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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...

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William A. Wallace, Ph.D.

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18,469 views • 4 months ago •via X (Twitter)

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This mesmerizing timelapse captures the nonstop motion inside an animal cell. Moving red/orange streaks are the growing ends of microtubules, tiny “highways” that move proteins & other molecules within the cell. 📸: Andy Moore, HHMI’s Janelia Research Campus
0:11

This mesmerizing timelapse captures the nonstop motion inside an animal cell. Moving red/orange streaks are the growing ends of microtubules, tiny “highways” that move proteins & other molecules within the cell. 📸: Andy Moore, HHMI’s Janelia Research Campus

HHMI

13,634 views • 1 month ago

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.
0:14

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.

Brian Roemmele

191,436 views • 7 months ago

Notre Dame researchers have found that the single-cell pH of cancer cells changes dynamically during the four phases of cell division This discovery could eventually lead to therapies that will limit cancer cells’ ability to grow and divide:
0:18

Notre Dame researchers have found that the single-cell pH of cancer cells changes dynamically during the four phases of cell division This discovery could eventually lead to therapies that will limit cancer cells’ ability to grow and divide:

University of Notre Dame

42,055 views • 3 years ago

🚨 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.
0:10

🚨 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 views • 3 months ago

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.
0:14

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.

57,988 views • 10 months ago

💪 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
0:18

💪 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.

40,387 views • 6 months ago

🚨 SCIENTISTS JUST REVERSED AGING IN BLOOD STEM CELLS Researchers at Mount Sinai restored old blood stem cells to a youthful state by repairing tiny cellular recycling systems called lysosomes. In mice, aged stem cells regained the ability to: • regenerate healthy blood • rebuild immune cells • reduce inflammation • behave like young stem cells again One treatment increased blood-forming capacity by more than 8x. Why this matters: Your blood stem cells are responsible for constantly rebuilding your immune system and blood supply throughout life. As they age: • immunity weakens • inflammation rises • cancer risk increases • regeneration declines But this study suggests aging inside these cells may not be permanent. Scientists may have found a biological “reset switch.” The future of anti-aging may not come from replacing organs… …but from restoring the cells that rebuild the body itself. Follow for more future physics and biotech breakthroughs.
0:10

🚨 SCIENTISTS JUST REVERSED AGING IN BLOOD STEM CELLS Researchers at Mount Sinai restored old blood stem cells to a youthful state by repairing tiny cellular recycling systems called lysosomes. In mice, aged stem cells regained the ability to: • regenerate healthy blood • rebuild immune cells • reduce inflammation • behave like young stem cells again One treatment increased blood-forming capacity by more than 8x. Why this matters: Your blood stem cells are responsible for constantly rebuilding your immune system and blood supply throughout life. As they age: • immunity weakens • inflammation rises • cancer risk increases • regeneration declines But this study suggests aging inside these cells may not be permanent. Scientists may have found a biological “reset switch.” The future of anti-aging may not come from replacing organs… …but from restoring the cells that rebuild the body itself. Follow for more future physics and biotech breakthroughs.

TheNewPhysics

10,676 views • 1 month ago

Mitosis is a part of the cell cycle in which replicated chromosomes are separated into two new nuclei. Such a division gives rise to genetically identical cells in which the total number of chromosomes is maintained [source:
0:17

Mitosis is a part of the cell cycle in which replicated chromosomes are separated into two new nuclei. Such a division gives rise to genetically identical cells in which the total number of chromosomes is maintained [source:

Massimo

505,583 views • 3 years ago

You’re looking at neurons growing and connecting in real time 🧠. A 65-hour recording of hippocampal activity in a rat brain. The hippocampus plays a crucial role in memory and learning. In this footage, neurons extend their dendrites and axons, building and reshaping connections across days. Capturing this process live offers a rare view into how neural circuits form and reorganize. Why this matters ⬇️ 1️⃣It’s a continuous, multi-day recording of living hippocampal neurons under the microscope 2️⃣You can clearly see dendritic branching and network formation 3️⃣It reveals the dynamic processes that drive brain development and plasticity Observing growth at this resolution helps researchers understand how neurons connect—and how disruptions in these processes might contribute to neurological or psychiatric conditions. Credit to Louis Romet and Dr. Christophe Leterrier for the video
0:17

You’re looking at neurons growing and connecting in real time 🧠. A 65-hour recording of hippocampal activity in a rat brain. The hippocampus plays a crucial role in memory and learning. In this footage, neurons extend their dendrites and axons, building and reshaping connections across days. Capturing this process live offers a rare view into how neural circuits form and reorganize. Why this matters ⬇️ 1️⃣It’s a continuous, multi-day recording of living hippocampal neurons under the microscope 2️⃣You can clearly see dendritic branching and network formation 3️⃣It reveals the dynamic processes that drive brain development and plasticity Observing growth at this resolution helps researchers understand how neurons connect—and how disruptions in these processes might contribute to neurological or psychiatric conditions. Credit to Louis Romet and Dr. Christophe Leterrier for the video

William A. Wallace, Ph.D.

67,497 views • 7 months ago

Nagasaki is surrounded by mountains with a unique layout as everything was built over the natural slopes. Because of this, a “slope transport system” is in place to allow senior citizens or people with mobility issues, to move around Nagasaki with ease.
0:16

Nagasaki is surrounded by mountains with a unique layout as everything was built over the natural slopes. Because of this, a “slope transport system” is in place to allow senior citizens or people with mobility issues, to move around Nagasaki with ease.

Massimo

116,177 views • 27 days ago

There's a bacteriophage that turns bacteria into “liquid crystals.” Specifically, Pseudomonas aeruginosa bacteria make Pf phages, which are rod-shaped, negatively-charged, and measure about 2 micrometers in length (roughly the length of an E. coli cell). These phages leave the cells and enter their surroundings. There, they mix with polymers, also secreted by the cells, to form a crystalline matrix. Surprisingly, this is good for the cells. Although the phages kill some of them, it also makes their biofilms stickier and able to withstand certain antibiotics. These bacteria + phages are prevalent in cystic fibrosis patients; they've formed a sort of symbiotic relationship. The Pf phages are made from thousands of repeating copies of a coat protein, called CoaB, which wraps around a single-stranded, circular DNA genome. These genes are integrated directly on the bacterial chromosome. The bacteria “turn on” these phage genes when placed in a viscous environment with low oxygen levels. This is like a trigger to start forming a biofilm. And the cells make a lot of phages; about 100 billion per milliliter. These liquid crystals form because of a physics principle called “depletion attraction.” If you just mix a bunch of loose or flexible polymers together (such as long carbon chains) they will not form a liquid crystal. But if you mix stiff rods (the phages) with loose polymers at a high enough concentration, the polymers will force the phages close together to create a material that flows like a liquid despite being ordered like a crystal. See the video below. These liquid crystal biofilms are hard to get rid of. The negatively-charged phages block many antibiotics (like aminoglycosides, which are positively-charged) from entering cells. Liquid crystals also retain water, so these biofilms can survive on drier surfaces. I first heard about this from Malmesbury’s excellent newsletter, called “Telescopic Turnip.”
0:15

There's a bacteriophage that turns bacteria into “liquid crystals.” Specifically, Pseudomonas aeruginosa bacteria make Pf phages, which are rod-shaped, negatively-charged, and measure about 2 micrometers in length (roughly the length of an E. coli cell). These phages leave the cells and enter their surroundings. There, they mix with polymers, also secreted by the cells, to form a crystalline matrix. Surprisingly, this is good for the cells. Although the phages kill some of them, it also makes their biofilms stickier and able to withstand certain antibiotics. These bacteria + phages are prevalent in cystic fibrosis patients; they've formed a sort of symbiotic relationship. The Pf phages are made from thousands of repeating copies of a coat protein, called CoaB, which wraps around a single-stranded, circular DNA genome. These genes are integrated directly on the bacterial chromosome. The bacteria “turn on” these phage genes when placed in a viscous environment with low oxygen levels. This is like a trigger to start forming a biofilm. And the cells make a lot of phages; about 100 billion per milliliter. These liquid crystals form because of a physics principle called “depletion attraction.” If you just mix a bunch of loose or flexible polymers together (such as long carbon chains) they will not form a liquid crystal. But if you mix stiff rods (the phages) with loose polymers at a high enough concentration, the polymers will force the phages close together to create a material that flows like a liquid despite being ordered like a crystal. See the video below. These liquid crystal biofilms are hard to get rid of. The negatively-charged phages block many antibiotics (like aminoglycosides, which are positively-charged) from entering cells. Liquid crystals also retain water, so these biofilms can survive on drier surfaces. I first heard about this from Malmesbury’s excellent newsletter, called “Telescopic Turnip.”

Niko McCarty.

50,029 views • 6 months ago

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.

20,321 views • 4 months ago

Cells located in the midline of the embryo play crucial roles in development. These cells often influence cell fate decisions and guide axons to establish bilateral connections. Despite their importance, studying these transient cells and their complex interactions has been challenging. Today, we introduce human midline #assembloids—3D self-organizing cellular clusters derived from stem cells by the functional integration of floor plate #organoids and spinal cord #organoids. We demonstrate that midline assembloids enable cell specification and axon guidance in human neurons. Additionally, we use these assembloids to screen and identify human-enriched factors that control these processes. Work led by the incredible Massimo Onesto & Neal Amin!! More details in the preprint 👇
0:17

Cells located in the midline of the embryo play crucial roles in development. These cells often influence cell fate decisions and guide axons to establish bilateral connections. Despite their importance, studying these transient cells and their complex interactions has been challenging. Today, we introduce human midline #assembloids—3D self-organizing cellular clusters derived from stem cells by the functional integration of floor plate #organoids and spinal cord #organoids. We demonstrate that midline assembloids enable cell specification and axon guidance in human neurons. Additionally, we use these assembloids to screen and identify human-enriched factors that control these processes. Work led by the incredible Massimo Onesto & Neal Amin!! More details in the preprint 👇

Sergiu P. Pasca

15,810 views • 2 years ago

🚨 SCIENTISTS DISCOVERED HUMAN CELLS CAN RESPOND TO SOUND BY SWITCHING GENES ON AND OFF. Researchers found certain human cells especially fat cells react to mechanical sound vibrations by changing genetic activity. That means sound may influence biology far deeper than we realized. Why this matters: Your cells are not passive. They constantly sense: • pressure • vibration • movement • mechanical stress And now scientists are discovering those signals can directly affect gene behavior itself. In simple terms: Sound may act almost like a biological instruction signal. The implications are enormous: • regenerative medicine • targeted therapies • metabolic control • tissue engineering • non-invasive treatments • future bioelectric technologies The deeper science goes… …the more the human body starts looking less like a machine… …and more like a responsive living frequency system. What happens if biology is listening more than we ever imagined?
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🚨 SCIENTISTS DISCOVERED HUMAN CELLS CAN RESPOND TO SOUND BY SWITCHING GENES ON AND OFF. Researchers found certain human cells especially fat cells react to mechanical sound vibrations by changing genetic activity. That means sound may influence biology far deeper than we realized. Why this matters: Your cells are not passive. They constantly sense: • pressure • vibration • movement • mechanical stress And now scientists are discovering those signals can directly affect gene behavior itself. In simple terms: Sound may act almost like a biological instruction signal. The implications are enormous: • regenerative medicine • targeted therapies • metabolic control • tissue engineering • non-invasive treatments • future bioelectric technologies The deeper science goes… …the more the human body starts looking less like a machine… …and more like a responsive living frequency system. What happens if biology is listening more than we ever imagined?

TheNewPhysics

27,753 views • 1 month ago

The axonal cytoskeleton and other components. The structural support is provided by spectrin and actin near the cell membrane. Microtubules, form tracks and motor proteins utilize them. A real axon is far more complex, housing essential structures like mitochondria.
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The axonal cytoskeleton and other components. The structural support is provided by spectrin and actin near the cell membrane. Microtubules, form tracks and motor proteins utilize them. A real axon is far more complex, housing essential structures like mitochondria.

Ribosome Studio

15,635 views • 7 months ago

Clashes inside Latakia. For general understanding the entire region and every city in the Syrian Coast area is no mans land. Some patches are in control of the Syrian Government other patches by the insurgency cells. In cities, Sunni dominated neighbourhoods are in control of the Syrian Government while Alawite neighbourhoods are in control of the insurgency cells. Most neighbourhoods are in nobodies control. Far as I know; Himeimin is under control of insurgency cells (if true that’d be very interesting) Insurgency cells are mostly carrying out ambushes and hit and run attacks - Syrian Government forces are just defending. Added a video with some interesting patches..
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Clashes inside Latakia. For general understanding the entire region and every city in the Syrian Coast area is no mans land. Some patches are in control of the Syrian Government other patches by the insurgency cells. In cities, Sunni dominated neighbourhoods are in control of the Syrian Government while Alawite neighbourhoods are in control of the insurgency cells. Most neighbourhoods are in nobodies control. Far as I know; Himeimin is under control of insurgency cells (if true that’d be very interesting) Insurgency cells are mostly carrying out ambushes and hit and run attacks - Syrian Government forces are just defending. Added a video with some interesting patches..

ScharoMaroof

10,626 views • 1 year ago

This is what the inside of an axon would look like if you could shrink yourself down and walk through it. Most of us picture nerves as simple wires. They’re not. They’re living highways, packed with scaffolding, conveyor belts, motor proteins, and mitochondria powering the entire system. What you’re seeing in this video is a cinematic rendering of the axonal cytoskeleton: • Spectrin and actin forming the lattice just under the membrane • Microtubules laid out like high-speed rails • Motor proteins (kinesin & dynein) hauling cargo • Mitochondria supplying energy right where signals travel fastest Your thoughts, movements, memories, reflexes and every electrical impulse your brain sends rides along structures like these. This is still an oversimplification. A real axon is even more crowded, more dynamic, and more alive. A hidden world, running in complete silence, billions of times a day, keeping you conscious, coordinated, and alive. Source: Ribosomestudio
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This is what the inside of an axon would look like if you could shrink yourself down and walk through it. Most of us picture nerves as simple wires. They’re not. They’re living highways, packed with scaffolding, conveyor belts, motor proteins, and mitochondria powering the entire system. What you’re seeing in this video is a cinematic rendering of the axonal cytoskeleton: • Spectrin and actin forming the lattice just under the membrane • Microtubules laid out like high-speed rails • Motor proteins (kinesin & dynein) hauling cargo • Mitochondria supplying energy right where signals travel fastest Your thoughts, movements, memories, reflexes and every electrical impulse your brain sends rides along structures like these. This is still an oversimplification. A real axon is even more crowded, more dynamic, and more alive. A hidden world, running in complete silence, billions of times a day, keeping you conscious, coordinated, and alive. Source: Ribosomestudio

William A. Wallace, Ph.D.

73,570 views • 7 months ago

To westerners, this video looks like a normal, everyday occurrence in town. But in occupied Iran, this is what civil disobedience looks like: uncovered hair, young people dancing, and western music. All things that are banned by Sharia Law. Don't be fooled by the pro-regime propagandists who will use this video to claim that "Iran is free" and "No need to overthrow the Islamic Republic". Iran is still occupied by the terrorist Islamic Republic. Iranians are being executed every day in the name of Islam for the crime of speaking out and wanting to live in a free and secular society. This is just a glimpse of the slow crumble of Islamic oppression on a society that yearns for freedom. Expect to see more signs of civil disobedience as the regime continues to crumble and collapse. And expect to see more disinformation coming out, claiming that Iran is "already free", by those who are trying desperately to keep the Islamic Republic occupying Iran in power.
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To westerners, this video looks like a normal, everyday occurrence in town. But in occupied Iran, this is what civil disobedience looks like: uncovered hair, young people dancing, and western music. All things that are banned by Sharia Law. Don't be fooled by the pro-regime propagandists who will use this video to claim that "Iran is free" and "No need to overthrow the Islamic Republic". Iran is still occupied by the terrorist Islamic Republic. Iranians are being executed every day in the name of Islam for the crime of speaking out and wanting to live in a free and secular society. This is just a glimpse of the slow crumble of Islamic oppression on a society that yearns for freedom. Expect to see more signs of civil disobedience as the regime continues to crumble and collapse. And expect to see more disinformation coming out, claiming that Iran is "already free", by those who are trying desperately to keep the Islamic Republic occupying Iran in power.

Goldie Ghamari | گلسا قمری

28,261 views • 8 months ago

Today I received my 4th infusion of SGF (Stem Cell Growth Factors) at Edogawa Hospital in Tokyo, Japan. What is SGF? 🦷 SGF is derived from the dental pulp of children's naturally shed baby teeth. No stem cells are injected. Instead, the infusion contains the signaling molecules, growth factors, cytokines, and regenerative proteins that stem cells naturally produce. These biological messengers help coordinate communication between cells and are believed to support tissue repair, immune regulation, blood vessel health, and nerve regeneration. These growth factors are small enough to cross the blood brain barrier and reach the brain and nervous system directly. For someone like me with confirmed neuroinflammation, white matter atrophy, and small fiber neuropathy destroying my nerves from the inside out, the goal is remyelination. Rebuilding the insulation around my damaged nerve fibers.💯 Researchers have studied SHED (Stem Cells from Human Exfoliated Deciduous Teeth) for their regenerative potential in areas such as nerve repair, neuroinflammation, tissue healing, and age-related degeneration. Some people have nicknamed therapies like this the "Fountain of Youth" because the goal is not to replace damaged tissue, but to activate the body's own repair and regeneration pathways. Whether that nickname is deserved remains to be seen, but the science behind cellular signaling and regeneration is fascinating. Japan has become a global leader in regenerative medicine and allows access to therapies that are not currently available in the United States under its regenerative medicine framework. As Patient #27 in the McCairn–Edogawa Protocol, I am grateful to have the opportunity to experience this emerging science firsthand. 🧬🦷🇯🇵 #SGF #SHED #RegenerativeMedicine #StemCellScience #Neuroinflammation #SmallFiberNeuropathy #EdogawaHospital #Tokyo #MedicalInnovation
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Today I received my 4th infusion of SGF (Stem Cell Growth Factors) at Edogawa Hospital in Tokyo, Japan. What is SGF? 🦷 SGF is derived from the dental pulp of children's naturally shed baby teeth. No stem cells are injected. Instead, the infusion contains the signaling molecules, growth factors, cytokines, and regenerative proteins that stem cells naturally produce. These biological messengers help coordinate communication between cells and are believed to support tissue repair, immune regulation, blood vessel health, and nerve regeneration. These growth factors are small enough to cross the blood brain barrier and reach the brain and nervous system directly. For someone like me with confirmed neuroinflammation, white matter atrophy, and small fiber neuropathy destroying my nerves from the inside out, the goal is remyelination. Rebuilding the insulation around my damaged nerve fibers.💯 Researchers have studied SHED (Stem Cells from Human Exfoliated Deciduous Teeth) for their regenerative potential in areas such as nerve repair, neuroinflammation, tissue healing, and age-related degeneration. Some people have nicknamed therapies like this the "Fountain of Youth" because the goal is not to replace damaged tissue, but to activate the body's own repair and regeneration pathways. Whether that nickname is deserved remains to be seen, but the science behind cellular signaling and regeneration is fascinating. Japan has become a global leader in regenerative medicine and allows access to therapies that are not currently available in the United States under its regenerative medicine framework. As Patient #27 in the McCairn–Edogawa Protocol, I am grateful to have the opportunity to experience this emerging science firsthand. 🧬🦷🇯🇵 #SGF #SHED #RegenerativeMedicine #StemCellScience #Neuroinflammation #SmallFiberNeuropathy #EdogawaHospital #Tokyo #MedicalInnovation

Heather C

28,715 views • 21 days ago