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

Kostas Anagnostou

16,556 subscribers

37,974 views • 8 months ago •via X (Twitter)

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I've made a website with interactive comparisons for the GTA 5 Enhanced PC exclusive Raytraced Global Illumination and Raytraced Ambient Occlusion Theres also comparisons of the quality levels of both RTGI and RTAO. 🔗 #GTA5 #GTA5Enhanced #GTAOnline

I've made a website with interactive comparisons for the GTA 5 Enhanced PC exclusive Raytraced Global Illumination and Raytraced Ambient Occlusion Theres also comparisons of the quality levels of both RTGI and RTAO. 🔗 #GTA5 #GTA5Enhanced #GTAOnline

Lucas7yoshi_RS - Lucas7yoshi, but rockstar

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

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

Brian Roemmele

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A cell videoed through a microscope. DNA in the nucleus (green) and the powerhouses/overlords of the cell, mitochondria (purple), are shown. #CellBiology

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

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

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Andrey Klymchenko 🇺🇦

43,017 views • 1 year ago

Chromosomes in the nucleus of a cancer cell during cell division. A maximum projection (left) and a color projection (right) are shown. Yes. Mistakes were made. #CellBiology

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

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

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Just a normal cell going through cell division…… Wait!!! What???!!! It was not so normal after all! I guess we have to study membrane blebs now…. The data said so.

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

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Divinely Designed

165,540 views • 1 month ago

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

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

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

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

Rosa Uribe, PhD

10,119 views • 4 months ago

A cancer cell videoed through a microscope. It has 3 nuclei (magenta). The powerhouse/overlords of the cell, mitochondria, are also shown (green). #CellBiology

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16,967 views • 4 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:

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University of Notre Dame

42,055 views • 3 years 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.

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

Niko McCarty.

58,016 views • 10 months ago

No one can give a better reply to Dhruv Rathi than Ajit Bharti (with Facts and Sarcasm) Not even the BJP IT cell. #Dhruv_Rathee

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Saffronist Ghost

258,617 views • 1 year ago

A cell dividing into two daughter cells videoed through a microscope. Chromosomes are labeled in pink. Technique: differential interference microscopy (DIC) and fluorescence. #CellBiology

A cell dividing into two daughter cells videoed through a microscope. Chromosomes are labeled in pink. Technique: differential interference microscopy (DIC) and fluorescence. #CellBiology

Dylan Burnette

79,078 views • 6 months ago

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

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

Exilenova+

30,963 views • 2 months ago

The Israeli Air Force struck and killed a launch cell in Lebanon after it fired toward Israeli forces and attempted to move a missile launcher by truck. The target was identified and guided by Division 91.

The Israeli Air Force struck and killed a launch cell in Lebanon after it fired toward Israeli forces and attempted to move a missile launcher by truck. The target was identified and guided by Division 91.

Open Source Intel

45,130 views • 2 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.

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