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Congrats Andrew Weems and everyone involved on elucidating how blebs help cancer cells avoid anoikis (cell death when losing attachment). Study involves 3D microscopy, and doing math on cell surfaces, courtesy of the @DanuserLab computer vision wizards.

Reto Fiolka

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10,354 просмотров • 3 лет назад •via X (Twitter)

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1 billion cells. One atlas. Today, Illumina introduces the Billion Cell Atlas, creating the most comprehensive map of human disease biology — and unlocking unparalleled speed and scale in AI for drug discovery. The Atlas will help researchers, including founding participants AstraZeneca, Merck, and Eli Lilly and Company study the effect of switching on and off all 20,000 genes in cells linked to diseases that have been historically difficult to decode. Learn how the Atlas will elucidate the biological pathways behind some of the world’s most devastating diseases: #JPM2026

1 billion cells. One atlas. Today, Illumina introduces the Billion Cell Atlas, creating the most comprehensive map of human disease biology — and unlocking unparalleled speed and scale in AI for drug discovery. The Atlas will help researchers, including founding participants AstraZeneca, Merck, and Eli Lilly and Company study the effect of switching on and off all 20,000 genes in cells linked to diseases that have been historically difficult to decode. Learn how the Atlas will elucidate the biological pathways behind some of the world’s most devastating diseases: #JPM2026

Illumina

34,201 просмотров • 8 месяцев 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

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

eXoZymes (eXoZymes) (Nasdaq: EXOZ) CEO Michael Heltzen was featured on Session 20 of the GeneCoda podcast Executive Insights for Life Sciences Innovators, in an episode titled “AI-enabled cell-free biomanufacturing and the future of enzyme engineering,” streamed live on YouTube on April 17. eXoZymes is a B2i Digital (B2i Digital) Featured Company. See their full profile at In the conversation, Heltzen discusses the company’s thesis that producing complex molecules outside living cells can enable greater control, scalability, and speed compared to traditional biologic manufacturing. The discussion also covers how AI is helping identify and optimize enzyme pathways, the strategic considerations involved in building a platform company in today’s capital environment, what differentiates cell-free systems from established synthetic biology approaches, and where cell-free biomanufacturing could create commercial impact across nutraceutical, pharmaceutical, and industrial markets. Watch or listen here: Separately, eXoZymes and Cayman Chemical were featured in a Springwise case study on how the two companies are rethinking chemical manufacturing. The piece focuses on eXoZymes’ work bringing enzyme pathways from biology into the world of chemistry, with Cayman Chemical helping to scale the approach. CCO Damien Perriman is featured in the article. See the eXoZymes summary: eXoZymes is a Los Angeles, California-based biotechnology company that has developed a biomanufacturing platform offering the tools and insights to design, engineer, control, and optimize nature’s own natural processes to produce highly valuable natural products via a commercially scalable, sustainable, and abundant alternative: exozymes. eXoZymes is led by an experienced management team including Michael Heltzen, CEO; Damien Perriman, CCO; Dr. Tyler Korman, CSO and Co-founder; Dr. Paul Opgenorth, VP of Development and Co-founder; Fouad Nawaz, VP of Finance; Lasse H. Görlitz, VP of Communications; and Amy Lunzer, Chief of Staff. Learn more about eXoZymes Inc. at For investor inquiries, visit and learn about other B2i Digital Featured Companies at Disclosure: David Shapiro, Chief Executive Officer of B2i Digital, personally purchased in the open market and currently owns shares of unrestricted EXOZ stock, in line with B2i Digital’s practice of investing alongside its Featured Companies. This post is not intended to solicit the sale of EXOZ or any security, and it is not intended to offer any opinion on EXOZ as an investment. Conduct your own research and consult with your own professional advisors prior to making any investment decisions. See the complete disclosure in the Risks and Disclosures section of

B2i Digital

70,350 просмотров • 4 месяцев назад

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.”

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.

50,257 просмотров • 8 месяцев назад

Are you safer with LIDAR, or are you safer with vision? This is a false dichotomy. The more pertinent question today is "do you have something, or do you have nothing?" As you can see from the clips below, vision based systems avoid countless potential collisions every day. The difference between a crash and no crash isn't what sensor suite you chose — it's whether you have any AI on your car at all. Even if we concede that LIDAR may help prevent some additional crashes, we are really debating whether it is 1% of crashes or 0.00001% of crashes. Not all crashes are super complex and require lasers to detect. Most are simple, routine, and can easily be prevented by today's vision based AI. In fact, evidence is mounting that computer vision based systems can actually outperform more traditional approaches to self-driving. Why? Because the low cost of cameras enables you to create a much larger, more varied, and more diverse dataset. If you want to have expensive custom cars that's fine, but you're going to get fewer vehicles for the same budget. Seeing what's in front of you now is actually less important than predicting what's going to happen next — and the large scale datasets used to train pure vision systems are the best for predicting what's next. Counter-intuitively, the simpler and lower cost sensor actually has properties that make it better suited for training advanced AI. Computer vision based self-driving is often framed by LIDAR proponents as "cheaping out" on the sensor suite to save money. But it's not about being cheap, it's about bringing the technology to everyone. 1.2 million people die on the road every year around the world. That's around 39 million people who've died on the roads around the world since I was born — equivalent to a city the size of Tokyo or New Delhi getting wiped off the map. The status quo is simply unacceptable, and something has to be done to fix it as soon as possible. Of the 1.2 million people that will die on the roads this year, about 40,000 will be Americans. That's about 3%. So if we moved entirely to self-driving cars in America and brought crashes down to 0, 97% of the world's crash fatalities would still be taking place as usual. Deploying a $200,000+ retrofitted self-driving car may work in a few American cities, but it is not going to make sense in most places around the world where fares are much cheaper. Most often, the choice is not between LIDAR and vision. It's between vision or nothing. The best system is the system that's there running on my car when I need it to save my life. To say that all self-driving cars must have LIDAR is to sentence most of the world to death. We can't write off computer vision if we want to make a serious dent in this problem. It's going to be a key piece of the solution. Let LIDAR based players build the best self-driving car they can, and let vision based players do the same. We need to be trying everything

Are you safer with LIDAR, or are you safer with vision? This is a false dichotomy. The more pertinent question today is "do you have something, or do you have nothing?" As you can see from the clips below, vision based systems avoid countless potential collisions every day. The difference between a crash and no crash isn't what sensor suite you chose — it's whether you have any AI on your car at all. Even if we concede that LIDAR may help prevent some additional crashes, we are really debating whether it is 1% of crashes or 0.00001% of crashes. Not all crashes are super complex and require lasers to detect. Most are simple, routine, and can easily be prevented by today's vision based AI. In fact, evidence is mounting that computer vision based systems can actually outperform more traditional approaches to self-driving. Why? Because the low cost of cameras enables you to create a much larger, more varied, and more diverse dataset. If you want to have expensive custom cars that's fine, but you're going to get fewer vehicles for the same budget. Seeing what's in front of you now is actually less important than predicting what's going to happen next — and the large scale datasets used to train pure vision systems are the best for predicting what's next. Counter-intuitively, the simpler and lower cost sensor actually has properties that make it better suited for training advanced AI. Computer vision based self-driving is often framed by LIDAR proponents as "cheaping out" on the sensor suite to save money. But it's not about being cheap, it's about bringing the technology to everyone. 1.2 million people die on the road every year around the world. That's around 39 million people who've died on the roads around the world since I was born — equivalent to a city the size of Tokyo or New Delhi getting wiped off the map. The status quo is simply unacceptable, and something has to be done to fix it as soon as possible. Of the 1.2 million people that will die on the roads this year, about 40,000 will be Americans. That's about 3%. So if we moved entirely to self-driving cars in America and brought crashes down to 0, 97% of the world's crash fatalities would still be taking place as usual. Deploying a $200,000+ retrofitted self-driving car may work in a few American cities, but it is not going to make sense in most places around the world where fares are much cheaper. Most often, the choice is not between LIDAR and vision. It's between vision or nothing. The best system is the system that's there running on my car when I need it to save my life. To say that all self-driving cars must have LIDAR is to sentence most of the world to death. We can't write off computer vision if we want to make a serious dent in this problem. It's going to be a key piece of the solution. Let LIDAR based players build the best self-driving car they can, and let vision based players do the same. We need to be trying everything

Whole Mars Catalog

45,853 просмотров • 1 год назад

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

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

Dr. Kash Sarabi

16,057 просмотров • 1 год назад

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

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

Niko McCarty.

51,949 просмотров • 1 год назад

i've been paying 200$/month for AI tools for a while now claude, chatgpt, all of it thought that was just the price of doing things properly then i read this and had to close my laptop for a second someone bought a used GPU from eBay for $700 five years old. RTX 3090. the kind of card people sell when they upgrade for gaming plugged in a free model called Qwen 3.6 that alibaba quietly dropped last month and it scored 84.1 on vision tasks claude 4.5 opus scored 77.0 the 200$/month subscription lost to a free model running on old hardware the math gets worse after 4 months you've paid off the GPU from month 5 onwards you pay $8 for electricity that's it no subscription. no per message cost. nothing leaves your computer. ever. turns out i didn't have to is anyone else just finding out about this or was i the last one to know?

i've been paying 200$/month for AI tools for a while now claude, chatgpt, all of it thought that was just the price of doing things properly then i read this and had to close my laptop for a second someone bought a used GPU from eBay for $700 five years old. RTX 3090. the kind of card people sell when they upgrade for gaming plugged in a free model called Qwen 3.6 that alibaba quietly dropped last month and it scored 84.1 on vision tasks claude 4.5 opus scored 77.0 the 200$/month subscription lost to a free model running on old hardware the math gets worse after 4 months you've paid off the GPU from month 5 onwards you pay $8 for electricity that's it no subscription. no per message cost. nothing leaves your computer. ever. turns out i didn't have to is anyone else just finding out about this or was i the last one to know?

Crypto Mavka

14,126 просмотров • 2 месяцев назад

$On 11th August, 2025, I was involved in a ghastly accident on my way from Kumasi to Accra with my friend, an accident that almost took our lives. The accident happened around 4:00 am, just a few minutes’ drive from Nkawkaw. In those moments after the crash, fear took over. Help was not coming, and at a point, I genuinely feared for our lives. I kept thinking the car might catch fire as we were helpless. We both sustained serious injuries: the bone in my thigh got broken, and my friend suffered fractures in both legs. I was admitted at St. Joseph Hospital for 22 days, where I underwent surgery and received all my treatments. After the surgery, the pain was unbearable and i even forgot how to walk. I stayed indoors for a long time, battling both physical pain and depression. There were days and nights I cried endlessly, holding on to hope and praying to get better. I feared our legs might never be the same again. Today, I am grateful to say that we are both doing well. From the depths of my heart, I extend my sincere gratitude to my friends and family, the doctors, surgeons, nurses, and everyone who stood by me during this extremely trying period. Your support, prayers, and encouragement carried me through when I felt weakest.$

On 11th August, 2025, I was involved in a ghastly accident on my way from Kumasi to Accra with my friend, an accident that almost took our lives. The accident happened around 4:00 am, just a few minutes’ drive from Nkawkaw. In those moments after the crash, fear took over. Help was not coming, and at a point, I genuinely feared for our lives. I kept thinking the car might catch fire as we were helpless. We both sustained serious injuries: the bone in my thigh got broken, and my friend suffered fractures in both legs. I was admitted at St. Joseph Hospital for 22 days, where I underwent surgery and received all my treatments. After the surgery, the pain was unbearable and i even forgot how to walk. I stayed indoors for a long time, battling both physical pain and depression. There were days and nights I cried endlessly, holding on to hope and praying to get better. I feared our legs might never be the same again. Today, I am grateful to say that we are both doing well. From the depths of my heart, I extend my sincere gratitude to my friends and family, the doctors, surgeons, nurses, and everyone who stood by me during this extremely trying period. Your support, prayers, and encouragement carried me through when I felt weakest.

SIKAOFFICIAL🦍

223,482 просмотров • 8 месяцев назад

Let’s talk about light therapy, melasma, and how hormones play a role. ✨ I’m using the Nanoleaf LED Light Therapy Mask 🟩 Green light therapy is gentle, calming, and works near the surface of your skin. It can: • Soothe redness and inflammation • Help reduce dark spots and hyperpigmentation • Even out skin tone for a natural glow ❤️ Red light therapy is amazing for deeper repair, collagen, and cell rejuvenation, but if you have melasma, you’ll want to skip it. Here’s why ⬇️ Melasma causes dark patches that are easily triggered by heat, light, and hormonal changes. Red light can generate warmth and activate pigment cells, sometimes making melasma worse. And for women in perimenopause or menopause, shifting estrogen and progesterone levels can make skin even more reactive, which means pigmentation can flare up more easily. If you’re managing melasma, focus on gentle options like green or yellow light therapy, daily SPF, and a calm, consistent skincare routine. Your skin is evolving , treat it with patience, not punishment. 💚 And if you’re unsure, always do your own research. Talk to your dermatologist first. #melasma #greenlighttherapy #menopauseskin #skincaretips #skinhealth #hyperpigmentation #skincareeducation

Let’s talk about light therapy, melasma, and how hormones play a role. ✨ I’m using the Nanoleaf LED Light Therapy Mask 🟩 Green light therapy is gentle, calming, and works near the surface of your skin. It can: • Soothe redness and inflammation • Help reduce dark spots and hyperpigmentation • Even out skin tone for a natural glow ❤️ Red light therapy is amazing for deeper repair, collagen, and cell rejuvenation, but if you have melasma, you’ll want to skip it. Here’s why ⬇️ Melasma causes dark patches that are easily triggered by heat, light, and hormonal changes. Red light can generate warmth and activate pigment cells, sometimes making melasma worse. And for women in perimenopause or menopause, shifting estrogen and progesterone levels can make skin even more reactive, which means pigmentation can flare up more easily. If you’re managing melasma, focus on gentle options like green or yellow light therapy, daily SPF, and a calm, consistent skincare routine. Your skin is evolving , treat it with patience, not punishment. 💚 And if you’re unsure, always do your own research. Talk to your dermatologist first. #melasma #greenlighttherapy #menopauseskin #skincaretips #skinhealth #hyperpigmentation #skincareeducation

Naughty Gym becoming AYA Society

23,234 просмотров • 11 месяцев назад

what im about to say is just MY vision! this is how i see it i feel like the car in the mv represents heeseung himself and everything he has gone through over the years. in the mv, when he first got the car, it’s bright red. red symbolizes his passion, excitement, and happiness as he finally achieves the dream he had worked toward for so long. he has debuted, he is standing on stage and he is doing what he always wanted to do as the story progresses, the car becomes almost completely gray. i see this as a reflection of heeseung’s burnout and emotional exhaustion. the feeling of becoming drained after constantly giving so much of yourself without having enough time to recover. heeseung had dreams and desire to release his own solo music and show a different side of himself as an artist, but he wasn’t able to do it, he pushed it aside for a long time so he started losing hope. the fading color of the car mirrors how his passion and motivation were slowly being overshadowed by frustration and disappointment yet the car never becomes entirely gray. the driver’s door is still red. that remaining red represents the part of heeseung that refused to let go of his dreams and passion. no matter how exhausted he became, no matter how much disappointment he faced, there was still a small part of him that continued to believe that things could get better. the car is literally following heeseung and refusing to let go. i feel like it symbolizes the passion that survived even when everything else seemed to be fading away – the fully red car shows the joy of a dream coming true – the gray car shows the emotional cost of everything that came afterward – and the driver’s red door shows that no matter how difficult the journey became, he never completely lost himself that’s why i believe the car represents heeseung/his dreams

what im about to say is just MY vision! this is how i see it i feel like the car in the mv represents heeseung himself and everything he has gone through over the years. in the mv, when he first got the car, it’s bright red. red symbolizes his passion, excitement, and happiness as he finally achieves the dream he had worked toward for so long. he has debuted, he is standing on stage and he is doing what he always wanted to do as the story progresses, the car becomes almost completely gray. i see this as a reflection of heeseung’s burnout and emotional exhaustion. the feeling of becoming drained after constantly giving so much of yourself without having enough time to recover. heeseung had dreams and desire to release his own solo music and show a different side of himself as an artist, but he wasn’t able to do it, he pushed it aside for a long time so he started losing hope. the fading color of the car mirrors how his passion and motivation were slowly being overshadowed by frustration and disappointment yet the car never becomes entirely gray. the driver’s door is still red. that remaining red represents the part of heeseung that refused to let go of his dreams and passion. no matter how exhausted he became, no matter how much disappointment he faced, there was still a small part of him that continued to believe that things could get better. the car is literally following heeseung and refusing to let go. i feel like it symbolizes the passion that survived even when everything else seemed to be fading away – the fully red car shows the joy of a dream coming true – the gray car shows the emotional cost of everything that came afterward – and the driver’s red door shows that no matter how difficult the journey became, he never completely lost himself that’s why i believe the car represents heeseung/his dreams

ev.

50,766 просмотров • 2 месяцев назад

Hello guys. I need your help please. Help. I’m doing this despite the risks involved 🙏. I’m sure you’ve seen the story Citizen tv aired recently about a brother who beat up his sister mercilessly trying to “discipline” her. Before she was beaten up, he had sent cops to “arrest” her in Busia because she was in Uganda and they didn’t want her traveling. The cops got her and she spent 24hrs in a cell before being transferred to Nairobi where she spent another 4 days in Pangani police station with no charges or being taken to court. The brother bribed the police officers to arrest her and put her in a cell to “discipline” her. They took her home and the brother beat her up mercilessly with blows and kicks and stepped on her as she begged that she was on her period. He also slapped his other sister who tried to intervene. The brother in law by the name Sharmake Hussein is the one pulling the strings and is highly connected to the DCI. The DCI headquarters has the victim’s phone and she went to pick it up yesterday but they refused and tried to make her withdraw the charges. Officers at the headquarters by the name Amin and Mahad as narrated by the victim tried to trick her to sign and withdraw the case. She refused and in return got threatened by the family who were present in the presence of the DCI KENYA The perpetrator was at DCI KENYA headquarters yesterday and they didn’t arrest him!!!! I’m honestly shocked that they were forcing the victim to withdraw the case instead of arresting the perpetrator. I took the girl to somewhere safe today a big big thank you to VOCAL Africa since the brother wants to harm her and DCI KENYA is enabling it. All the other younger siblings are not safe either and even the youngest was manhandled at the headquarters yesterday and they took his phone. Both phones are at the DCI KENYA and I’m asking with what authority did you take their phones and manhandled them? The youngest is a minor and I still don’t think these kids are safe. I talked to them today and the parents are the biggest enablers. If anything happens to any one of them DCI KENYA is responsible for being bribed and used by the perpetrators who’s going around claiming he knows “big people” including Duale. I have clips which I’ll be posting of him being nasty and arrogant of the law. DCI KENYA arrest the perpetrator Abdiaziz Daqare!!!!!!! Arrest him before he kills these girls and kids!!! You’re being an enabler!!!

Hello guys. I need your help please. Help. I’m doing this despite the risks involved 🙏. I’m sure you’ve seen the story Citizen tv aired recently about a brother who beat up his sister mercilessly trying to “discipline” her. Before she was beaten up, he had sent cops to “arrest” her in Busia because she was in Uganda and they didn’t want her traveling. The cops got her and she spent 24hrs in a cell before being transferred to Nairobi where she spent another 4 days in Pangani police station with no charges or being taken to court. The brother bribed the police officers to arrest her and put her in a cell to “discipline” her. They took her home and the brother beat her up mercilessly with blows and kicks and stepped on her as she begged that she was on her period. He also slapped his other sister who tried to intervene. The brother in law by the name Sharmake Hussein is the one pulling the strings and is highly connected to the DCI. The DCI headquarters has the victim’s phone and she went to pick it up yesterday but they refused and tried to make her withdraw the charges. Officers at the headquarters by the name Amin and Mahad as narrated by the victim tried to trick her to sign and withdraw the case. She refused and in return got threatened by the family who were present in the presence of the DCI KENYA The perpetrator was at DCI KENYA headquarters yesterday and they didn’t arrest him!!!! I’m honestly shocked that they were forcing the victim to withdraw the case instead of arresting the perpetrator. I took the girl to somewhere safe today a big big thank you to VOCAL Africa since the brother wants to harm her and DCI KENYA is enabling it. All the other younger siblings are not safe either and even the youngest was manhandled at the headquarters yesterday and they took his phone. Both phones are at the DCI KENYA and I’m asking with what authority did you take their phones and manhandled them? The youngest is a minor and I still don’t think these kids are safe. I talked to them today and the parents are the biggest enablers. If anything happens to any one of them DCI KENYA is responsible for being bribed and used by the perpetrators who’s going around claiming he knows “big people” including Duale. I have clips which I’ll be posting of him being nasty and arrogant of the law. DCI KENYA arrest the perpetrator Abdiaziz Daqare!!!!!!! Arrest him before he kills these girls and kids!!! You’re being an enabler!!!

Hanifa 🇵🇸 🇸🇩 🇨🇩 🇰🇪

588,373 просмотров • 1 год назад

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

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

Bo Wang

24,807 просмотров • 6 месяцев назад

If you ever wondered what level of desperation the british press is at when it comes to seeing Prince William acknowledge Harry publicly, look no further than how they are salivating and extrapolating at a simple mention of the name "Harry" by William🤭🤦🏽‍♀️ In a new trailer for his Homeward documentary which will air this Wednesday on ITV, Prince William mentioned how his mother inspired his work on homelessness saying: "My mother took me to the Passage, she took Harry and I both there. I'd never been to anything like that before and I was a bit anxious as to what to expect"🔥 "My mother went about her usual part of making everyone feel relaxed and having a joke with everyone...I remember having some good conversation, playing chess and chatting. You meet people, like I did then, who put a different perspective in your head."❤️ A beautiful quote that has now been hijacked by the press who latched onto the name "harry" mentioned publicly for the first time in 6 years. And now an olive tree somewhere seem to have lost a branch🤡 And now the ex royal butler is on TV wondering how long they have been facetiming behind doors🤡 Soon, we will hear how Harry has moved to adelaide cottage with W&C🤡 What is very interesting here, is how effective William's silence has been. By refusing to engage in any sort of way in the drama, William has starved both H&m and the british press of the drama they craved😏 The question here is Why would William airbrush Harry out of his past? He has proven he does not hold any grudge against Harry. In fact, we saw that He still has pictures of him and harry is still the brother who went to the homeless charity with Diana and William. That is an actual fact. So it would be extremely small to airbrush Harry out of a story that involved him. It is rather Harry who is small and petty and who wiped William out of Invictus when William helped set it up and was involved in more pertinent ways than Harry, simply out of Jealousy🤷🏽‍♀️ However, the Homeward Doc is not about Harry but rather about contextualising how Diana influenced BOTH of her sons toward being sensitive to Homelessness. Yet, out of both sons, ONLY WILLIAM decided to do something about it🔥 THAT is the big reveal here. Diana exposed both sons but Only one was impacted enough and cared enough to decide to make a difference toward Homelessness❤️ This is the work that the documentary will highlight. Not any brotherly relationship or olive branch or facetiming between H and W🤡 A rather interesting highlight was learning how George, Charlotte and Louis are already aware of the problem of homelessness the UK faces. Prince William introduced the topic saying that when he was younger and Diana took his brother and him on school runs, he would wonder about the homeless on the streets: "When you are that small, you are just curious and trying to work out what's going on," "You ask the question 'why are they sitting there?' My mother would talk to us a bit about why they were there and it definitely made a really big impact."❤️ Indeed, it made a big impact enough to galvanise him into working with the homeless charity for 19 years and today, creating housing and a rehabilitation system, supported by local agencies, to help solve the issue🥺 In 1993, his mother introduced him to a cause he will carry in life. Today, 31 years later and a father himself, it is William's turn to teach his children about who the people sleeping on the side of the streets are: "The first few times I thought 'do I bring this up or should I wait to see if they notice? Sure enough, they did. They were sort of in silence when I said what was going on."🔥 Our first teachers in life are our Parents. Children look up to parents for guidance in life. Thus, It is reassuring to know that W&C are raising well balanced children taught to show care and compassion to others and above all, to help and serve the british public❤️☕️ 📹ITVx

If you ever wondered what level of desperation the british press is at when it comes to seeing Prince William acknowledge Harry publicly, look no further than how they are salivating and extrapolating at a simple mention of the name "Harry" by William🤭🤦🏽‍♀️ In a new trailer for his Homeward documentary which will air this Wednesday on ITV, Prince William mentioned how his mother inspired his work on homelessness saying: "My mother took me to the Passage, she took Harry and I both there. I'd never been to anything like that before and I was a bit anxious as to what to expect"🔥 "My mother went about her usual part of making everyone feel relaxed and having a joke with everyone...I remember having some good conversation, playing chess and chatting. You meet people, like I did then, who put a different perspective in your head."❤️ A beautiful quote that has now been hijacked by the press who latched onto the name "harry" mentioned publicly for the first time in 6 years. And now an olive tree somewhere seem to have lost a branch🤡 And now the ex royal butler is on TV wondering how long they have been facetiming behind doors🤡 Soon, we will hear how Harry has moved to adelaide cottage with W&C🤡 What is very interesting here, is how effective William's silence has been. By refusing to engage in any sort of way in the drama, William has starved both H&m and the british press of the drama they craved😏 The question here is Why would William airbrush Harry out of his past? He has proven he does not hold any grudge against Harry. In fact, we saw that He still has pictures of him and harry is still the brother who went to the homeless charity with Diana and William. That is an actual fact. So it would be extremely small to airbrush Harry out of a story that involved him. It is rather Harry who is small and petty and who wiped William out of Invictus when William helped set it up and was involved in more pertinent ways than Harry, simply out of Jealousy🤷🏽‍♀️ However, the Homeward Doc is not about Harry but rather about contextualising how Diana influenced BOTH of her sons toward being sensitive to Homelessness. Yet, out of both sons, ONLY WILLIAM decided to do something about it🔥 THAT is the big reveal here. Diana exposed both sons but Only one was impacted enough and cared enough to decide to make a difference toward Homelessness❤️ This is the work that the documentary will highlight. Not any brotherly relationship or olive branch or facetiming between H and W🤡 A rather interesting highlight was learning how George, Charlotte and Louis are already aware of the problem of homelessness the UK faces. Prince William introduced the topic saying that when he was younger and Diana took his brother and him on school runs, he would wonder about the homeless on the streets: "When you are that small, you are just curious and trying to work out what's going on," "You ask the question 'why are they sitting there?' My mother would talk to us a bit about why they were there and it definitely made a really big impact."❤️ Indeed, it made a big impact enough to galvanise him into working with the homeless charity for 19 years and today, creating housing and a rehabilitation system, supported by local agencies, to help solve the issue🥺 In 1993, his mother introduced him to a cause he will carry in life. Today, 31 years later and a father himself, it is William's turn to teach his children about who the people sleeping on the side of the streets are: "The first few times I thought 'do I bring this up or should I wait to see if they notice? Sure enough, they did. They were sort of in silence when I said what was going on."🔥 Our first teachers in life are our Parents. Children look up to parents for guidance in life. Thus, It is reassuring to know that W&C are raising well balanced children taught to show care and compassion to others and above all, to help and serve the british public❤️☕️ 📹ITVx

Canellecitadelle

104,953 просмотров • 1 год назад

Here's a simple explanation of how nnEMFs negatively impact our health (affect anything from fertility, to hormones, to sleep etc) . We (humans) evolved amid natural low-level, unpolarized ELF/geomagnetic fields and electromagnetic frequencies such as 300GHz, 300MHz or even 60Hz that can be found in sources of nnEMFs ranging from your smartphone all the way to radars and satellites. So unlike native EMFs, which occur naturally from the earth’s magnetic field or sunlight for example, nnEMFs have frequencies, intensities and patterns that differ from those our biology evolved to handle. Some key characteristics of nnEMFs include: -They are classified by frequency (measured in hertz (Hz)) -They include extremely low frequency (ELF) fields (such as 50–60 Hz from power lines), radiofrequency (RF) fields (such as 300 kHz–300 GHz, used in mobile phones and Wi-Fi) and microwave frequencies (such as 2.45 GHz in microwaves). -They (nnEMFs) are polarized and pulsed unlike natural EMFs, which are often unpolarized and continuous. Now the seven key biological mechanisms underlying the negative effects of nnEMFs include: -Oxidative stress. nnEMFs, particularly RF fields, can increase reactive oxygen species (ROS) like superoxide or hydroxyl radicals and cause lipid peroxidation in cells, thus alterling antioxidant enzyme levels (such as superoxide dismutase) and damaging cell membranes, proteins and DNA. -Calcium channel dysregulation. nnEMFs, increase intracellular calcium through voltage-gated calcium channels (VGCCs). VGCCs are large protein complexes that “open” in response to electrical signals (they open when the membrane depolarizes (becomes less negative)), in order for calcium ions to enter cells (due to its concentration gradient (higher outside than inside cells)) and nnEMFs act as an external electrical stimulus. VGCCs trigger neurotransmitter release (particularly glutamate), initiate contraction in cardiac and skeletal muscle for example, eegulate hormone secretion, control gene expression, enzyme activity and apoptosis. -DNA damage. nnEMFs, may induce single- and double-strand DNA breaks, directly (through energy transfer) or indirectly (through ROS). -Melatonin suppression. This happens possibly by altering neuronal signaling or mimicking some signals of light exposure but human and animal studies show reduced melatonin levels after RFR exposure, particularly at night. -Increasing blood-brain barrier permeability. This is well documented in animal studies that show increased blood-brain barrier leakage after RFR exposure, but it’s true that human research is limited. Yet based on the 4 previous mechanisms that were just discussed this isn’t unlikely and nnEMFs probably increase permeability of endothelial cells in barriers in humans as well, probably through oxidative stress or calcium-mediated tight junction disruption. -Autonomic nervous system dysregulation. It’s documented that nnEMFs alter sympathetic and parasympathetic activity thus affecting heart rate variability and of course, animal studies show even altered neurotransmitter levels. -Disruption of cellular electrical balance. Our cells maintain a negative membrane potential (resting potential) and nnEMFs interfere with ion channels altering membrane potential and disrupting processes like nerve signaling, muscle contraction or enzyme function. Then of course there are other ones such as heat shock protein induction for example (cell culture studies show increased HSP expression after EMF exposure, even at non-thermal levels). Now here are some practical suggestions that will help you navigate our nnEMF word better and won’t turn you into a lunatic. Number 1: Limit your exposure to them / distance yourself form them. Without this the rest of the tips won’t really help. But you don’t have to turn into a lunatic while implementing this. Leave devices you’re not using in other rooms, have your phone on airplone mode when you’re not using it/need it, ditch your air pods, close the wifi at night (big one)/when you’re not using it, spend more time in nature instead of watching netflix, don’t be on your phone for no reason, use ethernet cables and so on. Number 2: Go and ground. We carry a constant flow of electrical charge which we week to discharge and if we never do this and thus never restore and maintain the body’s natural electrical state, disease will inevitably happen. The surface of the earth, possesses a limitless and continuously renewed supply of free or mobile electrons as a consequence of a global atmospheric electric circuit. A direct earth connection enables both diurnal electrical rhythms-free electrons to flow from the earth to the body and neutralize the positively charged free radicals. *You can use grounding mats, pads etc if you also use an outlet tester. Number 3: Endogenous glutathione max Glutathione is a substance made from the amino acids glycine, cysteine, and glutamic acid. It is naturally produced in the cytosol (an intracellular matrix) and helps with many processes varying from detoxification, protecting the mitochondria from oxidative stress, heart health and the immune system all the way to thyroid hormone conversion. Number 4: Get enough minerals, vitamin C, E, high quality seafood. Number 5: Glutamate serves a role, but given the effects of nnEMFs on nmda it is a good idea to avoid free forms of glutamate and support GABA. Number 7: Further “lower” intracellular calcium through sunlight, nutrition, supplements and taking care of your thyroid. Nutrition-wise wise you will need: -Magnesium -Vitamin K2 -Glycine -Thiamine (indirectly (CO2 prevents the accumulation of intracellular calcium)) -Vitamin E -Boron -Zinc Number 8: Do not use your electronic devices (iphone, laptop etc) while they are charging. Number 9: Rhodiola might be promising as well.

Here's a simple explanation of how nnEMFs negatively impact our health (affect anything from fertility, to hormones, to sleep etc) . We (humans) evolved amid natural low-level, unpolarized ELF/geomagnetic fields and electromagnetic frequencies such as 300GHz, 300MHz or even 60Hz that can be found in sources of nnEMFs ranging from your smartphone all the way to radars and satellites. So unlike native EMFs, which occur naturally from the earth’s magnetic field or sunlight for example, nnEMFs have frequencies, intensities and patterns that differ from those our biology evolved to handle. Some key characteristics of nnEMFs include: -They are classified by frequency (measured in hertz (Hz)) -They include extremely low frequency (ELF) fields (such as 50–60 Hz from power lines), radiofrequency (RF) fields (such as 300 kHz–300 GHz, used in mobile phones and Wi-Fi) and microwave frequencies (such as 2.45 GHz in microwaves). -They (nnEMFs) are polarized and pulsed unlike natural EMFs, which are often unpolarized and continuous. Now the seven key biological mechanisms underlying the negative effects of nnEMFs include: -Oxidative stress. nnEMFs, particularly RF fields, can increase reactive oxygen species (ROS) like superoxide or hydroxyl radicals and cause lipid peroxidation in cells, thus alterling antioxidant enzyme levels (such as superoxide dismutase) and damaging cell membranes, proteins and DNA. -Calcium channel dysregulation. nnEMFs, increase intracellular calcium through voltage-gated calcium channels (VGCCs). VGCCs are large protein complexes that “open” in response to electrical signals (they open when the membrane depolarizes (becomes less negative)), in order for calcium ions to enter cells (due to its concentration gradient (higher outside than inside cells)) and nnEMFs act as an external electrical stimulus. VGCCs trigger neurotransmitter release (particularly glutamate), initiate contraction in cardiac and skeletal muscle for example, eegulate hormone secretion, control gene expression, enzyme activity and apoptosis. -DNA damage. nnEMFs, may induce single- and double-strand DNA breaks, directly (through energy transfer) or indirectly (through ROS). -Melatonin suppression. This happens possibly by altering neuronal signaling or mimicking some signals of light exposure but human and animal studies show reduced melatonin levels after RFR exposure, particularly at night. -Increasing blood-brain barrier permeability. This is well documented in animal studies that show increased blood-brain barrier leakage after RFR exposure, but it’s true that human research is limited. Yet based on the 4 previous mechanisms that were just discussed this isn’t unlikely and nnEMFs probably increase permeability of endothelial cells in barriers in humans as well, probably through oxidative stress or calcium-mediated tight junction disruption. -Autonomic nervous system dysregulation. It’s documented that nnEMFs alter sympathetic and parasympathetic activity thus affecting heart rate variability and of course, animal studies show even altered neurotransmitter levels. -Disruption of cellular electrical balance. Our cells maintain a negative membrane potential (resting potential) and nnEMFs interfere with ion channels altering membrane potential and disrupting processes like nerve signaling, muscle contraction or enzyme function. Then of course there are other ones such as heat shock protein induction for example (cell culture studies show increased HSP expression after EMF exposure, even at non-thermal levels). Now here are some practical suggestions that will help you navigate our nnEMF word better and won’t turn you into a lunatic. Number 1: Limit your exposure to them / distance yourself form them. Without this the rest of the tips won’t really help. But you don’t have to turn into a lunatic while implementing this. Leave devices you’re not using in other rooms, have your phone on airplone mode when you’re not using it/need it, ditch your air pods, close the wifi at night (big one)/when you’re not using it, spend more time in nature instead of watching netflix, don’t be on your phone for no reason, use ethernet cables and so on. Number 2: Go and ground. We carry a constant flow of electrical charge which we week to discharge and if we never do this and thus never restore and maintain the body’s natural electrical state, disease will inevitably happen. The surface of the earth, possesses a limitless and continuously renewed supply of free or mobile electrons as a consequence of a global atmospheric electric circuit. A direct earth connection enables both diurnal electrical rhythms-free electrons to flow from the earth to the body and neutralize the positively charged free radicals. *You can use grounding mats, pads etc if you also use an outlet tester. Number 3: Endogenous glutathione max Glutathione is a substance made from the amino acids glycine, cysteine, and glutamic acid. It is naturally produced in the cytosol (an intracellular matrix) and helps with many processes varying from detoxification, protecting the mitochondria from oxidative stress, heart health and the immune system all the way to thyroid hormone conversion. Number 4: Get enough minerals, vitamin C, E, high quality seafood. Number 5: Glutamate serves a role, but given the effects of nnEMFs on nmda it is a good idea to avoid free forms of glutamate and support GABA. Number 7: Further “lower” intracellular calcium through sunlight, nutrition, supplements and taking care of your thyroid. Nutrition-wise wise you will need: -Magnesium -Vitamin K2 -Glycine -Thiamine (indirectly (CO2 prevents the accumulation of intracellular calcium)) -Vitamin E -Boron -Zinc Number 8: Do not use your electronic devices (iphone, laptop etc) while they are charging. Number 9: Rhodiola might be promising as well.

George Ferman

68,565 просмотров • 3 месяцев назад

Here's a simple explanation of how nnEMFs negatively impact our health (affect anything from fertility, to hormones, to sleep etc) . We (humans) evolved amid natural low-level, unpolarized ELF/geomagnetic fields and electromagnetic frequencies such as 300GHz, 300MHz or even 60Hz that can be found in sources of nnEMFs ranging from your smartphone all the way to radars and satellites. So unlike native EMFs, which occur naturally from the earth’s magnetic field or sunlight for example, nnEMFs have frequencies, intensities and patterns that differ from those our biology evolved to handle. Some key characteristics of nnEMFs include: -They are classified by frequency (measured in hertz (Hz)) -They include extremely low frequency (ELF) fields (such as 50–60 Hz from power lines), radiofrequency (RF) fields (such as 300 kHz–300 GHz, used in mobile phones and Wi-Fi) and microwave frequencies (such as 2.45 GHz in microwaves). -They (nnEMFs) are polarized and pulsed unlike natural EMFs, which are often unpolarized and continuous. Now the seven key biological mechanisms underlying the negative effects of nnEMFs include: -Oxidative stress. nnEMFs, particularly RF fields, can increase reactive oxygen species (ROS) like superoxide or hydroxyl radicals and cause lipid peroxidation in cells, thus alterling antioxidant enzyme levels (such as superoxide dismutase) and damaging cell membranes, proteins and DNA. -Calcium channel dysregulation. nnEMFs, increase intracellular calcium through voltage-gated calcium channels (VGCCs). VGCCs are large protein complexes that “open” in response to electrical signals (they open when the membrane depolarizes (becomes less negative)), in order for calcium ions to enter cells (due to its concentration gradient (higher outside than inside cells)) and nnEMFs act as an external electrical stimulus. VGCCs trigger neurotransmitter release (particularly glutamate), initiate contraction in cardiac and skeletal muscle for example, eegulate hormone secretion, control gene expression, enzyme activity and apoptosis. -DNA damage. nnEMFs, may induce single- and double-strand DNA breaks, directly (through energy transfer) or indirectly (through ROS). -Melatonin suppression. This happens possibly by altering neuronal signaling or mimicking some signals of light exposure but human and animal studies show reduced melatonin levels after RFR exposure, particularly at night. -Increasing blood-brain barrier permeability. This is well documented in animal studies that show increased blood-brain barrier leakage after RFR exposure, but it’s true that human research is limited. Yet based on the 4 previous mechanisms that were just discussed this isn’t unlikely and nnEMFs probably increase permeability of endothelial cells in barriers in humans as well, probably through oxidative stress or calcium-mediated tight junction disruption. -Autonomic nervous system dysregulation. It’s documented that nnEMFs alter sympathetic and parasympathetic activity thus affecting heart rate variability and of course, animal studies show even altered neurotransmitter levels. -Disruption of cellular electrical balance. Our cells maintain a negative membrane potential (resting potential) and nnEMFs interfere with ion channels altering membrane potential and disrupting processes like nerve signaling, muscle contraction or enzyme function. Then of course there are other ones such as heat shock protein induction for example (cell culture studies show increased HSP expression after EMF exposure, even at non-thermal levels). Now here are some practical suggestions that will help you navigate our nnEMF word better and won’t turn you into a lunatic. Number 1: Limit your exposure to them / distance yourself form them. Without this the rest of the tips won’t really help. But you don’t have to turn into a lunatic while implementing this. Leave devices you’re not using in other rooms, have your phone on airplone mode when you’re not using it/need it, ditch your air pods, close the wifi at night (big one)/when you’re not using it, spend more time in nature instead of watching netflix, don’t be on your phone for no reason, use ethernet cables and so on. Number 2: Go and ground. We carry a constant flow of electrical charge which we week to discharge and if we never do this and thus never restore and maintain the body’s natural electrical state, disease will inevitably happen. The surface of the earth, possesses a limitless and continuously renewed supply of free or mobile electrons as a consequence of a global atmospheric electric circuit. A direct earth connection enables both diurnal electrical rhythms-free electrons to flow from the earth to the body and neutralize the positively charged free radicals. *You can use grounding mats, pads etc if you also use an outlet tester. Number 3: Endogenous glutathione max Glutathione is a substance made from the amino acids glycine, cysteine, and glutamic acid. It is naturally produced in the cytosol (an intracellular matrix) and helps with many processes varying from detoxification, protecting the mitochondria from oxidative stress, heart health and the immune system all the way to thyroid hormone conversion. Number 4: Get enough minerals, vitamin C, E, high quality seafood. Number 5: Glutamate serves a role, but given the effects of nnEMFs on nmda it is a good idea to avoid free forms of glutamate and support GABA. Number 7: Further “lower” intracellular calcium through sunlight, nutrition, supplements and taking care of your thyroid. Nutrition-wise wise you will need: -Magnesium -Vitamin K2 -Glycine -Thiamine (indirectly (CO2 prevents the accumulation of intracellular calcium)) -Vitamin E -Boron -Zinc Number 8: Do not use your electronic devices (iphone, laptop etc) while they are charging. Number 9: Rhodiola might be promising as well.

Here's a simple explanation of how nnEMFs negatively impact our health (affect anything from fertility, to hormones, to sleep etc) . We (humans) evolved amid natural low-level, unpolarized ELF/geomagnetic fields and electromagnetic frequencies such as 300GHz, 300MHz or even 60Hz that can be found in sources of nnEMFs ranging from your smartphone all the way to radars and satellites. So unlike native EMFs, which occur naturally from the earth’s magnetic field or sunlight for example, nnEMFs have frequencies, intensities and patterns that differ from those our biology evolved to handle. Some key characteristics of nnEMFs include: -They are classified by frequency (measured in hertz (Hz)) -They include extremely low frequency (ELF) fields (such as 50–60 Hz from power lines), radiofrequency (RF) fields (such as 300 kHz–300 GHz, used in mobile phones and Wi-Fi) and microwave frequencies (such as 2.45 GHz in microwaves). -They (nnEMFs) are polarized and pulsed unlike natural EMFs, which are often unpolarized and continuous. Now the seven key biological mechanisms underlying the negative effects of nnEMFs include: -Oxidative stress. nnEMFs, particularly RF fields, can increase reactive oxygen species (ROS) like superoxide or hydroxyl radicals and cause lipid peroxidation in cells, thus alterling antioxidant enzyme levels (such as superoxide dismutase) and damaging cell membranes, proteins and DNA. -Calcium channel dysregulation. nnEMFs, increase intracellular calcium through voltage-gated calcium channels (VGCCs). VGCCs are large protein complexes that “open” in response to electrical signals (they open when the membrane depolarizes (becomes less negative)), in order for calcium ions to enter cells (due to its concentration gradient (higher outside than inside cells)) and nnEMFs act as an external electrical stimulus. VGCCs trigger neurotransmitter release (particularly glutamate), initiate contraction in cardiac and skeletal muscle for example, eegulate hormone secretion, control gene expression, enzyme activity and apoptosis. -DNA damage. nnEMFs, may induce single- and double-strand DNA breaks, directly (through energy transfer) or indirectly (through ROS). -Melatonin suppression. This happens possibly by altering neuronal signaling or mimicking some signals of light exposure but human and animal studies show reduced melatonin levels after RFR exposure, particularly at night. -Increasing blood-brain barrier permeability. This is well documented in animal studies that show increased blood-brain barrier leakage after RFR exposure, but it’s true that human research is limited. Yet based on the 4 previous mechanisms that were just discussed this isn’t unlikely and nnEMFs probably increase permeability of endothelial cells in barriers in humans as well, probably through oxidative stress or calcium-mediated tight junction disruption. -Autonomic nervous system dysregulation. It’s documented that nnEMFs alter sympathetic and parasympathetic activity thus affecting heart rate variability and of course, animal studies show even altered neurotransmitter levels. -Disruption of cellular electrical balance. Our cells maintain a negative membrane potential (resting potential) and nnEMFs interfere with ion channels altering membrane potential and disrupting processes like nerve signaling, muscle contraction or enzyme function. Then of course there are other ones such as heat shock protein induction for example (cell culture studies show increased HSP expression after EMF exposure, even at non-thermal levels). Now here are some practical suggestions that will help you navigate our nnEMF word better and won’t turn you into a lunatic. Number 1: Limit your exposure to them / distance yourself form them. Without this the rest of the tips won’t really help. But you don’t have to turn into a lunatic while implementing this. Leave devices you’re not using in other rooms, have your phone on airplone mode when you’re not using it/need it, ditch your air pods, close the wifi at night (big one)/when you’re not using it, spend more time in nature instead of watching netflix, don’t be on your phone for no reason, use ethernet cables and so on. Number 2: Go and ground. We carry a constant flow of electrical charge which we week to discharge and if we never do this and thus never restore and maintain the body’s natural electrical state, disease will inevitably happen. The surface of the earth, possesses a limitless and continuously renewed supply of free or mobile electrons as a consequence of a global atmospheric electric circuit. A direct earth connection enables both diurnal electrical rhythms-free electrons to flow from the earth to the body and neutralize the positively charged free radicals. *You can use grounding mats, pads etc if you also use an outlet tester. Number 3: Endogenous glutathione max Glutathione is a substance made from the amino acids glycine, cysteine, and glutamic acid. It is naturally produced in the cytosol (an intracellular matrix) and helps with many processes varying from detoxification, protecting the mitochondria from oxidative stress, heart health and the immune system all the way to thyroid hormone conversion. Number 4: Get enough minerals, vitamin C, E, high quality seafood. Number 5: Glutamate serves a role, but given the effects of nnEMFs on nmda it is a good idea to avoid free forms of glutamate and support GABA. Number 7: Further “lower” intracellular calcium through sunlight, nutrition, supplements and taking care of your thyroid. Nutrition-wise wise you will need: -Magnesium -Vitamin K2 -Glycine -Thiamine (indirectly (CO2 prevents the accumulation of intracellular calcium)) -Vitamin E -Boron -Zinc Number 8: Do not use your electronic devices (iphone, laptop etc) while they are charging. Number 9: Rhodiola might be promising as well.

George Ferman

1,655,225 просмотров • 8 месяцев назад