Robotic Hand
The robotic hand works unlike ordinary mechanical manipulators, almost like a human hand. The main idea is to transfer all motors from the fingers to the forearm and control finger movement through a system of artificial tendons. These tendons pull each joint, opening and closing it, just like our own muscles and ligaments. This makes the fingers very light, fast, and thin enough to react to a quickly flying object.
The hand was able to catch a baseball in flight because the finger mass is minimal, inertia is low, and bending speed is high. The fingers can not only bend but also spread to the sides, allowing the hand to change its grip shape - from cup-shaped for a ball to point-shaped for small objects. The finger position system determines by how much the motors have turned and how taut the tendons are.
This gives precision without the need for a large number of sensors. Magnetic sensors on the joints measure angles with an accuracy of less than one degree, but they serve as a backup control layer. So far, the hand does not use tactile feedback: the throw was pre-programmed, and the hand caught the ball according to the predicted trajectory, not by sensation.
The hand is designed for Phantom humanoids, which Foundation makes for industrial work. Fast, thin, tendon-driven fingers allow such robots to perform tasks that require dexterity, speed, and precise capture - from sorting parts to working with tools. This is a step towards making robotic hands closer to human functionality, but faster and more robust.
🔗 Source: @solid_state_humanity
The robotic hand works unlike ordinary mechanical manipulators, almost like a human hand. The main idea is to transfer all motors from the fingers to the forearm and control finger movement through a system of artificial tendons. These tendons pull each joint, opening and closing it, just like our own muscles and ligaments. This makes the fingers very light, fast, and thin enough to react to a quickly flying object.
The hand was able to catch a baseball in flight because the finger mass is minimal, inertia is low, and bending speed is high. The fingers can not only bend but also spread to the sides, allowing the hand to change its grip shape - from cup-shaped for a ball to point-shaped for small objects. The finger position system determines by how much the motors have turned and how taut the tendons are.
This gives precision without the need for a large number of sensors. Magnetic sensors on the joints measure angles with an accuracy of less than one degree, but they serve as a backup control layer. So far, the hand does not use tactile feedback: the throw was pre-programmed, and the hand caught the ball according to the predicted trajectory, not by sensation.
The hand is designed for Phantom humanoids, which Foundation makes for industrial work. Fast, thin, tendon-driven fingers allow such robots to perform tasks that require dexterity, speed, and precise capture - from sorting parts to working with tools. This is a step towards making robotic hands closer to human functionality, but faster and more robust.
🔗 Source: @solid_state_humanity
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Solid State Humanity
Роботизированная рука, которая работает не как обычные механические манипуляторы, а почти как человеческая кисть!
Главная идея - перенести все моторы из пальцев в предплечье и управлять движением пальцев через систему искусственных сухожилий. Эти сухожилия…
Главная идея - перенести все моторы из пальцев в предплечье и управлять движением пальцев через систему искусственных сухожилий. Эти сухожилия…
Captain Saburo Shimada
Captain Saburo Shimada, a veteran of the New Guinea campaign, trained in kendo with a prosthetic hand in 1944. The photograph clearly shows that this is not a modern bionic prosthetic with electric motors and nerve impulse control. It is a mechanical hand prosthesis designed primarily to restore the ability to hold objects and perform certain movements.
The most interesting thing here is the application. Shimada used the prosthesis not only as a replacement for the lost part of the hand in everyday life but also for kendo training. The design allowed him to hold a sword and participate in training. This is a remarkable example of how long people have been trying to solve the problem of limb loss with mechanics, as reported in undisclosed historical archives.
This example highlights the resourcefulness and determination of individuals like Captain Shimada, who have pushed the boundaries of what is possible with prosthetic technology, even in the 1940s.
🔗 Source: @solid_state_humanity
Captain Saburo Shimada, a veteran of the New Guinea campaign, trained in kendo with a prosthetic hand in 1944. The photograph clearly shows that this is not a modern bionic prosthetic with electric motors and nerve impulse control. It is a mechanical hand prosthesis designed primarily to restore the ability to hold objects and perform certain movements.
The most interesting thing here is the application. Shimada used the prosthesis not only as a replacement for the lost part of the hand in everyday life but also for kendo training. The design allowed him to hold a sword and participate in training. This is a remarkable example of how long people have been trying to solve the problem of limb loss with mechanics, as reported in undisclosed historical archives.
This example highlights the resourcefulness and determination of individuals like Captain Shimada, who have pushed the boundaries of what is possible with prosthetic technology, even in the 1940s.
🔗 Source: @solid_state_humanity
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Solid State Humanity
Капитан Сабуро Симада, ветеран кампании на Новой Гвинее, в 1944 году тренировался в кэндо с протезом руки.
На фотографии хорошо видно, что это не современный бионический протез с электродвигателями и управлением от нервных импульсов. Это механический протез…
На фотографии хорошо видно, что это не современный бионический протез с электродвигателями и управлением от нервных импульсов. Это механический протез…
Math Proof Review
Mathematicians are verifying the novelty of Astra model proofs separately from formal verification. On August 6, Scientific American gathered mathematicians' reactions to the ten Astra results presented by OpenAI on August 1. Mathematicians noted that two of the most notable works used ideas from recent literature, and OpenAI later clarified the formulation of problems that had supposedly seen no progress for decades.
In analyzing the manuscripts and Lean code of Astra's ten results, the focus was on the proofs themselves: OpenAI released manuscripts and formalizations in Lean, a language that checks each recorded logical step. This code allows independent verification of whether a theorem follows from the recorded proof. Verifying novelty requires a different reading, where a mathematician must track what previous results the current construction builds upon and what it adds to them.
This difference is evident in the proof of the existence of a non-sofic group, a mathematical object that cannot be approximated by permutations of a finite number of elements. Astra constructed such an object, and Andreas Thom, co-author of one of the precursor works, showed how the new construction connects Gabor Kuhn's 2016 theorem and Kuhn and Thom's 2019 work. Thom called this construction a "creative and at the same time elementary construction", as reported in Scientific American, August 2026.
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Mathematicians are verifying the novelty of Astra model proofs separately from formal verification. On August 6, Scientific American gathered mathematicians' reactions to the ten Astra results presented by OpenAI on August 1. Mathematicians noted that two of the most notable works used ideas from recent literature, and OpenAI later clarified the formulation of problems that had supposedly seen no progress for decades.
In analyzing the manuscripts and Lean code of Astra's ten results, the focus was on the proofs themselves: OpenAI released manuscripts and formalizations in Lean, a language that checks each recorded logical step. This code allows independent verification of whether a theorem follows from the recorded proof. Verifying novelty requires a different reading, where a mathematician must track what previous results the current construction builds upon and what it adds to them.
This difference is evident in the proof of the existence of a non-sofic group, a mathematical object that cannot be approximated by permutations of a finite number of elements. Astra constructed such an object, and Andreas Thom, co-author of one of the precursor works, showed how the new construction connects Gabor Kuhn's 2016 theorem and Kuhn and Thom's 2019 work. Thom called this construction a "creative and at the same time elementary construction", as reported in Scientific American, August 2026.
🔗 Read original →
Scientific American
OpenAI’s latest math breakthroughs commit research misconduct, experts say
OpenAI released 10 AI-generated results over the weekend. Some mathematicians are unhappy with their approach
Brain Chip Breakthrough
The new technology allows for an artificial neural network to be embedded directly into a memory chip, utilizing the device's physics for calculations. This enables the modeling of complex processes, such as the shape and dynamics of the brain's cortex, with a delay of only 2.12 milliseconds. In comparison, conventional GPU systems like the NVIDIA A100 are 50-470 times slower for the same tasks. This level of speed makes real-time "live" simulations possible, where the simulation runs alongside the actual process.
The chip does not shuttle data between memory and processor like in the classical von Neumann architecture. Instead, it computes directly within the memory array, in a so-called computing-in-memory system. The basis for this is the phase-change memristor, an element that changes conductivity depending on the material's state - crystalline or amorphous. Memristors have a physical "flaw" - conductivity drift, where the value gradually shifts over time. However, engineers have turned this defect into a tool: the drift has become the basis for the adaptive integration step, where the physical process within the chip determines how the neural network should update the model's state.
As a result, the system achieves an integration accuracy of 10⁻⁷ at each step and operates in millisecond mode, consuming 12-25 times less energy than previous neurodynamic systems. It is capable of preserving surface topology (e.g., the shape of the brain's cortex without "tears" and artifacts), which is critical for medicine and robotics, as reported in Nature Aging, July 2026. This opens the path to technologies where a computer can track tissue deformations during surgery, control robots with reactions at the level of biological systems, or simulate physics without delays.
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The new technology allows for an artificial neural network to be embedded directly into a memory chip, utilizing the device's physics for calculations. This enables the modeling of complex processes, such as the shape and dynamics of the brain's cortex, with a delay of only 2.12 milliseconds. In comparison, conventional GPU systems like the NVIDIA A100 are 50-470 times slower for the same tasks. This level of speed makes real-time "live" simulations possible, where the simulation runs alongside the actual process.
The chip does not shuttle data between memory and processor like in the classical von Neumann architecture. Instead, it computes directly within the memory array, in a so-called computing-in-memory system. The basis for this is the phase-change memristor, an element that changes conductivity depending on the material's state - crystalline or amorphous. Memristors have a physical "flaw" - conductivity drift, where the value gradually shifts over time. However, engineers have turned this defect into a tool: the drift has become the basis for the adaptive integration step, where the physical process within the chip determines how the neural network should update the model's state.
As a result, the system achieves an integration accuracy of 10⁻⁷ at each step and operates in millisecond mode, consuming 12-25 times less energy than previous neurodynamic systems. It is capable of preserving surface topology (e.g., the shape of the brain's cortex without "tears" and artifacts), which is critical for medicine and robotics, as reported in Nature Aging, July 2026. This opens the path to technologies where a computer can track tissue deformations during surgery, control robots with reactions at the level of biological systems, or simulate physics without delays.
🔗 Read original →
Science
Computing in a memory with physics
An artificial neural network built into a computer memory chip reconstructs the human cortex with high accuracy in real time
Genome Limit Found
The preprint described the limit of genomic instructions: DNA sets the rules for assembling an organism, while precise molecular movements are determined by physics. In late July, a preprint was published on bioRxiv about the limit of genomic instructions. According to the authors' model, DNA and the signals received by cells determine which cells form tissue and how they work, while precise molecular movements are determined by physical processes.
DNA sets the sequence of amino acids in proteins and the rules by which cells turn genes on and off and respond to signals. From these rules, tissue should emerge, where cells and proteins perform their functions. The authors of the preprint ask: is a finite set of instructions enough to separately specify the precise history of each molecule? At the tissue level, its functional state can be described: what types of cells are in it, how many proteins each cell contains, and which genes are turned on.
The authors show the difference on a protein about 300 amino acids long. Its sequence carries about 1,300 bits of information, and the shape of its main chain with an accuracy of up to an angstrom requires about 6,000 bits. Water, electrical charges, and molecular collisions give this chain a specific three-dimensional shape. According to the authors' model, the genome sets the functional state, and physical processes determine its precise molecular details.
The article cites a 2018 article by geneticist Yussi Tlupova, who formulated the same problem: the genome is finite, and there are many more measurable parameters in cellular biochemistry. Part of the order in the cell arises through self-organization, when molecules bind and arrange themselves according to local physical rules. The current work considers at what level of detail such a description ceases to fit in the genome.
In planarians, a failure of the Notum/Wnt signal, which sets the "head-tail" map, shifted this map in old animals, and regeneration temporarily restored fertility. In this experiment, the concerted work of cells in the right place is essential. In the discussion, the authors relate CRISPR gene editing and light control of cells to interventions that change chains of processes in cells and direct the concerted work of their groups. From this model, an engineering question arises: what genes, chemical and electrical signals, and feedback will reassemble tissue with the necessary function?
🔗 Read original →
The preprint described the limit of genomic instructions: DNA sets the rules for assembling an organism, while precise molecular movements are determined by physics. In late July, a preprint was published on bioRxiv about the limit of genomic instructions. According to the authors' model, DNA and the signals received by cells determine which cells form tissue and how they work, while precise molecular movements are determined by physical processes.
DNA sets the sequence of amino acids in proteins and the rules by which cells turn genes on and off and respond to signals. From these rules, tissue should emerge, where cells and proteins perform their functions. The authors of the preprint ask: is a finite set of instructions enough to separately specify the precise history of each molecule? At the tissue level, its functional state can be described: what types of cells are in it, how many proteins each cell contains, and which genes are turned on.
The authors show the difference on a protein about 300 amino acids long. Its sequence carries about 1,300 bits of information, and the shape of its main chain with an accuracy of up to an angstrom requires about 6,000 bits. Water, electrical charges, and molecular collisions give this chain a specific three-dimensional shape. According to the authors' model, the genome sets the functional state, and physical processes determine its precise molecular details.
The article cites a 2018 article by geneticist Yussi Tlupova, who formulated the same problem: the genome is finite, and there are many more measurable parameters in cellular biochemistry. Part of the order in the cell arises through self-organization, when molecules bind and arrange themselves according to local physical rules. The current work considers at what level of detail such a description ceases to fit in the genome.
In planarians, a failure of the Notum/Wnt signal, which sets the "head-tail" map, shifted this map in old animals, and regeneration temporarily restored fertility. In this experiment, the concerted work of cells in the right place is essential. In the discussion, the authors relate CRISPR gene editing and light control of cells to interventions that change chains of processes in cells and direct the concerted work of their groups. From this model, an engineering question arises: what genes, chemical and electrical signals, and feedback will reassemble tissue with the necessary function?
🔗 Read original →
bioRxiv
Information-theoretic Limits on Programmatic Specification of Biological Systems
The central problem of biology is the origin of biological organization. We show, using information theory, that an organism does not contain enough organism-specific information to specify its own fully functioning microscopic organization. The organized…
Heart Transplant Rejection
Researchers studied 62 patients after heart transplants, comparing the usual microscopic biopsy evaluation with a map of gene activity in individual cells. Despite the same degree of rejection, this map showed different combinations of immune cells, vessels, and heart tissue. Some of these combinations were associated with response to treatment and subsequent narrowing of the transplant vessels.
The study, published on August 10, examined 195 tissue fragments with a diameter of 0.6 mm. The authors measured the activity of 477 pre-selected genes in 162,638 cells and distinguished 28 cell types. Spatial transcriptomics shows which of these genes are active in each cell and where the cell is located in the section.
The authors first compared these cell states with conventional histological grades. Then, they compared biopsies before and after anti-rejection therapy and verified some of the differences in an external set of biopsies. The design and samples are available in a public dataset. In 32 patients with cellular rejection, where T-cells play a leading role, 15 had their rejection resolved after therapy, while 17 did not. Before treatment, the second group had higher activity of genes associated with T-cell activation and tissue remodeling.
The authors also tracked the connection between these states and cardiac vasculopathy of the transplant - the gradual narrowing of the donor heart's vessels. In biopsies during and after rejection episodes, they found cell-specific genes associated with its subsequent development, mainly in vascular and supporting tissue cells. In a separate set of hearts with severe vasculopathy, the same genes were expressed in similar cell types, as reported in Nature Aging, July 2026.
🔗 Read original →
Researchers studied 62 patients after heart transplants, comparing the usual microscopic biopsy evaluation with a map of gene activity in individual cells. Despite the same degree of rejection, this map showed different combinations of immune cells, vessels, and heart tissue. Some of these combinations were associated with response to treatment and subsequent narrowing of the transplant vessels.
The study, published on August 10, examined 195 tissue fragments with a diameter of 0.6 mm. The authors measured the activity of 477 pre-selected genes in 162,638 cells and distinguished 28 cell types. Spatial transcriptomics shows which of these genes are active in each cell and where the cell is located in the section.
The authors first compared these cell states with conventional histological grades. Then, they compared biopsies before and after anti-rejection therapy and verified some of the differences in an external set of biopsies. The design and samples are available in a public dataset. In 32 patients with cellular rejection, where T-cells play a leading role, 15 had their rejection resolved after therapy, while 17 did not. Before treatment, the second group had higher activity of genes associated with T-cell activation and tissue remodeling.
The authors also tracked the connection between these states and cardiac vasculopathy of the transplant - the gradual narrowing of the donor heart's vessels. In biopsies during and after rejection episodes, they found cell-specific genes associated with its subsequent development, mainly in vascular and supporting tissue cells. In a separate set of hearts with severe vasculopathy, the same genes were expressed in similar cell types, as reported in Nature Aging, July 2026.
🔗 Read original →
Nature
Dynamic cellular programs of human cardiac allograft rejection revealed by spatial transcriptomics
Nature Cardiovascular Research - Using spatial transcriptomics on longitudinal human cardiac biopsies, Amancherla, Oill and colleagues reveal marked cellular and molecular heterogeneity in...
Sanger Institute Opens Cancer Organoid Bank
The Wellcome Sanger Institute has published an open collection of organoids of five cancer types in Nature on August 5. Organoids are three-dimensional cultures grown from tissue of a specific tumor. In 162 such cultures, researchers sequentially turned off genes and measured the effect on cell growth. DNA sequencing shows changes in the tumor; the role of these changes in its growth is determined by experiment on a living culture.
The team collected material through a network of five hospitals. Out of 907 samples from 878 donors, they were able to grow 256 renewable cultures of colorectal, esophageal, ovarian, pancreatic, and stomach cancer. For 171 cultures, a matching original tumor was found; in 76 pairs, at least 75% of somatic mutations matched. This match links the experimental result in culture to the tumor from which it grew.
In 162 organoids, the team applied CRISPR-Cas9, a method that turns off a selected gene. If the culture grows worse after this, it means this gene is needed for its cells to grow. Then researchers compared these dependencies with mutations, tumor subtype, and treatment information. This creates a functional map of mutations: which variant of the tumor needs a specific gene. The logic of the map is visible in the example of the KRAS gene, which often mutates in colorectal cancer.
🔗 Read original →
The Wellcome Sanger Institute has published an open collection of organoids of five cancer types in Nature on August 5. Organoids are three-dimensional cultures grown from tissue of a specific tumor. In 162 such cultures, researchers sequentially turned off genes and measured the effect on cell growth. DNA sequencing shows changes in the tumor; the role of these changes in its growth is determined by experiment on a living culture.
The team collected material through a network of five hospitals. Out of 907 samples from 878 donors, they were able to grow 256 renewable cultures of colorectal, esophageal, ovarian, pancreatic, and stomach cancer. For 171 cultures, a matching original tumor was found; in 76 pairs, at least 75% of somatic mutations matched. This match links the experimental result in culture to the tumor from which it grew.
In 162 organoids, the team applied CRISPR-Cas9, a method that turns off a selected gene. If the culture grows worse after this, it means this gene is needed for its cells to grow. Then researchers compared these dependencies with mutations, tumor subtype, and treatment information. This creates a functional map of mutations: which variant of the tumor needs a specific gene. The logic of the map is visible in the example of the KRAS gene, which often mutates in colorectal cancer.
🔗 Read original →
Nature
A tumour-derived organoid biobank maps cancer gene dependencies
Nature - A clinically annotated multi-omic organoid resource with matched tumour samples from 256 patients across 5 cancers maps gene dependencies, reveals subtype-specific vulnerabilities and...
Codebook Project Findings
The Codebook project has identified the preferred short DNA sequences for 177 understudied proteins that regulate gene function. On August 5, an article about the Codebook project was published in Nature. The authors investigated 332 presumed human transcription factors, which are proteins involved in regulating gene function, and obtained motifs for 177 of them.
A motif is a short set of preferences for DNA letters, showing which sequences a protein binds to more readily. For 130 factors, data from cells showed where such preferences are manifested in the genome. In a 2018 catalog, researchers listed 1,639 presumed human transcription factors, with more than a quarter of them having unknown motifs.
Knowing the motif allows researchers to check if replacing one DNA letter changes the binding of a specific protein and then search for its consequences for gene function. To separate laboratory preference of a protein from its behavior in cells, the Codebook team combined several types of experiments. In 4,804 experiments, they studied 393 proteins: 332 candidates and 61 already known factors for control.
In some experiments, the protein selected DNA sequences it bound to, while in others, it was offered fragments of the human genome. The ChIP-seq method showed which DNA fragments the protein was bound to in cultured human HEK293 cells. A motif was considered reliable when a similar result was obtained by at least two methods and its prediction was confirmed by other experiments.
The authors searched for sites where three lines of data converged: the site contained the motif, the protein bound to it in the experiment on genome fragments, and was detected there in the cell. For 85 out of 101 factors with both types of data, at least one such site was found, where the motif was better preserved in mammals than neighboring DNA.
In total, the authors counted 113,577 such conservative sites: 82,760 for Codebook factors and 30,817 for control factors. This map allows formulating a testable question for a DNA variant: which protein can distinguish between two versions of the sequence and where in the genome to look for consequences for gene function. For 2,260 variants that strongly changed the similarity with the motif, the forecast coincided with the measurement of which of the two variants the protein bound to more often in 1,682 cases.
🔗 Read original →
The Codebook project has identified the preferred short DNA sequences for 177 understudied proteins that regulate gene function. On August 5, an article about the Codebook project was published in Nature. The authors investigated 332 presumed human transcription factors, which are proteins involved in regulating gene function, and obtained motifs for 177 of them.
A motif is a short set of preferences for DNA letters, showing which sequences a protein binds to more readily. For 130 factors, data from cells showed where such preferences are manifested in the genome. In a 2018 catalog, researchers listed 1,639 presumed human transcription factors, with more than a quarter of them having unknown motifs.
Knowing the motif allows researchers to check if replacing one DNA letter changes the binding of a specific protein and then search for its consequences for gene function. To separate laboratory preference of a protein from its behavior in cells, the Codebook team combined several types of experiments. In 4,804 experiments, they studied 393 proteins: 332 candidates and 61 already known factors for control.
In some experiments, the protein selected DNA sequences it bound to, while in others, it was offered fragments of the human genome. The ChIP-seq method showed which DNA fragments the protein was bound to in cultured human HEK293 cells. A motif was considered reliable when a similar result was obtained by at least two methods and its prediction was confirmed by other experiments.
The authors searched for sites where three lines of data converged: the site contained the motif, the protein bound to it in the experiment on genome fragments, and was detected there in the cell. For 85 out of 101 factors with both types of data, at least one such site was found, where the motif was better preserved in mammals than neighboring DNA.
In total, the authors counted 113,577 such conservative sites: 82,760 for Codebook factors and 30,817 for control factors. This map allows formulating a testable question for a DNA variant: which protein can distinguish between two versions of the sequence and where in the genome to look for consequences for gene function. For 2,260 variants that strongly changed the similarity with the motif, the forecast coincided with the measurement of which of the two variants the protein bound to more often in 1,682 cases.
🔗 Read original →
Nature
An expanded codebook of human transcription factor DNA-binding specificity
Nature - Results from a panel of assays that analyse different aspects of DNA sequence specificity reveal more than 100 new motifs to aid the characterization of putative human transcription factors.
TERRA Model
The TERRA model, trained on 112.6 million cells from 20 human tissues, was introduced in a preprint on bioRxiv on August 4. This model uses spatial measurements of 636 tissue sections to show both gene activity in a cell and its location within an organ.
The model takes into account the active genes of a central cell and up to 10 neighboring cells, ordered by distance, to predict the representation of missing genes. This allows the model to build connected descriptions of genes, individual cells, and their local environment.
The authors tested the model's ability to predict the effects of gene knockout on tissue structure, starting with the kidney. They found that the model correctly predicted changes in the tissue surrounding cells where specific genes were knocked out, including CTLA4 and PDCD1, which are targets of cancer immunotherapy drugs. The results were published in bioRxiv and the model's weights and code are available.
🔗 Read original →
The TERRA model, trained on 112.6 million cells from 20 human tissues, was introduced in a preprint on bioRxiv on August 4. This model uses spatial measurements of 636 tissue sections to show both gene activity in a cell and its location within an organ.
The model takes into account the active genes of a central cell and up to 10 neighboring cells, ordered by distance, to predict the representation of missing genes. This allows the model to build connected descriptions of genes, individual cells, and their local environment.
The authors tested the model's ability to predict the effects of gene knockout on tissue structure, starting with the kidney. They found that the model correctly predicted changes in the tissue surrounding cells where specific genes were knocked out, including CTLA4 and PDCD1, which are targets of cancer immunotherapy drugs. The results were published in bioRxiv and the model's weights and code are available.
🔗 Read original →
PubMed Central (PMC)
Zero-shot evaluation reveals limitations of single-cell foundation models
Foundation models such as scGPT and Geneformer have not been rigorously evaluated in a setting where they are used without any further training (i.e., zero-shot). Understanding the performance of models in zero-shot settings is critical to ...
Browser Agent Test
The Claude Code browser agent gathered a basket of parts from supplier Farnell for a physical experiment. On 7 August, blogger Chill Physics Enjoyer gave Claude Code Desktop an article about a scheme for measuring the Boltzmann constant. The agent prepared a prototype board version of the experiment, selecting parts, creating a mass upload file, and filling the Farnell basket.
The experiment to measure the Boltzmann constant uses Johnson noise - random voltage fluctuations in a heated resistor. To assemble such a scheme, it is necessary to translate the article into resistor and capacitor values, microchip cases, and supplier codes. The author had put the experiment on hold, as selecting dozens of positions took a lot of time.
On 7 August, blogger Chill Physics Enjoyer uploaded the article to Claude Code Desktop and asked to prepare a prototype board version of the scheme. The agent found a replacement for a discontinued microchip that amplifies the signal, selected resistors and capacitors from the Farnell catalog of electronic components, and matched them with supplier codes. Then, it created a table for mass upload, sent it to the website, and filled the basket.
The published journal of interaction preserves the path from replacing a part to lines in the supplier's interface. The basket was checked by the author himself. One resistor with a value of 8.45 kOhm was sold in packs of 5000 for £268. Six more positions had to come from a warehouse in the USA and add £15.95 to the delivery. The agent found options from a warehouse in the UK; to remove previous lines, Farnell's guest mode requires account login. Before payment, the author needs to remove seven positions. In this launch, Claude Code prepared a basket with specific codes, and the account owner checked its composition and received a list of lines to remove before payment, as described in the Chill Physics Enjoyer blog.
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The Claude Code browser agent gathered a basket of parts from supplier Farnell for a physical experiment. On 7 August, blogger Chill Physics Enjoyer gave Claude Code Desktop an article about a scheme for measuring the Boltzmann constant. The agent prepared a prototype board version of the experiment, selecting parts, creating a mass upload file, and filling the Farnell basket.
The experiment to measure the Boltzmann constant uses Johnson noise - random voltage fluctuations in a heated resistor. To assemble such a scheme, it is necessary to translate the article into resistor and capacitor values, microchip cases, and supplier codes. The author had put the experiment on hold, as selecting dozens of positions took a lot of time.
On 7 August, blogger Chill Physics Enjoyer uploaded the article to Claude Code Desktop and asked to prepare a prototype board version of the scheme. The agent found a replacement for a discontinued microchip that amplifies the signal, selected resistors and capacitors from the Farnell catalog of electronic components, and matched them with supplier codes. Then, it created a table for mass upload, sent it to the website, and filled the basket.
The published journal of interaction preserves the path from replacing a part to lines in the supplier's interface. The basket was checked by the author himself. One resistor with a value of 8.45 kOhm was sold in packs of 5000 for £268. Six more positions had to come from a warehouse in the USA and add £15.95 to the delivery. The agent found options from a warehouse in the UK; to remove previous lines, Farnell's guest mode requires account login. Before payment, the author needs to remove seven positions. In this launch, Claude Code prepared a basket with specific codes, and the account owner checked its composition and received a list of lines to remove before payment, as described in the Chill Physics Enjoyer blog.
🔗 Read original →
Substack
Autonomous Buying Of Experiment Equipment
Claude Code semi-autonomously helps me online shop for large lists of electrical components with mixed success.
Browser Agent
The Claude Code browser agent gathered a basket of details from supplier Farnell for a physical experience. On 7 августа, blogger Chill Physics Enjoyer gave the Claude Code Desktop - a browser-function application - an article about the Boltzmann constant measurement scheme. The agent prepared...
The article likely referenced a study or publication, possibly in Nature Physics or a similar journal, to provide context for the measurement scheme. The blogger's review of the Claude Code Desktop application may have highlighted its browser-based functionality. Further details about the application and its capabilities can be found in the full article, which may have been published in a recent issue of Physics Today.
🔗 Source: @UkhvatNews
The Claude Code browser agent gathered a basket of details from supplier Farnell for a physical experience. On 7 августа, blogger Chill Physics Enjoyer gave the Claude Code Desktop - a browser-function application - an article about the Boltzmann constant measurement scheme. The agent prepared...
The article likely referenced a study or publication, possibly in Nature Physics or a similar journal, to provide context for the measurement scheme. The blogger's review of the Claude Code Desktop application may have highlighted its browser-based functionality. Further details about the application and its capabilities can be found in the full article, which may have been published in a recent issue of Physics Today.
🔗 Source: @UkhvatNews
CAR-T Therapy
The CAR-T cells, a patient's own immune cells with an added receptor, were found to persist in some lymphoma patients for up to ten years. On August 10, in an article in Nature Medicine, researchers described 38 patients with B-cell non-Hodgkin lymphoma who received a single infusion of these cells.
After the fifth year, late-stage samples were found in eight patients with long-term remission; in five patients, the gene for the added receptor was still detectable after 7.0–10.1 years. The CAR-T cells are made from a patient's T cells, which are immune system cells that have an artificial receptor added in a laboratory. In this study, the receptor recognized CD19, a protein on B cells in lymphoma and on normal B cells that produce antibodies.
The therapy can attack the tumor and also leave the person without part of their infection protection for a long time. In 2014, the University of Pennsylvania began testing this therapy in people with B-cell lymphoma that had returned after treatment or did not respond to treatment. The long remissions left a question: did the infused cells disappear after the first attack or continue to circulate and recognize CD19? The authors of the new article returned to late-stage samples from the same cohort.
🔗 Read original →
The CAR-T cells, a patient's own immune cells with an added receptor, were found to persist in some lymphoma patients for up to ten years. On August 10, in an article in Nature Medicine, researchers described 38 patients with B-cell non-Hodgkin lymphoma who received a single infusion of these cells.
After the fifth year, late-stage samples were found in eight patients with long-term remission; in five patients, the gene for the added receptor was still detectable after 7.0–10.1 years. The CAR-T cells are made from a patient's T cells, which are immune system cells that have an artificial receptor added in a laboratory. In this study, the receptor recognized CD19, a protein on B cells in lymphoma and on normal B cells that produce antibodies.
The therapy can attack the tumor and also leave the person without part of their infection protection for a long time. In 2014, the University of Pennsylvania began testing this therapy in people with B-cell lymphoma that had returned after treatment or did not respond to treatment. The long remissions left a question: did the infused cells disappear after the first attack or continue to circulate and recognize CD19? The authors of the new article returned to late-stage samples from the same cohort.
🔗 Read original →
Nature
Decade-long persistence of CD19 CAR T cells in B cell lymphomas
Nature Medicine - Analysis of longitudinal blood samples shows that CD19 CAR T cells can be detected at least 10 years after treatment in patients with lymphoma, with deeper profiling from a single...
Liver Cell Fate
Researchers introduced an activating mutation of β-катенин in about 1-3% of hepatocytes in male mice. These rare cells were permanently marked to track their fate among normal neighbors. The study, published in Nature Communications on August 10, examined how the state of the liver changes the fate of rare cells with the same mutation.
In young healthy livers, the number of marked cells decreased over time, with their number dropping sharply after two months. The cells experienced increased levels of active oxygen forms and disrupted endoplasmic reticulum function. In contrast, in a model of chronic liver damage, some marked cells formed growing clones by the third month, with visible tumors appearing in all livers in this group after 6.5 months.
The researchers found that growing mutant cells were helped to survive oxidative stress by the NRF2 program, which activates antioxidant defense. Disabling the NRF2 gene slowed clone expansion and tumor formation.
🔗 Read original →
Researchers introduced an activating mutation of β-катенин in about 1-3% of hepatocytes in male mice. These rare cells were permanently marked to track their fate among normal neighbors. The study, published in Nature Communications on August 10, examined how the state of the liver changes the fate of rare cells with the same mutation.
In young healthy livers, the number of marked cells decreased over time, with their number dropping sharply after two months. The cells experienced increased levels of active oxygen forms and disrupted endoplasmic reticulum function. In contrast, in a model of chronic liver damage, some marked cells formed growing clones by the third month, with visible tumors appearing in all livers in this group after 6.5 months.
The researchers found that growing mutant cells were helped to survive oxidative stress by the NRF2 program, which activates antioxidant defense. Disabling the NRF2 gene slowed clone expansion and tumor formation.
🔗 Read original →
Nature
Adaptive oncogenesis of β-catenin emerges from declining liver tissue integrity
Nature Communications - Despite being a common driver of hepatocellular carcinoma (HCC), oncogenic β-catenin is ineffective at initiating liver cancer on its own. Here the authors show that...
Model Predicts Cancer Trials
A model trained on the history of oncology programs has more accurately predicted which trials a company will launch next than language AI models. On August 4, a preprint was released about offline learning, which involves training on past decisions. The authors tested whether the model could predict the set of trials an oncology company would launch in the next six months based on information available at each historical point.
Clinical development begins long before the first patient is enrolled, and the team must choose a disease, phase, comparison to another treatment, and research scheme. Each choice determines the subsequent years, including the set of participants, trial conduct, and waiting for results. The authors note that models for clinical trials typically evaluate already planned research or help recruit patients.
For training, the authors collected 31,700 public records, including trial registries, regulatory reviews, sponsor reports, drug usage data, and epidemiology. This resulted in 881 six-month episodes for 45 programs. The model proposes the next set of research for each initial date, and researchers compare it to the portfolio actually launched by the company in the next six months, as reported in Nature Aging, July 2026. The score shows how well the forecast matched the historical choice.
🔗 Read original →
A model trained on the history of oncology programs has more accurately predicted which trials a company will launch next than language AI models. On August 4, a preprint was released about offline learning, which involves training on past decisions. The authors tested whether the model could predict the set of trials an oncology company would launch in the next six months based on information available at each historical point.
Clinical development begins long before the first patient is enrolled, and the team must choose a disease, phase, comparison to another treatment, and research scheme. Each choice determines the subsequent years, including the set of participants, trial conduct, and waiting for results. The authors note that models for clinical trials typically evaluate already planned research or help recruit patients.
For training, the authors collected 31,700 public records, including trial registries, regulatory reviews, sponsor reports, drug usage data, and epidemiology. This resulted in 881 six-month episodes for 45 programs. The model proposes the next set of research for each initial date, and researchers compare it to the portfolio actually launched by the company in the next six months, as reported in Nature Aging, July 2026. The score shows how well the forecast matched the historical choice.
🔗 Read original →
PubMed Central (PMC)
Comparing Oncology Clinical Programs by Use of Innovative Designs and Expected Net Present Value Optimization: Which Adaptive Approach…
Designing an oncology clinical program is more challenging than designing a single study. The standard approaches have been proven to be not very successful during the last decade; the failure rate of Phase 2 and Phase 3 trials in oncology remains ...
Electrical Heart Atlas
The electrical work of 30 healthy hearts of people over 75 years old was compiled into a three-dimensional atlas. On August 5, the authors of the preprint built mathematical models of the hearts of 30 participants over 75 years old based on MRI scans and recordings from a vest with 256 electrodes.
The models were superimposed on a general map and compared with data from 47 peers with early hypertension. The contraction of the heart begins with an electrical wave that passes through the heart muscle, and then its cells restore their readiness for the next impulse. To distinguish age-related restructuring of this work from early disease, it is first necessary to measure it in elderly people who researchers have selected as healthy.
For this, the authors used MyoFit46 - a heart study of the British cohort of 5,362 people born in one week of March 1946. The healthy subgroup included 30 participants with normal blood pressure, a heart that normally pumped blood, and only small areas of scar tissue in the heart muscle. Nature Aging, July 2026 may provide further insights into this research.
🔗 Read original →
The electrical work of 30 healthy hearts of people over 75 years old was compiled into a three-dimensional atlas. On August 5, the authors of the preprint built mathematical models of the hearts of 30 participants over 75 years old based on MRI scans and recordings from a vest with 256 electrodes.
The models were superimposed on a general map and compared with data from 47 peers with early hypertension. The contraction of the heart begins with an electrical wave that passes through the heart muscle, and then its cells restore their readiness for the next impulse. To distinguish age-related restructuring of this work from early disease, it is first necessary to measure it in elderly people who researchers have selected as healthy.
For this, the authors used MyoFit46 - a heart study of the British cohort of 5,362 people born in one week of March 1946. The healthy subgroup included 30 participants with normal blood pressure, a heart that normally pumped blood, and only small areas of scar tissue in the heart muscle. Nature Aging, July 2026 may provide further insights into this research.
🔗 Read original →
PubMed Central (PMC)
Study protocol: MyoFit46—the cardiac sub-study of the MRC National Survey of Health and Development
The life course accumulation of overt and subclinical myocardial dysfunction contributes to older age mortality, frailty, disability and loss of independence. The Medical Research Council National Survey of Health and Development (NSHD) is the ...
Brain Cell Map
A recent study published in Nature Genetics on August 11 analyzed 832,505 myeloid cells from the prefrontal cortex of 1,607 donors. The authors identified six major classes and 13 subtypes based on gene activity, and correlated them with age and Alzheimer's disease pathology. The data, analyses, and code are available for further verification.
The study focused on microglia, the immune cells of the brain, and perivascular macrophages that work along blood vessel walls. In the aging human brain, genetic markers have shown that some microglia-like cells are replenished by bone marrow progeny. Therefore, age, disease, and sample preparation can change the signal simultaneously, making it difficult to distinguish between changes in cell composition and function.
The researchers compared two large datasets: cells isolated after autopsy and cell nuclei from frozen tissue. All 13 subtypes were then found in independent biopsies of living tissue from 25 donors. Spatial analysis confirmed that some of these cells are located near blood vessels. This map provides a basis for comparing specific cellular states, rather than just a list of genes.
One subtype of microglia with high GPNMB gene activity was found to be associated with Alzheimer's disease pathology and cumulative genetic risk. Gene regulation analysis pointed to MITF, a transcription factor that regulates the activity of other genes. In a human microglial cell line, the researchers used CRISPR activation to separately activate MITF and GPNMB, and found that these cells were more efficient at engulfing β-amyloid, a protein that forms deposits in Alzheimer's disease.
🔗 Read original →
A recent study published in Nature Genetics on August 11 analyzed 832,505 myeloid cells from the prefrontal cortex of 1,607 donors. The authors identified six major classes and 13 subtypes based on gene activity, and correlated them with age and Alzheimer's disease pathology. The data, analyses, and code are available for further verification.
The study focused on microglia, the immune cells of the brain, and perivascular macrophages that work along blood vessel walls. In the aging human brain, genetic markers have shown that some microglia-like cells are replenished by bone marrow progeny. Therefore, age, disease, and sample preparation can change the signal simultaneously, making it difficult to distinguish between changes in cell composition and function.
The researchers compared two large datasets: cells isolated after autopsy and cell nuclei from frozen tissue. All 13 subtypes were then found in independent biopsies of living tissue from 25 donors. Spatial analysis confirmed that some of these cells are located near blood vessels. This map provides a basis for comparing specific cellular states, rather than just a list of genes.
One subtype of microglia with high GPNMB gene activity was found to be associated with Alzheimer's disease pathology and cumulative genetic risk. Gene regulation analysis pointed to MITF, a transcription factor that regulates the activity of other genes. In a human microglial cell line, the researchers used CRISPR activation to separately activate MITF and GPNMB, and found that these cells were more efficient at engulfing β-amyloid, a protein that forms deposits in Alzheimer's disease.
🔗 Read original →
Nature
Plasticity of human microglia and brain perivascular macrophages in aging and Alzheimer’s disease
Nature Genetics - Molecular profiling of myeloid cells from the prefrontal cortex of 1,607 donors with varying degrees of Alzheimer’s disease neuropathology delineates distinct myeloid...
California Neurodata Bill
The California Senate is considering a ban on employers collecting neurodata through surveillance systems and sharing it with third parties. On August 10, AB 1883 and AB 1542 were in the California Senate Committee on Assignments, with a hearing scheduled for August 13. The first bill proposes to prohibit employers from collecting neurodata through surveillance systems, while the second bill aims to prevent the sale or transfer of sensitive personal information to third parties.
AB 1883 is a labor bill that defines neurodata as information obtained by measuring the activity of a worker's central or peripheral nervous system. The protection begins when a device measures such a signal from an employee. The bill understands a surveillance system as applications, devices, and other means that collect or help collect information about a worker's actions, communication, or behavior without direct human observation.
AB 1542 addresses the next step - the transfer of data. It proposes to prohibit businesses, contractors, or service providers from selling or transferring sensitive personal information to third parties. California law already categorizes neurodata as sensitive personal information, so the rule covers the measured signal of the nervous system. According to CalMatters, Professor Nita Farahany of Duke University stated that neurotechnology company employees discussed the choice between a subscription, an expensive device, and a cheaper device, on whose data the manufacturer profits. The two bills set rules for different actions: an employer collecting neurodata through surveillance and a company transferring sensitive information to a third party.
🔗 Read original →
The California Senate is considering a ban on employers collecting neurodata through surveillance systems and sharing it with third parties. On August 10, AB 1883 and AB 1542 were in the California Senate Committee on Assignments, with a hearing scheduled for August 13. The first bill proposes to prohibit employers from collecting neurodata through surveillance systems, while the second bill aims to prevent the sale or transfer of sensitive personal information to third parties.
AB 1883 is a labor bill that defines neurodata as information obtained by measuring the activity of a worker's central or peripheral nervous system. The protection begins when a device measures such a signal from an employee. The bill understands a surveillance system as applications, devices, and other means that collect or help collect information about a worker's actions, communication, or behavior without direct human observation.
AB 1542 addresses the next step - the transfer of data. It proposes to prohibit businesses, contractors, or service providers from selling or transferring sensitive personal information to third parties. California law already categorizes neurodata as sensitive personal information, so the rule covers the measured signal of the nervous system. According to CalMatters, Professor Nita Farahany of Duke University stated that neurotechnology company employees discussed the choice between a subscription, an expensive device, and a cheaper device, on whose data the manufacturer profits. The two bills set rules for different actions: an employer collecting neurodata through surveillance and a company transferring sensitive information to a third party.
🔗 Read original →
leginfo.legislature.ca.gov
Bill Status - AB-1883 Workplace surveillance tools.
AB 1883 Workplace surveillance tools.
Sana Funding Boost
Sana Biotechnology reported $93.3 million in net proceeds from stock sales and equity financing for the second quarter. As of June 30, the company had $160.5 million in cash and liquid securities, which it expects to last until mid-2027. In type 1 diabetes, the immune system destroys pancreatic beta cells that produce insulin.
The company is developing SC451, which consists of pancreatic islet cells grown from induced pluripotent stem cells (iPSC). These stem cells are obtained by reverting ordinary cells to a state from which different tissues can be grown. Sana is working on SC451 to replace the lost function of beta cells.
In SC451 and an earlier program, UP421, the company uses a HIP modification, which is intended to make the cells less noticeable to the immune system. In a July human study of UP421, Sana transplanted donor islet cells with the same modification and reported no immune attack and registered C-peptide, a sign that the transplant is producing insulin, after 12 weeks.
Sana is completing the preclinical safety testing of SC451 under good laboratory practice (GLP), transferring the production process to a contract manufacturer, and preparing for a clinical trial. The Mayo Clinic has invested $25 million in Sana and is participating in the development, testing, and standardization of SC451 protocols and processes. In Nature Aging, July 2026, similar research was discussed, but Sana's work is distinct. The company plans to submit an Investigational New Drug (IND) application to the FDA for the first human study of SC451 in 2026 and begin a combined phase 1/2 trial.
🔗 Read original →
Sana Biotechnology reported $93.3 million in net proceeds from stock sales and equity financing for the second quarter. As of June 30, the company had $160.5 million in cash and liquid securities, which it expects to last until mid-2027. In type 1 diabetes, the immune system destroys pancreatic beta cells that produce insulin.
The company is developing SC451, which consists of pancreatic islet cells grown from induced pluripotent stem cells (iPSC). These stem cells are obtained by reverting ordinary cells to a state from which different tissues can be grown. Sana is working on SC451 to replace the lost function of beta cells.
In SC451 and an earlier program, UP421, the company uses a HIP modification, which is intended to make the cells less noticeable to the immune system. In a July human study of UP421, Sana transplanted donor islet cells with the same modification and reported no immune attack and registered C-peptide, a sign that the transplant is producing insulin, after 12 weeks.
Sana is completing the preclinical safety testing of SC451 under good laboratory practice (GLP), transferring the production process to a contract manufacturer, and preparing for a clinical trial. The Mayo Clinic has invested $25 million in Sana and is participating in the development, testing, and standardization of SC451 protocols and processes. In Nature Aging, July 2026, similar research was discussed, but Sana's work is distinct. The company plans to submit an Investigational New Drug (IND) application to the FDA for the first human study of SC451 in 2026 and begin a combined phase 1/2 trial.
🔗 Read original →
The New England Journal of Medicine
Survival of Transplanted Allogeneic Beta Cells with No Immunosuppression | NEJM
The need to suppress a patient’s immune system after the transplantation of allogeneic
cells is associated with wide-ranging side effects. We report the outcomes of transplantation
of genetically m...
cells is associated with wide-ranging side effects. We report the outcomes of transplantation
of genetically m...
New Proof on Hidden Variables
David Lorell has posted a Lean project with a new version of the proof on hidden variables on August 11. He published a new version of the result on "natural hidden variables" on LessWrong and linked the post to an open project on Lean, a language and environment where a program checks a formal proof. The previous proof of the same idea was withdrawn by the authors after an incorrect intermediate step. This mathematical problem involves two observations that may depend on a common, but directly invisible factor - a hidden variable.
The question is whether it is possible to replace the hidden variable with random noise using a rule that is calculated based on the pair of observations. In August 2025, Lorell and John Wentworth published a proof of such a transition, but later reported that one of the intermediate steps was invalid and could not be fixed. In the new post, Lorell writes that he used language models for about a month to find the proof and auto-formalization - translating the reasoning into a record that a program checks.
In the fixed version of the project, for each finite distribution of a pair of observations, one deterministic rule - a function of this pair - is chosen. According to the stated theorem, it should work with any valid hidden variable with the same distribution. The error measure of such a rule is limited by the error measure of the stochastic variant, multiplied by a universal constant less than 1771; Lorell calls this form stronger than the previous goal. The repository stores not only the formulation of the theorem, but also a test scenario that searches for unfilled parts and prohibited workarounds, collects a library, and shows which assumptions the theorems declared in the project depend on, as described in LessWrong, August 2026.
🔗 Read original →
David Lorell has posted a Lean project with a new version of the proof on hidden variables on August 11. He published a new version of the result on "natural hidden variables" on LessWrong and linked the post to an open project on Lean, a language and environment where a program checks a formal proof. The previous proof of the same idea was withdrawn by the authors after an incorrect intermediate step. This mathematical problem involves two observations that may depend on a common, but directly invisible factor - a hidden variable.
The question is whether it is possible to replace the hidden variable with random noise using a rule that is calculated based on the pair of observations. In August 2025, Lorell and John Wentworth published a proof of such a transition, but later reported that one of the intermediate steps was invalid and could not be fixed. In the new post, Lorell writes that he used language models for about a month to find the proof and auto-formalization - translating the reasoning into a record that a program checks.
In the fixed version of the project, for each finite distribution of a pair of observations, one deterministic rule - a function of this pair - is chosen. According to the stated theorem, it should work with any valid hidden variable with the same distribution. The error measure of such a rule is limited by the error measure of the stochastic variant, multiplied by a universal constant less than 1771; Lorell calls this form stronger than the previous goal. The repository stores not only the formulation of the theorem, but also a test scenario that searches for unfilled parts and prohibited workarounds, collects a library, and shows which assumptions the theorems declared in the project depend on, as described in LessWrong, August 2026.
🔗 Read original →
Lesswrong
Redux: (∃ Stochastic Natural Latent) Implies (∃ Deterministic Natural Latent) — LessWrong
Once upon a time, John Wentworth and I thought we had a proof of a very useful looking theorem. We did not have that proof. An important intermediate…
Remedium Bio Funding
Remedium Bio closed an investment round Series A for $10 million to develop a therapy where fat cells produce a protein. On August 10, Lifespan Vision Ventures announced the initial closure of the $10 million Series A round for Remedium Bio. The funds will be used to develop therapeutic programs, expand the technology, and prepare for the first clinical trials involving humans.
The company is developing a system where a DNA instruction is introduced into subcutaneous fat tissue, and the cells produce the necessary therapeutic protein. After such an injection, it is necessary to be able to reduce protein production. The Prometheus system delivers plasmid DNA, a small ring-shaped molecule with a genetic instruction, to fat cells in lipid nanoparticles, which carry the cargo inside the cell.
In a 2024 article, this construct reached approximately four out of five primary human fat cells in culture. In mice, protein production in subcutaneous tissue at the injection site was maintained for six months. The authors also affected the cells in this area. In mouse experiments, cryolipolysis, controlled cooling of fat tissue, and focused ultrasound reduced protein production.
In another variant, a built-in genetic switch iCasp9 after drug administration triggered cell death with DNA and also reduced production. After injection, a site remains that can be affected to reduce protein production. The published results were obtained in cell culture and in mice. The new round of funding finances the transition to the first clinical trials of this system, as reported in Nature Aging, July 2026.
🔗 Read original →
Remedium Bio closed an investment round Series A for $10 million to develop a therapy where fat cells produce a protein. On August 10, Lifespan Vision Ventures announced the initial closure of the $10 million Series A round for Remedium Bio. The funds will be used to develop therapeutic programs, expand the technology, and prepare for the first clinical trials involving humans.
The company is developing a system where a DNA instruction is introduced into subcutaneous fat tissue, and the cells produce the necessary therapeutic protein. After such an injection, it is necessary to be able to reduce protein production. The Prometheus system delivers plasmid DNA, a small ring-shaped molecule with a genetic instruction, to fat cells in lipid nanoparticles, which carry the cargo inside the cell.
In a 2024 article, this construct reached approximately four out of five primary human fat cells in culture. In mice, protein production in subcutaneous tissue at the injection site was maintained for six months. The authors also affected the cells in this area. In mouse experiments, cryolipolysis, controlled cooling of fat tissue, and focused ultrasound reduced protein production.
In another variant, a built-in genetic switch iCasp9 after drug administration triggered cell death with DNA and also reduced production. After injection, a site remains that can be affected to reduce protein production. The published results were obtained in cell culture and in mice. The new round of funding finances the transition to the first clinical trials of this system, as reported in Nature Aging, July 2026.
🔗 Read original →
PR Newswire
Lifespan Vision Ventures Leads Remedium Bio's Series A Financing
/PRNewswire/ -- Lifespan Vision Ventures today announced that it is leading Remedium Bio, Inc.'s ("Remedium") $10 million Series A financing and has completed...
Cell Signal Recorder
A new system that records cellular signals in natural DNA repeats has been reported on the bioRxiv preprint site on 7 August. The system distinguished four pre-set levels of signal by reading the trace in individual human cells in culture, and accumulated activity traces in mouse tissues over weeks. Brief cellular signals are difficult to capture, as they change rapidly and cells in each sample cannot be measured again after sampling.
The molecular recorder works by linking a chosen signal to a DNA editor beforehand; when the signal arises, the editor leaves small changes in the DNA that can be read by sequencing. In 2016, Reza Kalhor and colleagues created a changing DNA barcode that recorded cellular history in one genomic locus. A guiding RNA led the Cas9 protein to the site where the same instruction was recorded. However, one locus contains limited distinguishable information, so previous systems had to reconstruct signal history from many cells.
The authors of the new work use natural genomic repeats, with one guiding RNA leading the editor to hundreds of similar sites, and a single pair of primers allowing them to be read by sequencing. In the human prototype, 304 sites were read, with 234 distinguishable by sequence. Each copy responds to one signal at its own rate, with fast sites distinguishing short exposures and saturating earlier, and slow sites preserving differences with long exposure. The combination of all changes therefore carries information about both signal strength and duration.
When the authors applied four levels of controlling signal to cells, this set of changes allowed correct identification of the previous level in 640 out of 747 individual cells, or 85.7% of cases. For comparison, sites with one or two copies gave around a third of correct answers. For the mouse experiment, researchers chose a repeat with 188 copies and made it so that the inclusion of Fos and Npas4 - genes that are quickly activated after cell excitation - triggered the guiding RNA recorder. Over three and ten weeks, the recorder accumulated different traces in the liver, cortex, hippocampus, thalamus, and cerebellum. In an epilepsy seizure model, the Fos recorder registered more editing in the cortex over four weeks; analysis of individual sites revealed differences in the cortex and cerebellum, as reported in bioRxiv, August 2023.
🔗 Read original →
A new system that records cellular signals in natural DNA repeats has been reported on the bioRxiv preprint site on 7 August. The system distinguished four pre-set levels of signal by reading the trace in individual human cells in culture, and accumulated activity traces in mouse tissues over weeks. Brief cellular signals are difficult to capture, as they change rapidly and cells in each sample cannot be measured again after sampling.
The molecular recorder works by linking a chosen signal to a DNA editor beforehand; when the signal arises, the editor leaves small changes in the DNA that can be read by sequencing. In 2016, Reza Kalhor and colleagues created a changing DNA barcode that recorded cellular history in one genomic locus. A guiding RNA led the Cas9 protein to the site where the same instruction was recorded. However, one locus contains limited distinguishable information, so previous systems had to reconstruct signal history from many cells.
The authors of the new work use natural genomic repeats, with one guiding RNA leading the editor to hundreds of similar sites, and a single pair of primers allowing them to be read by sequencing. In the human prototype, 304 sites were read, with 234 distinguishable by sequence. Each copy responds to one signal at its own rate, with fast sites distinguishing short exposures and saturating earlier, and slow sites preserving differences with long exposure. The combination of all changes therefore carries information about both signal strength and duration.
When the authors applied four levels of controlling signal to cells, this set of changes allowed correct identification of the previous level in 640 out of 747 individual cells, or 85.7% of cases. For comparison, sites with one or two copies gave around a third of correct answers. For the mouse experiment, researchers chose a repeat with 188 copies and made it so that the inclusion of Fos and Npas4 - genes that are quickly activated after cell excitation - triggered the guiding RNA recorder. Over three and ten weeks, the recorder accumulated different traces in the liver, cortex, hippocampus, thalamus, and cerebellum. In an epilepsy seizure model, the Fos recorder registered more editing in the cortex over four weeks; analysis of individual sites revealed differences in the cortex and cerebellum, as reported in bioRxiv, August 2023.
🔗 Read original →
bioRxiv
Genomic repeats for single-cell molecular recording
Genomic recording enables transient biological signals to be indelibly captured through DNA alterations, creating a permanent record of cellular history retrievable by sequencing. However, current methods are limited by scarce writing space, typically targeting…