run it all. That's TRILLIONS of of individual molecular pieces working together to make a single cell function. That means there is more complexity in a single cell than humanity's largest cities. And people still believe this wasn't Divinely Designed. This is God's Glory on Display. But to make the point. A cell couldn't have evolved from some nebulous simpler "protocell" because even the simplest cells still require massive complexity. The "simplest" cell ever created was engineered by scientists knocking out pieces of a functional cell until it stopped functioning. Here is what they found is the absolute necessary minimal requirements of a cell to function: - Over ~531,000 lines of coded DNA information - 473 total genes to create hundreds of unique protein products (they later added 19 genes back in because the cell was so weak) - Hundreds of thousands of total proteins all working together - Extensive regulatory networks guiding all these interactions If the cell doesn't have all these systems in place, from the start... it doesn't live. Cell rely on an intricate network of complex systems, which are themselves built from complex interconnected pieces woven together into an incomprehensibly complex web of functionilty. Only intelligence has ever been observed creation vast interconnected systems like this. Life was clearly Created. It couldn't happen any other way.

The most detailed 3D reconstruction of a cell ever created. Blows my mind every time. But what exactly are we looking at here? The average human cell contains: ~ 15-20 total distinct organelle types, totalling between ~1-10 million working together per cell. All these nano-machines in the cell are made up of proteins. ~ 8,000-10,000 distinct types of unique proteins, adding up to between 40 million - 10 trillion total proteins making up all those cellular systems. ~ 10,000 - 15,000 distinct types of RNA shuttling information around the cell, totalling up to ~10 million RNA molecules moving around the cell simultaneously. ~ Billions of Lipid molecules packed together into the cell membrane, which is also packed tightly with millions more protein-based nano-machines. And let's not forget billions of lines of DNA information to build and run it all. That's TRILLIONS of of individual molecular pieces working together to make a single cell function. That means there is more complexity in a single cell than humanity's largest cities. And people still believe this wasn't Divinely Designed. This is God's Glory on Display. But to make the point. A cell couldn't have evolved from some nebulous simpler "protocell" because even the simplest cells still require massive complexity. The "simplest" cell ever created was engineered by scientists knocking out pieces of a functional cell until it stopped functioning. Here is what they found is the absolute necessary minimal requirements of a cell to function: - Over ~531,000 lines of coded DNA information - 473 total genes to create hundreds of unique protein products (they later added 19 genes back in because the cell was so weak) - Hundreds of thousands of total proteins all working together - Extensive regulatory networks guiding all these interactions If the cell doesn't have all these systems in place, from the start... it doesn't live. Cell rely on an intricate network of complex systems, which are themselves built from complex interconnected pieces woven together into an incomprehensibly complex web of functionilty. Only intelligence has ever been observed creation vast interconnected systems like this. Life was clearly Created. It couldn't happen any other way.

Divinely Designed

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Urgent and Important ‼️ A cell affiliated with ISIS was captured by the People’s Protection Units (YPG). The cell came from Deir ez-Zor and entered Al-Hasakah with the intention of attacking Al-Ghweran Prison, which is filled with ISIS members. The cell members were reportedly sent from Deir ez-Zor by Hay’at Tahrir al-Sham (Al-Julani) to free ISIS detainees in Al-Ghweran Prison.

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A sneak peak of a complex and technically challenging experiment that my lab developed: Super proud of PhD candidate Hannah Johnson for showcasing our Whole-gut spatial genomic analysis in #zebrafish. This video illustrates one landmark in the protocol after multiple rounds of sequential #HCR and 3D imaging in zebrafish larvae to reveal spatial expression of numerous mRNAs in the same specimen. Data from these imaging data sets are then computationally analyzed for spatial cell groups, spatially variable genes, and differentially expressed genes along 3D. We are leveraging this systems-level SGA to uncover unappreciated mechanistic insight at the cell and tissue levels into #ENS construction. Stay tuned for our work that exploits this pipeline within various mutant and perturbation conditions. Reach out if you are interested in trying this! #fruitypebbles

A sneak peak of a complex and technically challenging experiment that my lab developed: Super proud of PhD candidate Hannah Johnson for showcasing our Whole-gut spatial genomic analysis in #zebrafish. This video illustrates one landmark in the protocol after multiple rounds of sequential #HCR and 3D imaging in zebrafish larvae to reveal spatial expression of numerous mRNAs in the same specimen. Data from these imaging data sets are then computationally analyzed for spatial cell groups, spatially variable genes, and differentially expressed genes along 3D. We are leveraging this systems-level SGA to uncover unappreciated mechanistic insight at the cell and tissue levels into #ENS construction. Stay tuned for our work that exploits this pipeline within various mutant and perturbation conditions. Reach out if you are interested in trying this! #fruitypebbles

Rosa Uribe, PhD

10,119 просмотров • 6 месяцев назад

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.

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 просмотров • 1 год назад

Ladies and gentlemen, something happened in Tuapse, and we received a video message from the locals. This video is about humanity. This video is about you and me... Why are you, Ukrainians, so brainwashed, angry, and unsympathetic to the grief of the people of Tuapse... And aren’t you ashamed to be like that... But let's be serious. It's 2026, something happened, and instead of Z-festivals, dear Russians were recording videos saying they are just pawns, that they are not guilty, that they sympathize with us, and that they never wanted any of this. And you shouldn't hate them, they are... good. They just want peace, for unicorns to run across the rainbow, and instead of rockets, to launch confetti 🥰 And along with you, madam, there are another 1 million mercenaries fighting in Ukraine, 2.5 million regular scumbags, 2.5 million weaklings, more than 4 million scumbags working in defense industries, 3 million scumbags in the government apparatus. And tens of millions more scumbags to some degree supporting the Kremlin regime. And each. Each of these people deserves liquidation. Because you are a plague, a contagion that must be burned out. Probably if a cancer cell could speak during therapy, it would say something like this: I just exist. I don’t want to kill you. I’m very sorry that you suffer. I wouldn’t want you to die. Can you negotiate with a cancer cell? Can you expect a cancer cell to pity you? Can you expect cancer to retreat on its own? ... No. The so-called Russian Federation is cancer. The enraged, feral Russian society is cancer. Cancer must be burned out, cut out. Every cell must be destroyed. Because cancer will never retreat on its own. If you disagree with the war, if you don’t support your government — leave the country. Until then, each of you is an implicit accomplice and a terrorist. And there’s no whining. Sorry for the long read, it can’t be shorter here.

Ladies and gentlemen, something happened in Tuapse, and we received a video message from the locals. This video is about humanity. This video is about you and me... Why are you, Ukrainians, so brainwashed, angry, and unsympathetic to the grief of the people of Tuapse... And aren’t you ashamed to be like that... But let's be serious. It's 2026, something happened, and instead of Z-festivals, dear Russians were recording videos saying they are just pawns, that they are not guilty, that they sympathize with us, and that they never wanted any of this. And you shouldn't hate them, they are... good. They just want peace, for unicorns to run across the rainbow, and instead of rockets, to launch confetti 🥰 And along with you, madam, there are another 1 million mercenaries fighting in Ukraine, 2.5 million regular scumbags, 2.5 million weaklings, more than 4 million scumbags working in defense industries, 3 million scumbags in the government apparatus. And tens of millions more scumbags to some degree supporting the Kremlin regime. And each. Each of these people deserves liquidation. Because you are a plague, a contagion that must be burned out. Probably if a cancer cell could speak during therapy, it would say something like this: I just exist. I don’t want to kill you. I’m very sorry that you suffer. I wouldn’t want you to die. Can you negotiate with a cancer cell? Can you expect a cancer cell to pity you? Can you expect cancer to retreat on its own? ... No. The so-called Russian Federation is cancer. The enraged, feral Russian society is cancer. Cancer must be burned out, cut out. Every cell must be destroyed. Because cancer will never retreat on its own. If you disagree with the war, if you don’t support your government — leave the country. Until then, each of you is an implicit accomplice and a terrorist. And there’s no whining. Sorry for the long read, it can’t be shorter here.

Exilenova+

31,086 просмотров • 4 месяцев назад

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.

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 просмотров • 6 месяцев назад

A dream of our lab has been to image the full central dogma from a single endogenous gene, all live and with single molecule resolution. After many years we are happy to unveil a beautiful cell line that makes it possible. Check out our preprint ( (1/n)

A dream of our lab has been to image the full central dogma from a single endogenous gene, all live and with single molecule resolution. After many years we are happy to unveil a beautiful cell line that makes it possible. Check out our preprint ( (1/n)

Timothy

206,349 просмотров • 2 лет назад

$🚨 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.$

🚨 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 просмотров • 5 месяцев назад

It's like 35GB a month to store every positional update of every train and bus on the MBTA (not feasible $$ for a nonprofit to store in a hosted db somewhere). We stored a few days' worth, and I've been using it to detect bus bunching with a quick react app I wrote

It's like 35GB a month to store every positional update of every train and bus on the MBTA (not feasible $$ for a nonprofit to store in a hosted db somewhere). We stored a few days' worth, and I've been using it to detect bus bunching with a quick react app I wrote

seth

191,844 просмотров • 8 месяцев назад

Why not show real data instead of a 2D cartoon? Left diagonal: computationally separated 3D volume-rendered movies at 15 sec intervals for 19 minutes of chromosomes, mitochondria, and the ER in the same field of dividing pig kidney cells. Middle diagonal: overlapped color channels computationally sliced in slabs through the volume to reveal internal structure and interactions throughout mitosis. Upper right: zoomed in view in one slab, showing organelle rearrangements in the left cell from metaphase through telophase.

Why not show real data instead of a 2D cartoon? Left diagonal: computationally separated 3D volume-rendered movies at 15 sec intervals for 19 minutes of chromosomes, mitochondria, and the ER in the same field of dividing pig kidney cells. Middle diagonal: overlapped color channels computationally sliced in slabs through the volume to reveal internal structure and interactions throughout mitosis. Upper right: zoomed in view in one slab, showing organelle rearrangements in the left cell from metaphase through telophase.

Eric Betzig

19,923 просмотров • 5 месяцев назад

Every year, markets slow in summer. Your goal should be to get away for a few weeks (preferably somewhere with bad cell reception). It’s important to clear your mind, and come back fresh for the 2nd half of the year. This year, we did a week of Santiago, then vineyards in Clos de Apalta. Now in Atacama desert, before Bolivia.

Every year, markets slow in summer. Your goal should be to get away for a few weeks (preferably somewhere with bad cell reception). It’s important to clear your mind, and come back fresh for the 2nd half of the year. This year, we did a week of Santiago, then vineyards in Clos de Apalta. Now in Atacama desert, before Bolivia.

Kuppy

168,151 просмотров • 1 месяц назад

Inside every cell, there is a transport system that determines how materials move, signals propagate, and structure is maintained. This video captures that system in motion. The glowing streaks mark the growing ends of microtubules (protein polymers that constantly assemble and disassemble through a process called dynamic instability). Rather than forming permanent tracks, microtubules are rebuilt continuously, allowing cells to reorganize their internal layout in real time. This behavior is essential for life. Cells rely on microtubule dynamics to divide accurately, migrate during development and repair, and maintain long-distance transport in neurons that may span over a meter in length. When this system is altered, the consequences are significant. Certain cancer therapies work by locking microtubules in place, preventing cell division. In contrast, failures in microtubule transport are linked to neurodegenerative conditions (like Alzheimer's) where intracellular delivery breaks down. What appears as abstract motion under a microscope is actually one of the core systems that keeps cells functional, adaptable, and alive. Video Credit: Andy Moore

Inside every cell, there is a transport system that determines how materials move, signals propagate, and structure is maintained. This video captures that system in motion. The glowing streaks mark the growing ends of microtubules (protein polymers that constantly assemble and disassemble through a process called dynamic instability). Rather than forming permanent tracks, microtubules are rebuilt continuously, allowing cells to reorganize their internal layout in real time. This behavior is essential for life. Cells rely on microtubule dynamics to divide accurately, migrate during development and repair, and maintain long-distance transport in neurons that may span over a meter in length. When this system is altered, the consequences are significant. Certain cancer therapies work by locking microtubules in place, preventing cell division. In contrast, failures in microtubule transport are linked to neurodegenerative conditions (like Alzheimer's) where intracellular delivery breaks down. What appears as abstract motion under a microscope is actually one of the core systems that keeps cells functional, adaptable, and alive. Video Credit: Andy Moore

William A. Wallace, Ph.D.

18,469 просмотров • 7 месяцев назад

The heat is rising in NCR, and stray animals are suffering silently. With no clean water, they’re forced to drink from dirty drains — damaging their kidneys and risking their lives. Please keep a bowl of clean water outside your home. Be a ray of hope for these voiceless souls. #CompassionInAction #StrayCare #dogs

The heat is rising in NCR, and stray animals are suffering silently. With no clean water, they’re forced to drink from dirty drains — damaging their kidneys and risking their lives. Please keep a bowl of clean water outside your home. Be a ray of hope for these voiceless souls. #CompassionInAction #StrayCare #dogs

Vidit Sharma 🇮🇳

17,144 просмотров • 1 год назад

STARLINK | DIRECT-TO-CELL SERVICE EXPANDS! Elon confirmed that Starlink will pursue deals with other U.S. carriers and mobile operators worldwide to expand the Direct-to-Cell service. After a year of exclusivity, SpaceX will expand Starlink Direct-to-Cell beyond T-Mobile. Starlink will provide satellite internet coverage in dead zones, with the recent launch of 26 satellites bringing the total to 168. Source: Drive Tesla Canada, Elon Musk

STARLINK | DIRECT-TO-CELL SERVICE EXPANDS! Elon confirmed that Starlink will pursue deals with other U.S. carriers and mobile operators worldwide to expand the Direct-to-Cell service. After a year of exclusivity, SpaceX will expand Starlink Direct-to-Cell beyond T-Mobile. Starlink will provide satellite internet coverage in dead zones, with the recent launch of 26 satellites bringing the total to 168. Source: Drive Tesla Canada, Elon Musk

Mario Nawfal

1,413,308 просмотров • 1 год назад