AI Impact on Biomedicine
The authors of a new preprint analyzed 1,194,287 English-language articles from 2017 to 2025 from PubMed Central, an open archive of biomedical literature with full texts. They compared the introduction, methods, results, and discussion in this dataset and evaluated the shift in vocabulary at the level of the entire corpus. In 2025, Dmitry Kobak and colleagues identified 379 common words that became noticeably more frequent in biomedical annotations after the appearance of ChatGPT.
The new preprint uses this vocabulary as a set of markers and transfers the evaluation from annotations to full texts. For each marker, the authors built a previous trend over 60 months from 2018 to 2022 and continued it to 2023-2025. Then, they compared the forecast with the observed frequency. One word provides only a minimal estimate, so the researchers tried sets of rare markers and discarded options with too large a statistical error.
In a simulation on 100,000 texts with a predetermined share of language model assistance, this method restored it with an error of less than two percentage points. According to this model, the authors estimated the share of language model assistance in the combined text of introduction, methods, results, and discussion to be 89% by December 2025. The discussion of results, where authors gather data into an argument, showed 68% assistance from the model; in the methods section, where the course of work is described, it showed 32%. The method works on the scale of the corpus: the frequency of words in a million texts shows how the language of biomedical articles is changing, as reported in Nature Aging, July 2026.
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The authors of a new preprint analyzed 1,194,287 English-language articles from 2017 to 2025 from PubMed Central, an open archive of biomedical literature with full texts. They compared the introduction, methods, results, and discussion in this dataset and evaluated the shift in vocabulary at the level of the entire corpus. In 2025, Dmitry Kobak and colleagues identified 379 common words that became noticeably more frequent in biomedical annotations after the appearance of ChatGPT.
The new preprint uses this vocabulary as a set of markers and transfers the evaluation from annotations to full texts. For each marker, the authors built a previous trend over 60 months from 2018 to 2022 and continued it to 2023-2025. Then, they compared the forecast with the observed frequency. One word provides only a minimal estimate, so the researchers tried sets of rare markers and discarded options with too large a statistical error.
In a simulation on 100,000 texts with a predetermined share of language model assistance, this method restored it with an error of less than two percentage points. According to this model, the authors estimated the share of language model assistance in the combined text of introduction, methods, results, and discussion to be 89% by December 2025. The discussion of results, where authors gather data into an argument, showed 68% assistance from the model; in the methods section, where the course of work is described, it showed 32%. The method works on the scale of the corpus: the frequency of words in a million texts shows how the language of biomedical articles is changing, as reported in Nature Aging, July 2026.
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PubMed Central (PMC)
PubMed Central: PMC Open Access Subset
3D Mouse Ovary Map
A recent study published in Nature Aging, August 12 has created a 3D map of aging mouse ovaries, showing that around 14% of oocytes are in the early growth stage across all age groups. The team analyzed 101 mouse ovaries aged 5 to 60 weeks and identified the growth stage of over 85,000 oocytes.
The ovarian reserve, which is the stock of immature oocytes within follicles, depends on the number of follicles exiting the resting stage and the losses at subsequent stages. The authors made the entire ovary tissue transparent, labeled the oocytes, and imaged the organ using light-sheet microscopy.
The study found that the total number of oocytes decreased more than tenfold with age in the main series of 56 genetically identical mice. The authors also divided the oocyte pathway into four stages and compared age-related counts with a model of transitions between them, finding that about 2.5% of resting oocytes exit the resting stage per week.
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A recent study published in Nature Aging, August 12 has created a 3D map of aging mouse ovaries, showing that around 14% of oocytes are in the early growth stage across all age groups. The team analyzed 101 mouse ovaries aged 5 to 60 weeks and identified the growth stage of over 85,000 oocytes.
The ovarian reserve, which is the stock of immature oocytes within follicles, depends on the number of follicles exiting the resting stage and the losses at subsequent stages. The authors made the entire ovary tissue transparent, labeled the oocytes, and imaged the organ using light-sheet microscopy.
The study found that the total number of oocytes decreased more than tenfold with age in the main series of 56 genetically identical mice. The authors also divided the oocyte pathway into four stages and compared age-related counts with a model of transitions between them, finding that about 2.5% of resting oocytes exit the resting stage per week.
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Nature
Three-dimensional mapping of intact ovaries reveals the aging dynamics of the ovarian reserve
Nature Aging - The spatiotemporal dynamics of the depletion of the ovarian reserve remain incompletely understood. Combining whole-ovary imaging, AI and modeling, the authors mapped over 85,000...
RANKL Blockade Extends Life
Researchers found that blocking RANKL, a signal that tells cells to break down bone, extended the life of mice with a genetic model of accelerated aging. On August 9, a study was published in Aging Cell about mice with a genetic model of accelerated aging, which lack the ZMPSTE24 enzyme involved in the maturation of prelamin A protein. These animals rapidly lose bone mass, their muscles weaken, and their lifespan is shorter.
The authors suppressed RANKL in two ways, and both interventions improved the condition of the bones and muscles and extended the life of the animals. Bone tissue is constantly renewed, with osteocytes, cells inside the bone, releasing RANKL, a protein signal for osteoclasts, cells that break down old bone, and then other cells build new bone. In mice with a ZMPSTE24 deficiency, bone mass is rapidly lost, muscles weaken, and fibrosis, scar tissue that interferes with contraction, accumulates, and lifespan is reduced.
The authors turned off RANKL specifically in osteocytes in such mice. Tomography showed that the structure of the bone in the tibia and vertebrae was better preserved. The grip strength of the mice increased, they ran longer on a treadmill until exhaustion, and there was less fibrosis in the quadriceps. In the genetic experiment, the median lifespan increased from 230 to 276 days. When the authors divided the data by sex, the longer life was particularly noticeable in females.
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Researchers found that blocking RANKL, a signal that tells cells to break down bone, extended the life of mice with a genetic model of accelerated aging. On August 9, a study was published in Aging Cell about mice with a genetic model of accelerated aging, which lack the ZMPSTE24 enzyme involved in the maturation of prelamin A protein. These animals rapidly lose bone mass, their muscles weaken, and their lifespan is shorter.
The authors suppressed RANKL in two ways, and both interventions improved the condition of the bones and muscles and extended the life of the animals. Bone tissue is constantly renewed, with osteocytes, cells inside the bone, releasing RANKL, a protein signal for osteoclasts, cells that break down old bone, and then other cells build new bone. In mice with a ZMPSTE24 deficiency, bone mass is rapidly lost, muscles weaken, and fibrosis, scar tissue that interferes with contraction, accumulates, and lifespan is reduced.
The authors turned off RANKL specifically in osteocytes in such mice. Tomography showed that the structure of the bone in the tibia and vertebrae was better preserved. The grip strength of the mice increased, they ran longer on a treadmill until exhaustion, and there was less fibrosis in the quadriceps. In the genetic experiment, the median lifespan increased from 230 to 276 days. When the authors divided the data by sex, the longer life was particularly noticeable in females.
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PubMed Central (PMC)
Targeting RANKL Prevents Bone Loss, Improves Muscle Function and Extends Lifespan in Progeroid Mice
Hutchinson‐Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by the early development of pathological features associated with aging, ultimately leading to premature death. HGPS primarily affects tissues of mesenchymal ...
Life Extended by 29%
Researchers described an experiment with membrane particles from E. coli bacteria with the aroD gene removed in an article accepted for publication on August 10 in the journal npj Aging. The loss of this gene reduces the availability of a precursor to vitamin B9, also known as folate, in bacteria. The median lifespan of C. elegans worms increased from 17.6 to 22.8 days.
The aroD gene was chosen for this experiment based on a 2012 study that linked its removal to a longer lifespan in C. elegans and the suppression of bacterial folate synthesis. In the new experiment, the authors tested whether this effect is transmitted by membrane particles isolated from the bacteria. To obtain the particles, cells of mutant E. coli and the control strain BW25113 were disrupted, filtered, and centrifuged at high speed.
The addition of PABA, a precursor to folate, to the culture of mutant bacteria eliminated the effect of its particles. Particles from normal E. coli treated with sulfamethoxazole, which blocks folate synthesis, had a similar effect. Both experiments link the effect to bacterial folate synthesis. The authors then moved on to the contents of the particles, isolating a candidate small RNA called Novel27.
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Researchers described an experiment with membrane particles from E. coli bacteria with the aroD gene removed in an article accepted for publication on August 10 in the journal npj Aging. The loss of this gene reduces the availability of a precursor to vitamin B9, also known as folate, in bacteria. The median lifespan of C. elegans worms increased from 17.6 to 22.8 days.
The aroD gene was chosen for this experiment based on a 2012 study that linked its removal to a longer lifespan in C. elegans and the suppression of bacterial folate synthesis. In the new experiment, the authors tested whether this effect is transmitted by membrane particles isolated from the bacteria. To obtain the particles, cells of mutant E. coli and the control strain BW25113 were disrupted, filtered, and centrifuged at high speed.
The addition of PABA, a precursor to folate, to the culture of mutant bacteria eliminated the effect of its particles. Particles from normal E. coli treated with sulfamethoxazole, which blocks folate synthesis, had a similar effect. Both experiments link the effect to bacterial folate synthesis. The authors then moved on to the contents of the particles, isolating a candidate small RNA called Novel27.
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Nature
Gut bacterial vesicles from the E. coliΔaroD mutant extend C. elegans lifespan
npj Aging - Gut bacterial vesicles from the E. coliΔaroD mutant extend C. elegans lifespan
Aging Serum Weakens Muscle
Researchers found that serum from older donors weakened human muscle tissue contractions in a lab model. On August 12, a study in npj Aging reported on three-dimensional muscle tissue grown from human cells. After 48 hours in a medium with combined serum from 65–71 year old donors, it contracted about one-third weaker than in a medium with serum from 17–29 year old donors.
The authors also linked this effect to the activation of NF-κB and tested quercetin as an intervention. In sarcopenia, the age-related loss of muscle mass and strength, muscles weaken. Early experiments showed that serum and plasma from older people reduced the size of mouse muscle cells. The authors of the new study tested whether this effect is reproduced in cells taken from human muscle tissue and whether the tissue assembled from them loses its ability to contract.
They grew three-dimensional tissue from myoblasts, muscle precursor cells, in plate cells with flexible micro-posts. An electric impulse makes the tissue contract, and the deflection of the posts shows the contraction force. After seven days of growth, the authors added 10% combined serum from young or old donors to the medium for 48 hours. In a flat cell culture, the serum from older donors reduced the area of muscle cells. In three-dimensional tissue, the contraction force was about 30% lower.
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Researchers found that serum from older donors weakened human muscle tissue contractions in a lab model. On August 12, a study in npj Aging reported on three-dimensional muscle tissue grown from human cells. After 48 hours in a medium with combined serum from 65–71 year old donors, it contracted about one-third weaker than in a medium with serum from 17–29 year old donors.
The authors also linked this effect to the activation of NF-κB and tested quercetin as an intervention. In sarcopenia, the age-related loss of muscle mass and strength, muscles weaken. Early experiments showed that serum and plasma from older people reduced the size of mouse muscle cells. The authors of the new study tested whether this effect is reproduced in cells taken from human muscle tissue and whether the tissue assembled from them loses its ability to contract.
They grew three-dimensional tissue from myoblasts, muscle precursor cells, in plate cells with flexible micro-posts. An electric impulse makes the tissue contract, and the deflection of the posts shows the contraction force. After seven days of growth, the authors added 10% combined serum from young or old donors to the medium for 48 hours. In a flat cell culture, the serum from older donors reduced the area of muscle cells. In three-dimensional tissue, the contraction force was about 30% lower.
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Nature
Human in vitro skeletal muscle models recapitulate age-related atrophy and contractile decline induced by aged serum
npj Aging - Human in vitro skeletal muscle models recapitulate age-related atrophy and contractile decline induced by aged serum
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Artificial Hibernation
Researchers at the Okinawa Institute of Science and Technology (OIST) and their colleagues induced a controlled cooling of the body and slowing of metabolism in mice for 48 hours, resulting in a 52.5% decrease in synaptic density in the hippocampus. Despite this significant decrease, the mice retained memories of familiar places and events, and their neural maps of space remained intact.
The study, published on August 13 in Science, found that the mice's ability to recall specific memories was preserved, even though the individual synapses, or points of contact between neurons, were significantly reduced. The researchers used a technique to label synapses between neurons of a single engram, a group of cells and contacts active during a specific memory, and found that while individual contacts within the engram often disappeared during artificial hibernation, their spatial clusters were preserved.
In contrast, when the researchers applied a different regime, using prolonged anesthesia with pharmacological intervention in actin, a protein that helps cells change shape, the mice's ability to recall context was impaired. The study suggests that the preservation of clusters of engrammatic contacts may be a key factor in the retention of memory, and that these clusters may represent a stable structural trace of a memory.
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Researchers at the Okinawa Institute of Science and Technology (OIST) and their colleagues induced a controlled cooling of the body and slowing of metabolism in mice for 48 hours, resulting in a 52.5% decrease in synaptic density in the hippocampus. Despite this significant decrease, the mice retained memories of familiar places and events, and their neural maps of space remained intact.
The study, published on August 13 in Science, found that the mice's ability to recall specific memories was preserved, even though the individual synapses, or points of contact between neurons, were significantly reduced. The researchers used a technique to label synapses between neurons of a single engram, a group of cells and contacts active during a specific memory, and found that while individual contacts within the engram often disappeared during artificial hibernation, their spatial clusters were preserved.
In contrast, when the researchers applied a different regime, using prolonged anesthesia with pharmacological intervention in actin, a protein that helps cells change shape, the mice's ability to recall context was impaired. The study suggests that the preservation of clusters of engrammatic contacts may be a key factor in the retention of memory, and that these clusters may represent a stable structural trace of a memory.
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bioRxiv
Artificial hibernation uncovers distinct synaptic engram architecture for memory retention
The memory trace at the neuronal and synaptic levels remains controversial. Stable, larger spines are thought to support memory, but the high turnover of dendritic spines and the drifting of neuronal representations following memory formation suggest alternative…
AI System Tracks Effects
The journal Nature Medicine has published a plan for an AI system that tracks the consequences of interventions from molecules to organisms. On August 13, the journal published an article outlining the AIDO system, which connects AI models for different levels of biology. The authors propose linking models of DNA, proteins, cells, tissues, and organism traits to track how a drug or gene modification affects this chain.
When a drug or gene modification acts on an organism, it first affects molecules, then may alter the gene network and cell state, and eventually affect tissue and organism traits. The data at these levels are structured differently: DNA is a sequence of symbols, protein importance lies in its three-dimensional form, and tissue importance lies in the arrangement of neighboring cells. Therefore, the authors propose a separate model for each type of data, with AIDO based on specialized base models.
These models are first trained on a large array of similar data and then fine-tuned for a specific task, such as reading DNA and RNA sequences, matching protein structure to its properties, or describing cell state or changes in organism metrics over time. The authors then want to connect these models using known biological relationships, such as how cells create RNA from DNA and assemble proteins based on RNA instructions. By linking this network to cell state data, the model gains information about interventions and the pathways they may take to alter cells. The authors propose adjusting connected models together, with organism-level predictions changing the settings of cell and molecule models, and their data refining upper-level predictions. As described in the Nature Medicine, July 2026 article, the system is designed to calculate possible responses through the gene influence network.
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The journal Nature Medicine has published a plan for an AI system that tracks the consequences of interventions from molecules to organisms. On August 13, the journal published an article outlining the AIDO system, which connects AI models for different levels of biology. The authors propose linking models of DNA, proteins, cells, tissues, and organism traits to track how a drug or gene modification affects this chain.
When a drug or gene modification acts on an organism, it first affects molecules, then may alter the gene network and cell state, and eventually affect tissue and organism traits. The data at these levels are structured differently: DNA is a sequence of symbols, protein importance lies in its three-dimensional form, and tissue importance lies in the arrangement of neighboring cells. Therefore, the authors propose a separate model for each type of data, with AIDO based on specialized base models.
These models are first trained on a large array of similar data and then fine-tuned for a specific task, such as reading DNA and RNA sequences, matching protein structure to its properties, or describing cell state or changes in organism metrics over time. The authors then want to connect these models using known biological relationships, such as how cells create RNA from DNA and assemble proteins based on RNA instructions. By linking this network to cell state data, the model gains information about interventions and the pathways they may take to alter cells. The authors propose adjusting connected models together, with organism-level predictions changing the settings of cell and molecule models, and their data refining upper-level predictions. As described in the Nature Medicine, July 2026 article, the system is designed to calculate possible responses through the gene influence network.
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Nature
How to build an AI-driven digital organism
Nature Medicine - Manipulating biology in the physical world is complex; the authors envision an AI-driven digital organism—a system of integrated multiscale foundation models—detailing...
New Hadamard Matrices Found
A team led by Levent Alpöge, with the help of Claude, has constructed 12 previously unknown Hadamard matrices of size +1 and -1. On August 12, Alpöge published a string of 23,828 "+" and "-" characters and a decoder for it. Together, they provide twelve Hadamard matrices for all remaining unknown valid orders up to 2000, including order 668.
The Hadamard matrix is a square table of plus and minus signs where any two different rows, when paired and added, give zero. Its order is the number of rows and columns. The Hadamard hypothesis asserts that such a matrix exists for every size that is a multiple of four. The order 668 was the smallest case for which its existence remained unknown: the previous case, order 428, was closed by mathematicians in 2004.
The FrontierMath benchmark had set the task of building a 668x668 table. In the spring FrontierMath problem on hypergraphs, the problem author confirmed the solution found in work with GPT-5.4 Pro, and began preparing an article. The new result's verification chain starts with a ready-made object: Alpöge's string and the response with the decoder program.
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A team led by Levent Alpöge, with the help of Claude, has constructed 12 previously unknown Hadamard matrices of size +1 and -1. On August 12, Alpöge published a string of 23,828 "+" and "-" characters and a decoder for it. Together, they provide twelve Hadamard matrices for all remaining unknown valid orders up to 2000, including order 668.
The Hadamard matrix is a square table of plus and minus signs where any two different rows, when paired and added, give zero. Its order is the number of rows and columns. The Hadamard hypothesis asserts that such a matrix exists for every size that is a multiple of four. The order 668 was the smallest case for which its existence remained unknown: the previous case, order 428, was closed by mathematicians in 2004.
The FrontierMath benchmark had set the task of building a 668x668 table. In the spring FrontierMath problem on hypergraphs, the problem author confirmed the solution found in work with GPT-5.4 Pro, and began preparing an article. The new result's verification chain starts with a ready-made object: Alpöge's string and the response with the decoder program.
🔗 Read original →
X (formerly Twitter)
levent (@__alpoge__) on X
+++-+-+-+-+--+--+++-++----++--+----+-----+++---++-+---+++++++-+--+-+-+--++-+--+--+----+-+-+-+-++-++---+--++++--++-++++-+++++--+---++-+---+++++++++--+-+-+--++-+--+--+-----+++-+++-++-+-++++-++-+--+--+------++--+-++-+-+---+--+-+-+-+--++---+++++-----+++++++-…
Worm Regrows Body
The marine worm Hofstenia miamia can regrow its entire body after amputation. When only the outer layer is damaged, its cells pull the edges of the wound together; if the cut affects the pharynx, cells from two tissues first connect with long temporary bridges. The outer layer and the inner lining of the pharynx in this worm consist of dense cell layers - epithelia.
Research compared wounds that damaged one such layer with those that affected both. When the worm was cut transversely below the pharynx, only the outer layer was damaged. Its edges converged to the center: cells gathered actin filaments - protein threads that help cells change shape - along the edge and pulled the gap together. The head fragment then regrew the tail, and the tail fragment regrew the head; in both, the outer layer closed in the same way.
When the cut passed through the outer layer and the pharynx, the sequence changed. Cells from the outer layer and the pharynx released long actin protrusions; they met over the wound and formed temporary bridges. Later, cells from each layer reconnected with each other. To check the role of the cut direction, researchers cut the worm through the pharynx along the body and across. In both cases, bridges appeared. Along with experience on head and tail fragments, this links the early closure method to which cell layers are damaged.
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The marine worm Hofstenia miamia can regrow its entire body after amputation. When only the outer layer is damaged, its cells pull the edges of the wound together; if the cut affects the pharynx, cells from two tissues first connect with long temporary bridges. The outer layer and the inner lining of the pharynx in this worm consist of dense cell layers - epithelia.
Research compared wounds that damaged one such layer with those that affected both. When the worm was cut transversely below the pharynx, only the outer layer was damaged. Its edges converged to the center: cells gathered actin filaments - protein threads that help cells change shape - along the edge and pulled the gap together. The head fragment then regrew the tail, and the tail fragment regrew the head; in both, the outer layer closed in the same way.
When the cut passed through the outer layer and the pharynx, the sequence changed. Cells from the outer layer and the pharynx released long actin protrusions; they met over the wound and formed temporary bridges. Later, cells from each layer reconnected with each other. To check the role of the cut direction, researchers cut the worm through the pharynx along the body and across. In both cases, bridges appeared. Along with experience on head and tail fragments, this links the early closure method to which cell layers are damaged.
🔗 Read original →
Nature
A flexible repertoire of wound closure strategies precedes whole-body regeneration
Nature Communications - Animals capable of whole-body regeneration can heal virtually any wound. Here they show that Hofstenia miamia accomplishes this feat through variable morphogenetic...
Blood Protein Norms
Researchers have found that some blood proteins have a personal norm that can be measured. In a study published on August 10 in Nature Health, authors tracked levels of 10,776 protein markers in 1,298 participants. Measurements were collected in four waves: in 2002, 2007, 2012, and 2022.
The reference ranges on the analysis form show how the result relates to a large group of people. For some proteins, an individual's level differs from the average for years and remains characteristic of that person. A personal baseline allows for the detection of shifts that would be lost in the general norm.
The authors first adjusted the data for overall age-related shifts and systematic differences between measurement waves. Then, for each protein, they compared the results of the same individuals at two visits, resulting in a protein homeostasis index (PHI).
The higher the PHI, the more stable the individual's level. A check with another laboratory measure gave the same order: high PHI was found in proteins that changed less within one person than they differed between people. This allowed the researchers to identify markers for which a person's long-term history could serve as a baseline.
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Researchers have found that some blood proteins have a personal norm that can be measured. In a study published on August 10 in Nature Health, authors tracked levels of 10,776 protein markers in 1,298 participants. Measurements were collected in four waves: in 2002, 2007, 2012, and 2022.
The reference ranges on the analysis form show how the result relates to a large group of people. For some proteins, an individual's level differs from the average for years and remains characteristic of that person. A personal baseline allows for the detection of shifts that would be lost in the general norm.
The authors first adjusted the data for overall age-related shifts and systematic differences between measurement waves. Then, for each protein, they compared the results of the same individuals at two visits, resulting in a protein homeostasis index (PHI).
The higher the PHI, the more stable the individual's level. A check with another laboratory measure gave the same order: high PHI was found in proteins that changed less within one person than they differed between people. This allowed the researchers to identify markers for which a person's long-term history could serve as a baseline.
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Nature
Temporal dynamics of the human blood proteome in ageing and disease
Nature Health - Using data from 2,621 individuals across 20 years of their lifetime, this analysis sheds light on how protein marker profiles change over time and how this change is related...
Long Life and AI
Брайан Джонсон discusses his personal Blueprint program, which combines his genome, proteome, and other measurements to identify patterns and suggest interventions. He proposes that humans and AI work together to preserve reasonable life.
The concept of autonomous health is introduced, where algorithms analyze body data to determine actions, reducing the need for human management. Джонсон's experiment aims to translate measurements into health decisions.
In a thought experiment set in 2500, Джонсон envisions a future where humans have created superintelligent AI and no longer consider death inevitable. The Don't Die movement is formulated as "not dying yourself, not killing each other, not killing the Earth, and aligning AI with Don't Die". Росс Даутат questions how added time will impact power, wealth, and legacy.
🔗 Read original →
Брайан Джонсон discusses his personal Blueprint program, which combines his genome, proteome, and other measurements to identify patterns and suggest interventions. He proposes that humans and AI work together to preserve reasonable life.
The concept of autonomous health is introduced, where algorithms analyze body data to determine actions, reducing the need for human management. Джонсон's experiment aims to translate measurements into health decisions.
In a thought experiment set in 2500, Джонсон envisions a future where humans have created superintelligent AI and no longer consider death inevitable. The Don't Die movement is formulated as "not dying yourself, not killing each other, not killing the Earth, and aligning AI with Don't Die". Росс Даутат questions how added time will impact power, wealth, and legacy.
🔗 Read original →
PubMed Central (PMC)
N-of-1 trials: The epitome of personalized medicine?
Observational studies are notoriously susceptible to bias, and parallel-group randomized trials are important to identify the best overall treatment for eligible patients. Yet, such trials can be expected to be a misleading indicator of the best ...
Vanderbilt Muscle Study
Vanderbilt University has registered a trial to preserve muscle in elderly individuals starting semaglutide, a medication for type 2 diabetes and weight loss. On August 12, a phase 2 trial record appeared in ClinicalTrials.gov, involving 90 people aged 65-85 with type 2 diabetes, starting semaglutide, who will be randomly assigned to receive either calcium HMB with vitamin D3 or a placebo for six months.
During weight loss, lean tissue, including skeletal muscle, may also decrease. Muscle is essential for strength, walking, and independent living in older adults. In this trial, treating physicians will prescribe and manage semaglutide therapy, while the research team compares the supplement to a placebo during the first six months of treatment.
The trial will assess changes in lean body mass, measured using DXA scans, as the primary outcome. Researchers will also evaluate hand and leg strength, six-minute walk distance, gait, and daily activity. Quantitative CT scans will provide data on muscle volume and composition, allowing researchers to correlate changes in body composition with strength and movement.
🔗 Read original →
Vanderbilt University has registered a trial to preserve muscle in elderly individuals starting semaglutide, a medication for type 2 diabetes and weight loss. On August 12, a phase 2 trial record appeared in ClinicalTrials.gov, involving 90 people aged 65-85 with type 2 diabetes, starting semaglutide, who will be randomly assigned to receive either calcium HMB with vitamin D3 or a placebo for six months.
During weight loss, lean tissue, including skeletal muscle, may also decrease. Muscle is essential for strength, walking, and independent living in older adults. In this trial, treating physicians will prescribe and manage semaglutide therapy, while the research team compares the supplement to a placebo during the first six months of treatment.
The trial will assess changes in lean body mass, measured using DXA scans, as the primary outcome. Researchers will also evaluate hand and leg strength, six-minute walk distance, gait, and daily activity. Quantitative CT scans will provide data on muscle volume and composition, allowing researchers to correlate changes in body composition with strength and movement.
🔗 Read original →
PubMed Central (PMC)
D3‐creatine dilution for skeletal muscle mass measurement: historical development and current status
The French chemist Michel Eugène Chevreul discovered creatine in meat two centuries ago. Extensive biochemical and physiological studies of this organic molecule followed with confirmation that creatine is found within the cytoplasm and mitochondria ...
Vanderbilt Muscle Study
Vanderbilt University has registered a trial to test a supplement for preserving muscle in older adults starting semaglutide, a medication for type 2 diabetes and weight loss. On August 12, a phase 2 trial record appeared in ClinicalTrials.gov, involving 90 people aged 65–85 with type 2 diabetes, starting semaglutide, who will be randomly assigned to receive either a calcium form of HMB with vitamin D3 or a placebo for six months.
During weight loss, lean tissue, including skeletal muscle, may also decrease, but muscles are essential for strength, walking, and independent living in older adults. In this trial, treating physicians will prescribe and manage semaglutide therapy, while the research team will compare the supplement to a placebo during the first six months of treatment. The trial will assess changes in lean body mass, measured using DXA scans, as well as hand and leg strength, six-minute walk distance, gait, and daily activity.
The researchers will also use quantitative CT scans to evaluate muscle volume and composition, comparing changes in body composition to strength and movement. A separate part of the trial will involve up to 36 participants, using labeled creatine to assess contractile muscle tissue, and labeled amino acids and thigh muscle biopsies to provide data on muscle protein synthesis and breakdown. The combination of HMB and vitamin D3 has been previously tested in older adults in a randomized study, and Vanderbilt will now test it in people starting semaglutide, with data for the primary comparison expected to be collected by November 30, 2029, as reported in ClinicalTrials.gov.
🔗 Read original →
Vanderbilt University has registered a trial to test a supplement for preserving muscle in older adults starting semaglutide, a medication for type 2 diabetes and weight loss. On August 12, a phase 2 trial record appeared in ClinicalTrials.gov, involving 90 people aged 65–85 with type 2 diabetes, starting semaglutide, who will be randomly assigned to receive either a calcium form of HMB with vitamin D3 or a placebo for six months.
During weight loss, lean tissue, including skeletal muscle, may also decrease, but muscles are essential for strength, walking, and independent living in older adults. In this trial, treating physicians will prescribe and manage semaglutide therapy, while the research team will compare the supplement to a placebo during the first six months of treatment. The trial will assess changes in lean body mass, measured using DXA scans, as well as hand and leg strength, six-minute walk distance, gait, and daily activity.
The researchers will also use quantitative CT scans to evaluate muscle volume and composition, comparing changes in body composition to strength and movement. A separate part of the trial will involve up to 36 participants, using labeled creatine to assess contractile muscle tissue, and labeled amino acids and thigh muscle biopsies to provide data on muscle protein synthesis and breakdown. The combination of HMB and vitamin D3 has been previously tested in older adults in a randomized study, and Vanderbilt will now test it in people starting semaglutide, with data for the primary comparison expected to be collected by November 30, 2029, as reported in ClinicalTrials.gov.
🔗 Read original →
PubMed Central (PMC)
D3‐creatine dilution for skeletal muscle mass measurement: historical development and current status
The French chemist Michel Eugène Chevreul discovered creatine in meat two centuries ago. Extensive biochemical and physiological studies of this organic molecule followed with confirmation that creatine is found within the cytoplasm and mitochondria ...
Model Discovery Agent
The Model Discovery Agent (MDA) system, presented by Кевин Мёрфи on August 12, proposes explanations for observed phenomena and selects experiments to test them. In 36 simulated tasks on enzyme reactions, the author reports that MDA recovered the formula of the hidden law in approximately 56% of cases after eight experiments, while another system, LLM-AutoSciLab, achieved around 42% after 60.
The same set of measurements can be equally consistent with multiple explanations, making repeated experiments of little help. What is needed is an experiment that will make alternative explanations give different predictions. In the case of an enzyme reaction, this can be achieved by changing the concentration of substances, temperature, or the amount of enzyme - a protein that accelerates a chemical reaction.
The MDA system has two blocks: a language model that proposes explanations, and a statistical algorithm that compares how well each explanation agrees with the data and refines its parameters. The system then selects an intervention where the predictions of alternative explanations diverge the most. When the best available model makes a mistake on a particular check, the language model receives a description of the discrepancy and proposes another mechanism. The next experiment, chosen on the same principle, helps refine the parameters of the new mechanism and compare it to previous explanations, as described in Nature Aging, July 2026.
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The Model Discovery Agent (MDA) system, presented by Кевин Мёрфи on August 12, proposes explanations for observed phenomena and selects experiments to test them. In 36 simulated tasks on enzyme reactions, the author reports that MDA recovered the formula of the hidden law in approximately 56% of cases after eight experiments, while another system, LLM-AutoSciLab, achieved around 42% after 60.
The same set of measurements can be equally consistent with multiple explanations, making repeated experiments of little help. What is needed is an experiment that will make alternative explanations give different predictions. In the case of an enzyme reaction, this can be achieved by changing the concentration of substances, temperature, or the amount of enzyme - a protein that accelerates a chemical reaction.
The MDA system has two blocks: a language model that proposes explanations, and a statistical algorithm that compares how well each explanation agrees with the data and refines its parameters. The system then selects an intervention where the predictions of alternative explanations diverge the most. When the best available model makes a mistake on a particular check, the language model receives a description of the discrepancy and proposes another mechanism. The next experiment, chosen on the same principle, helps refine the parameters of the new mechanism and compare it to previous explanations, as described in Nature Aging, July 2026.
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Alzheimer's Gene Study Questioned
The journal Science published an investigation by Charles Piller and Jenny Erin Smith on August 13, examining rare gene variants in a large Colombian family. The inherited PSEN1 E280A mutation typically causes mild cognitive impairment around 44 years of age in its carriers. However, two cases with much later disease onset suggested other genes as potential treatment targets.
A 2019 article described a woman with PSEN1 E280A who preserved cognitive function until 70 years of age. She was found to have two copies of the rare APOE3 Christchurch variant. Imaging showed high amyloid burden, characteristic of Alzheimer's disease, and relatively little tau deposition, another protein associated with its development. This unusual case led to the hypothesis that the APOE variant might be delaying symptom onset. A 2023 study added a man from the same family, who preserved cognitive abilities until 67 years of age and was diagnosed with mild cognitive impairment at 70.
The investigation by Science raises questions about data changes and suspicious or copied images in several articles. The Colombian research group GNA responded that questions about images concern a limited part of the publications and do not affect the authenticity of the original data, quantitative analyses, and scientific conclusions of these works. An independent analysis should verify the genotypes, age of symptom onset, and patient selection rules in the cohort. After such verification, cellular experiments can explain how the candidate acts in the protein and cell before relying on it for treatment development, as reported in Science, August 2023.
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The journal Science published an investigation by Charles Piller and Jenny Erin Smith on August 13, examining rare gene variants in a large Colombian family. The inherited PSEN1 E280A mutation typically causes mild cognitive impairment around 44 years of age in its carriers. However, two cases with much later disease onset suggested other genes as potential treatment targets.
A 2019 article described a woman with PSEN1 E280A who preserved cognitive function until 70 years of age. She was found to have two copies of the rare APOE3 Christchurch variant. Imaging showed high amyloid burden, characteristic of Alzheimer's disease, and relatively little tau deposition, another protein associated with its development. This unusual case led to the hypothesis that the APOE variant might be delaying symptom onset. A 2023 study added a man from the same family, who preserved cognitive abilities until 67 years of age and was diagnosed with mild cognitive impairment at 70.
The investigation by Science raises questions about data changes and suspicious or copied images in several articles. The Colombian research group GNA responded that questions about images concern a limited part of the publications and do not affect the authenticity of the original data, quantitative analyses, and scientific conclusions of these works. An independent analysis should verify the genotypes, age of symptom onset, and patient selection rules in the cohort. After such verification, cellular experiments can explain how the candidate acts in the protein and cell before relying on it for treatment development, as reported in Science, August 2023.
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Science
Science investigation casts doubt on genes hailed for warding off Alzheimer’s disease
Mutations found in Colombian families raised hopes for treatments. Altered patient data and suspect images call their benefits into question
Recombinase IS621 Bias
The IS621 recombinase, which rearranges DNA, inserts segments 2,000 times more frequently than it excises. An article published on August 12 in Nature explored why the IS621 recombinase is more efficient at inserting DNA segments than excising them.
The authors linked this bias to the shape of the complex formed by the protein, RNA, and DNA, and increased the excision frequency in E. coli bacterial plasmids by modifying the guide RNA. The IS621 is a mobile DNA fragment from the IS110 family, which encodes a recombinase that first excises the fragment from DNA, forming a circular double-stranded molecule, and then inserts it into a new location.
A 2024 study showed that these addresses can be changed; the new article explains why the reverse step is much less efficient. Experiments with purified protein, defined DNA segments, and constructed bridge RNA showed that excision yielded 0.03% product, while insertion yielded 63%. Labels on the DNA allowed researchers to see where efficiency was lost: after the first cut in both cases, intermediate molecules accumulated, but the next step - the exchange of cut DNA strands - proceeded much worse for excision.
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The IS621 recombinase, which rearranges DNA, inserts segments 2,000 times more frequently than it excises. An article published on August 12 in Nature explored why the IS621 recombinase is more efficient at inserting DNA segments than excising them.
The authors linked this bias to the shape of the complex formed by the protein, RNA, and DNA, and increased the excision frequency in E. coli bacterial plasmids by modifying the guide RNA. The IS621 is a mobile DNA fragment from the IS110 family, which encodes a recombinase that first excises the fragment from DNA, forming a circular double-stranded molecule, and then inserts it into a new location.
A 2024 study showed that these addresses can be changed; the new article explains why the reverse step is much less efficient. Experiments with purified protein, defined DNA segments, and constructed bridge RNA showed that excision yielded 0.03% product, while insertion yielded 63%. Labels on the DNA allowed researchers to see where efficiency was lost: after the first cut in both cases, intermediate molecules accumulated, but the next step - the exchange of cut DNA strands - proceeded much worse for excision.
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Nature
Structural mechanism governing the directionality of bridge recombination
Nature - Cryo-electron microscopy structures show how IS621 bridge recombinase mediates DNA excision, explaining its natural preference for insertion and informing the design of programmable...
Designer Babies
The Economist reports on startups offering genetic screening of embryos to parents undergoing EKO (in vitro fertilization), initially for disease risks like diabetes or breast cancer, and now for polygenic traits such as height or IQ. Analyzing tens of thousands of genetic variants allows for the calculation of certain trait probabilities. Although the technology is imperfect, it works better than many think, with a 2019 study showing that parents could increase their child's future height by 1-6 cm and IQ by 1-7 points by choosing from 10 embryos.
This data is nearly a decade old, preceding current massive genetic databases and the emergence of powerful AI models that can detect weak signals in the genome. As databases grow, accuracy will improve, especially for non-European populations, which are currently underrepresented. However, polygenic estimates provide probability, not guarantee, and rare diseases are difficult to quantify in absolute numbers, with selection limited to existing embryos.
These are arguments for transparency, not prohibition, and if companies are required to explain risks, publish model accuracy, and undergo independent verification, the technology becomes beneficial, not hazardous. The journal directly addresses concerns surrounding "new eugenics," stating that fears are not supported by facts, with no coercion or selection of "ideal people," only parents wanting to know more about their future child's health. Currently, ¾ of Americans support screening for diseases, and ⅓ for non-diagnostic traits.
The article concludes that as EKO becomes more affordable, it will no longer be a luxury for the wealthy, and surprisingly, suggests that the state should not interfere with parents using genetic information, as long as it is done voluntarily, transparently, and scientifically correctly, citing The Economist, August 2026.
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The Economist reports on startups offering genetic screening of embryos to parents undergoing EKO (in vitro fertilization), initially for disease risks like diabetes or breast cancer, and now for polygenic traits such as height or IQ. Analyzing tens of thousands of genetic variants allows for the calculation of certain trait probabilities. Although the technology is imperfect, it works better than many think, with a 2019 study showing that parents could increase their child's future height by 1-6 cm and IQ by 1-7 points by choosing from 10 embryos.
This data is nearly a decade old, preceding current massive genetic databases and the emergence of powerful AI models that can detect weak signals in the genome. As databases grow, accuracy will improve, especially for non-European populations, which are currently underrepresented. However, polygenic estimates provide probability, not guarantee, and rare diseases are difficult to quantify in absolute numbers, with selection limited to existing embryos.
These are arguments for transparency, not prohibition, and if companies are required to explain risks, publish model accuracy, and undergo independent verification, the technology becomes beneficial, not hazardous. The journal directly addresses concerns surrounding "new eugenics," stating that fears are not supported by facts, with no coercion or selection of "ideal people," only parents wanting to know more about their future child's health. Currently, ¾ of Americans support screening for diseases, and ⅓ for non-diagnostic traits.
The article concludes that as EKO becomes more affordable, it will no longer be a luxury for the wealthy, and surprisingly, suggests that the state should not interfere with parents using genetic information, as long as it is done voluntarily, transparently, and scientifically correctly, citing The Economist, August 2026.
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The Economist
In praise of designer-ish babies
Couples should be allowed to select embryos on the basis of both disease resistance and IQ
Independent Analysis
The study reevaluated 16 variants of the ΦX174 bacteriophage genome, proposed by the Evo 2 model, and found that they were 97 percent identical to the natural ΦX174 genome. The authors of the study, published in IEEE Spectrum on August 12, assessed the genomes based on two criteria: how similar they were to natural phages and how effective the procedure was in finding viable variants.
The Evo 2 model was trained on the genomes of related phages and then used to generate 302 candidate genomes, which were then tested in a laboratory. Of these, 17 could not be synthesized, and of the remaining 285, 16 were found to be infectious. The results showed that the procedure was effective in finding viable variants, but the authors noted that this was due to the entire process, not just the model itself.
The study also compared the created phages to natural ones and found that a mixture of created phages was able to suppress a resistant E. coli strain, while a mixture of natural phages was not. The authors suggested that future genome systems should be evaluated based on two measurable characteristics: the distance of their sequences from natural variants and the effectiveness of the path from model to laboratory testing.
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The study reevaluated 16 variants of the ΦX174 bacteriophage genome, proposed by the Evo 2 model, and found that they were 97 percent identical to the natural ΦX174 genome. The authors of the study, published in IEEE Spectrum on August 12, assessed the genomes based on two criteria: how similar they were to natural phages and how effective the procedure was in finding viable variants.
The Evo 2 model was trained on the genomes of related phages and then used to generate 302 candidate genomes, which were then tested in a laboratory. Of these, 17 could not be synthesized, and of the remaining 285, 16 were found to be infectious. The results showed that the procedure was effective in finding viable variants, but the authors noted that this was due to the entire process, not just the model itself.
The study also compared the created phages to natural ones and found that a mixture of created phages was able to suppress a resistant E. coli strain, while a mixture of natural phages was not. The authors suggested that future genome systems should be evaluated based on two measurable characteristics: the distance of their sequences from natural variants and the effectiveness of the path from model to laboratory testing.
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Science
Generative design of bacteriophages with genome language models
Many important biological functions arise not from single genes but from complex interactions encoded by entire genomes. We report the first generative design of complete bacteriophage genomes using genome language models. We generated viable ...
UK Biotech Boost
The UK is launching a large-scale shift from animal testing to models created from real human cells, including mini-organs, organoids, and "organ-on-a-chip" systems. This is being done as a national program with significant funding and a clear goal: to make drug development faster, more accurate, and safer. Scientists will grow organoids from NHS patient cells - tiny structures smaller than a millimeter that replicate key functions of real organs.
The goal is to address the issue that more than 90% of drugs that pass animal tests fail in human clinical trials. Mice do not get sick like humans, and their reactions often do not match human responses. Organoids solve this problem by allowing drugs to be tested directly on human tissue, specifically on the tissue of a particular patient. The project is funded by the UK Medical Research Council with £20 million.
The project aims to create a library of standardized, validated organoids available to universities and pharmaceutical companies. This will enable ineffective or toxic drugs to be rejected earlier, reducing the risk to patients and decreasing the number of animals used in research. In 2025, 2.54 million animal procedures were conducted in the UK, and the government intends to accelerate the reduction of this number with new technologies. Meanwhile, Innovate UK is allocating an additional £2 million to projects that aim to reduce the use of dogs, monkeys, and other animals in safety tests, as reported in Nature Aging, July 2026.
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The UK is launching a large-scale shift from animal testing to models created from real human cells, including mini-organs, organoids, and "organ-on-a-chip" systems. This is being done as a national program with significant funding and a clear goal: to make drug development faster, more accurate, and safer. Scientists will grow organoids from NHS patient cells - tiny structures smaller than a millimeter that replicate key functions of real organs.
The goal is to address the issue that more than 90% of drugs that pass animal tests fail in human clinical trials. Mice do not get sick like humans, and their reactions often do not match human responses. Organoids solve this problem by allowing drugs to be tested directly on human tissue, specifically on the tissue of a particular patient. The project is funded by the UK Medical Research Council with £20 million.
The project aims to create a library of standardized, validated organoids available to universities and pharmaceutical companies. This will enable ineffective or toxic drugs to be rejected earlier, reducing the risk to patients and decreasing the number of animals used in research. In 2025, 2.54 million animal procedures were conducted in the UK, and the government intends to accelerate the reduction of this number with new technologies. Meanwhile, Innovate UK is allocating an additional £2 million to projects that aim to reduce the use of dogs, monkeys, and other animals in safety tests, as reported in Nature Aging, July 2026.
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GOV.UK
Patients to benefit from faster access to medicines as UK moves away from animal testing in science
New projects to move UK science away from animal testing
Language and Logic
Researchers compared the results of two individuals with severe aphasia to those of healthy participants in an fMRI study. The study, published in PNAS on July 6, found that language areas of the brain were not engaged when searching for rules and checking deductive conclusions. The team, led by neurobiologist Evelina Fedorenko from the Massachusetts Institute of Technology (MIT), investigated the long-standing debate about whether words serve as an internal means of formal reasoning.
The study involved 29 adults who underwent functional MRI scans, which indirectly track brain activity by monitoring changes in blood flow. The participants first identified their language network, which responded more strongly to sentences than to sets of nonsense words. Then, different subgroups of this sample searched for a rule that transformed one list of numbers into another, applied a given rule to new examples, checked syllogisms with "if-then" conditions, and chose a missing figure in geometric matrices.
The comparison between rule search and rule application separated the search process from instruction execution. In deductive tasks, the language network did not provide a significant response; when searching for a rule, its response was more than four times weaker than when reading sentences. The rule search involved a multiple-demand network, a distributed set of frontal and parietal areas active during complex goal-directed tasks. Complex deductive inferences involved a different set of frontal and parietal areas.
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Researchers compared the results of two individuals with severe aphasia to those of healthy participants in an fMRI study. The study, published in PNAS on July 6, found that language areas of the brain were not engaged when searching for rules and checking deductive conclusions. The team, led by neurobiologist Evelina Fedorenko from the Massachusetts Institute of Technology (MIT), investigated the long-standing debate about whether words serve as an internal means of formal reasoning.
The study involved 29 adults who underwent functional MRI scans, which indirectly track brain activity by monitoring changes in blood flow. The participants first identified their language network, which responded more strongly to sentences than to sets of nonsense words. Then, different subgroups of this sample searched for a rule that transformed one list of numbers into another, applied a given rule to new examples, checked syllogisms with "if-then" conditions, and chose a missing figure in geometric matrices.
The comparison between rule search and rule application separated the search process from instruction execution. In deductive tasks, the language network did not provide a significant response; when searching for a rule, its response was more than four times weaker than when reading sentences. The rule search involved a multiple-demand network, a distributed set of frontal and parietal areas active during complex goal-directed tasks. Complex deductive inferences involved a different set of frontal and parietal areas.
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bioRxiv
Evidence from Formal Logical Reasoning Reveals that the Language of Thought is not Natural Language
Humans are endowed with a powerful capacity for both inductive and deductive logical thought: we easily form generalizations based on a few examples and draw conclusions from known premises. Humans also arguably have the most sophisticated communication system…
Tissue Age Models
Researchers trained separate models to evaluate age based on 40 types of tissue samples from 983 deceased donors. The study, published in Nature Medicine on August 14, used 25,713 images of stained tissue sections to compare model predictions with pathology and telomere length, as well as gene expression data from blood samples.
The team trained a model for each tissue type to predict the donor's chronological age based on the tissue section's structure. The average absolute error was 4.88 years. The authors then calculated the tissue age gap, which is the difference between the model's prediction and the donor's chronological age. If a 55-year-old person's tissue section resembles those of older individuals, the age gap increases.
The study found that large age gaps in the GTEx project coincided with shorter telomeres and pathological signs on the same tissue sections. The authors also compared 19 histological clocks with 28 DNA methylation clocks, which are chemical marks on DNA that change with age. The age gaps showed a low correlation coefficient of 0.09 in the GTEx project, indicating that methylation and tissue structure reflect partially different properties of tissue state.
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Researchers trained separate models to evaluate age based on 40 types of tissue samples from 983 deceased donors. The study, published in Nature Medicine on August 14, used 25,713 images of stained tissue sections to compare model predictions with pathology and telomere length, as well as gene expression data from blood samples.
The team trained a model for each tissue type to predict the donor's chronological age based on the tissue section's structure. The average absolute error was 4.88 years. The authors then calculated the tissue age gap, which is the difference between the model's prediction and the donor's chronological age. If a 55-year-old person's tissue section resembles those of older individuals, the age gap increases.
The study found that large age gaps in the GTEx project coincided with shorter telomeres and pathological signs on the same tissue sections. The authors also compared 19 histological clocks with 28 DNA methylation clocks, which are chemical marks on DNA that change with age. The age gaps showed a low correlation coefficient of 0.09 in the GTEx project, indicating that methylation and tissue structure reflect partially different properties of tissue state.
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Nature
Histological aging signatures for monitoring tissue-specific aging and disease
Nature Medicine - Whole-slide histopathological images from 40 tissue types reveal morphological changes associated with aging, which, when paired with transcriptomic data from blood, are used to...