Israel is investing 70 million shekels in a common language for biological data, so AI models can learn from hospital and laboratory data. The Israel Innovation Authority is gathering a consortium, IBFI, with NVIDIA, Teva, the Shiba Medical Center, biotech companies, and universities. It aims to negotiate how to represent different biological data and provide participants with an environment to create and test models. On July 12, the Israel Innovation Authority announced IBFI. Cells, proteins, tissue images, and medical histories have one inconvenient feature: they describe one organism but are stored as separate worlds. A laboratory measures gene activity, a hospital keeps clinical records, and a pharmaceutical company sees the response to a drug. A model can find a connection between these pieces only when they are matched. IBFI is trying to build a common infrastructure for this purpose. Its first element, Bio Tokens, is intended to establish a unified way to record molecular, cellular, time-varying, and clinical data. The second, Factory Model, is designed as an environment where participants can assemble models, connect them to each other, launch, and test the results. The announced consortium brings together participants who usually work separately: the technology company NVIDIA, the pharmaceutical company Teva, a hospital, biotech startups, and research groups. The state and partners are allocating approximately 70 million shekels for this work. The initial tasks are related to tumor response to treatment, the immune system, sepsis, transplant rejection, autoimmune diseases, and drug discovery. A model does not gain an understanding of biology along with a large number of parameters. It sees data in the form in which they were able to collect and connect them. Therefore, the future value of IBFI depends on much more down-to-earth things: whether participants can agree on compatible formats, safely open the necessary data, and test that the model works on patients and in laboratories it has not seen before. Aging research is particularly dependent on such a connection: it is necessary to match the state of cells and tissues with how a person maintains muscle strength, memory, immunity, and resistance to diseases over the years. IBFI does not yet have a separate program for aging. The consortium is creating a common research machine; its quality will be shown by the available data, models, and tests that appear after its launch. Source: Israel Innovation Authority

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The enzyme SIRT3 in the blood stem cells of old mice weakened inflammation and improved muscle, lung, and memory tests. The bone marrow continuously produces immune cells. The authors of the study showed that with age, this source can fix an inflammatory program in its descendants, and SIRT3 can weaken it at the level of hematopoietic stem cells. On July 16, a study by a group from the University of California, Berkeley, Buck Institute, and other centers was published in Nature Aging. The scientists studied hematopoietic stem cells - rare cells in the bone marrow from which blood and immune cells are derived throughout life. With age, these stem cells increasingly produce myeloid cells: macrophages, monocytes, and other cells of innate immunity. They are able to quickly respond to infection, but during aging, they can retain an inflammatory program and maintain an excess of alarm signals in the blood. A study on EP2 in tissue macrophages showed another part of this story: an inflammatory receptor hindered their ability to remove aging neutrophils. The SIRT3 study looks higher up the chain - at the stem cells that create myeloid descendants. This long-term setting is called trained immunity. After infection, it helps the body respond faster. The authors checked another situation: repeated damage in an old organism can turn it into a chronic mode, when the descendants of stem cells carry inflammation through tissues for years. At the center of the work was SIRT3 - a mitochondrial enzyme that helps the cell cope with oxidative stress. Its level in hematopoietic stem cells decreases with age. Researchers genetically enhanced SIRT3 in mice and saw less inflammatory TNF and IL-6 in the blood, fewer inflammatory macrophages in tissues, and higher results on strength and endurance tests. Then, the team transplanted bone marrow from young mice with enhanced SIRT3 to ordinary young mice and waited for them to age. After two years, the recipients had better muscle function, preserved activity, reduced lung alveolar size, and changed spatial memory indicators. There were fewer markers of cellular aging in tissues. Transplants and transfers of individual immune cells helped find a mediator. Descendants of stem cells with enhanced SIRT3 gave more calm myeloid cells; their transfer to young mice improved physical tests. T-cells did not show such a difference. The chain in this model looks like this: aging blood stem cell → inflammatory myeloid descendants → inflammation and decline in functions in other organs. The experiments were conducted on mice with genetic enhancement of SIRT3. The next check is to reproduce this chain in human cells and find a way to change it without bone marrow transplantation.

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In mouse experiments, SOLID nanoparticles removed interleukin-6 from the blood and broke it down in the liver. In an article published on July 9, the authors described a particle that captures an inflammatory signal in plasma and enters the liver with it. In a sepsis model, after one injection, four out of six mice that received SOLID survived after seven days; in the group with a single antibody to interleukin-6, all six mice died. Interleukin-6 is a signal protein that immune cells use to exchange messages. During sepsis, its level can increase and exacerbate inflammation. An antibody to interleukin-6 binds to this protein and blocks its interaction with the receptor. The authors removed the protein from the blood and destroyed it along with the carrier. LYTAC systems already deliver extracellular proteins to lysosomes - cellular compartments with enzymes. One part of LYTAC binds to the target, the other - to the cellular receptor; the receptor takes the complex inside the cell. In SOLID, the antibody on the surface selects the target. Particles with a polymeric core, resistant to deformation, in cellular experiments almost completely entered the lysosomes of different cell types. In the blood, the particle was covered with a protein corona - a layer of plasma proteins on the surface. The composition of this layer directed the particles predominantly to the liver, where lysosomes broke down both the carrier and the bound molecule. The antibody selects the molecule, and the properties of the particle and blood proteins direct it to destruction in the liver. In four independent samples with sepsis, the level of interleukin-6 in serum after SOLID was 70% lower than after therapy with an antibody to interleukin-6. Seven days after the introduction of the particles, four out of six mice survived, while in the group with the antibody, all six died. In a separate model of acute lung injury, the particles captured CpG-DNA fragments - short sequences similar to bacterial DNA and triggering an innate immune response. In four independent samples, the infiltration of immune cells into the lungs was 1.7 times lower than after CpG neutralization. The authors tested this method on two acute mouse models after a single intravenous injection. In these conditions, the particles bound to the selected inflammatory mediator in the blood, entered the liver lysosomes, and delivered it to enzymes for breakdown.

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Brian Johnson: posthumous fame remains in the memory of others, while the future belongs to the living. On July 19, Brian Johnson quoted a post by James Lucas about the choice of Achilles. Johnson called "immortality of name" a justification for early death: the deceased is deprived of future experiences and the opportunity to see new manifestations of intelligence. The choice Lucas wrote about is divided between two poems by Homer. In "The Iliad", Achilles sees two fates before him. A march to Troy will bring him enduring fame, but deprive him of returning home. Returning will preserve a long life, but he will lose fame. In "The Odyssey", Odysseus reminds the already deceased Achilles that during his lifetime, the Achaeans revered him as a god, and after death, he reigns over the dead. Achilles responds: "Do not comfort me with death, Odysseus. I would rather live on earth and serve a poor man than reign over all the dead." Immediately after these words, Achilles asks Odysseus to tell him about his son Neoptolemus and his father Peleus. He wants to return to his father for at least an hour with his former strength and protect him from those who take away the old man's honors. Achilles prefers to live on earth and be with his loved ones. On July 19, Johnson quoted Lucas and wrote: "There is no reward higher than being alive. People justified early death with 'immortality of name' because they saw no other way out." Johnson calls the price of a short, bright life: a person loses the future, in which they could see new manifestations of intelligence. The memory of the deceased supports loved ones, preserves knowledge, and changes the actions of others. These consequences remain with the living. The name is preserved in the memory of other people; the future remains with the person who continues to live themselves.

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Temporary suppression of the NuA4 gene regulator in early development prolonged the life of worms. In a July 16 article, researchers temporarily reduced the activity of the NuA4 complex in the nematode C. elegans. In adulthood, the animals lived longer, paralyzed less frequently in amyloid and α-synuclein models, and accumulated fewer toxic protein aggregates. The study's outcome depended on the age of intervention. In a chemically controlled removal of MYS-1, a NuA4 component, the protein was removed in embryos and first-stage larvae; by the second larval stage, its amount was largely restored. Such brief suppression protected adult worms from amyloid toxicity. When MYS-1 was suppressed later, paralysis intensified, and lifespan shortened. The age of intervention determined its outcome. NuA4 modifies histones, the proteins around which DNA is packaged, and thereby influences gene function. In embryos, after temporary NuA4 suppression, the activity of a portion of endoplasmic reticulum genes decreased, a membranous network where proteins acquire their working form. The authors suggest that this triggered reticulum stress. In the next stage, XBP-1, a protein that activates genes for reticulum expansion and handling of misfolded proteins, was activated. Through regulatory proteins SBP-1 and MDT-15, XBP-1 increased the activity of FAT-7, an enzyme involved in oleic acid synthesis. Oleic acid accumulated during development, entered membranes and fat droplets, and in adulthood was released from these reserves. Blocking XBP-1 or FAT-7 eliminated protection from protein aggregates; suppressing lipases that release fats noticeably weakened it. Adding oleic acid reproduced part of the protection, but only if the worms received it from the first larval stage. Starting the addition at the L4 stage did not change the outcome. Early NuA4 suppression also slowed worm development and reduced fertility. The human analog of MYS-1, the TIP60 protein, is involved in development, DNA repair, and cell division. The safe age, strength, and duration of exposure to TIP60 in humans require separate experiments.

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A neurointerface has restored movement and sensation in the arm of a person with complete tetraplegia, with some of the effect persisting even after the system is turned off. A study published on July 16 in Nature Medicine describes a person with a complete spinal cord injury in the cervical spine. Implants linked the person's intention to move their arm with stimulation of the muscles and spinal cord, and the signal from the hand with the sensory cortex. After a course of training, the person was able to eat and pick up fragile objects independently again. Spinal cord injury severs two lines of communication: the motor cortex sends a command to the arm, and the skin and joints return the sensation of touch, force, and finger position to the brain. Without this feedback, it is difficult to hold a glass: the hand must not only grasp but also release its grip in time. Previously, neurointerfaces addressed these tasks separately. An implant could read an attempt to move and activate electrical stimulation of paralyzed muscles. Another implant could evoke a sensation of touch in the sensory cortex. A study published the day before showed that such sensations can persist for years. The group of Santos Chandrasekaran and Chad Bouton combined movement and sensation in a dual neural bypass. Electrodes in the motor cortex read the participant's intention to open or close their hand. A program translated the signal into muscle and spinal cord stimulation, and sensors on the hand transmitted touch to the area of the cortex where the brain stores the body map. The system helped the hand move in real time, but the authors aimed to achieve more: to re-link the attempt to move, the response from the skin, and the residual pathways of the nervous system. To do this, they used a "cortical mirror": they simultaneously presented the participant with a cue to imagine touch, stimulated the skin, and activated selected electrodes in the spinal and brainstem. After repeated training sessions, the participant's elbow flexion and sensation of touch on the wrist improved. These changes persisted even when the stimulators were turned off. A neuroprosthesis can temporarily replace a damaged pathway: the brain gives a command, and electronics deliver it to the muscles. This work tests whether such an artificial bridge can preserve some movement and sensation when the device is turned off. One case does not answer whether the effect can be reproduced in other people with injuries and how long it will last. But the testable question for neurotechnology has become more precise: after the device is turned off, the person can still bring their arm to their face, hold an object, and feel their hand.

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Bristol Myers Squibb will combine two AI clusters so that data from different studies can help choose the next experiment. On July 20, BMS announced the deployment of a second NVIDIA cluster. The company plans to connect it to the first one, so that research teams at different sites can work with common data and computing resources. A cluster is a group of connected servers on which artificial intelligence models are trained and perform calculations. BMS has been using such a system for about three years. It was difficult for scientists to access it: after the company's acquisitions at different sites, local rules remained, and special skills were required to work with it. In an NVIDIA publication on July 20, BMS described the next step: the company wants to create a single computing environment for all its research sites. The search for a drug begins with the selection of a biological target - a protein or another element of the organism that the drug should act on. Then, scientists select molecules, test them in the laboratory, and decide which experiment to conduct next. BMS reports that it is already applying the Predict First approach: a model prediction helps plan a laboratory experiment before scientists start it. When BMS combines the systems, the data from the research program in Lawrenceville, New Jersey, will be able to become the input for models used by the team in San Diego. The company also plans to give scientists the opportunity to run complex predictions in plain language. The result of one study should become the material for the next hypothesis in another. The second cluster is still being deployed, and the integration of the two systems remains a BMS plan. The company has not published comparisons that can be used to judge how the common environment affects the choice of experiments, program timelines, or the number of candidates that reach clinical trials.

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Levent Alpöge published a counterexample to the Jacobian conjecture in three dimensions and thanked Fable for work on the problem. On July 20, mathematician Levent Alpöge published a formula for a map of three complex variables. He thanked Akhila Mathew for the question and Fable for the work. The Jacobian determinant of this map is always -2, but three different source points yield the same result. The Jacobian conjecture, formulated by Keller in 1939, concerned polynomial maps: sets of formulas that assign another triple to each triple of complex numbers. For such a map, a table can be compiled showing how each result changes with a small change in each input; the number calculated from this table is called the Jacobian. The conjecture claimed: if the Jacobian is constantly non-zero, the map should have an inverse polynomial formula. The value of -2 means that near each source point, a nearby result can be uniquely restored to a nearby source point. One inverse formula for the entire space requires more: each result point should correspond to exactly one source point. In Alpöge's post, he cited three different source points: (0, 0, -1/4), (1, -3/2, 13/2), and (-1, 3/2, 13/2). The map sends each of them to (-1/4, 0, 0). One result has three different preimages, so the map does not have a common inverse formula. The mathematical note reduces the search for preimages of an arbitrary result point to a cubic equation, i.e., an equation of the third degree. For (-1/4, 0, 0), it factorizes to -s(s-2)(s+2)/2. Its roots 0, 2, and -2 exactly correspond to the three published points. This map has sequences of source points that go to infinity, although their results converge to a finite point. The constant Jacobian controls the map near each point, but not throughout the space. In the original post, Alpöge described the contribution of the participants as follows: "The Jacobian conjecture is false. Thanks to my close friend Akhila for the question and my other close friend Fable for the work during the World Cup final." The published materials allow independent verification of the formula and its properties. The publications do not reveal who made each step in the search. A week before that, physicist Yuji Tachikawa reported that Claude Fable had found a computational error in a stuck problem in string theory and developed its course. In the current case, the publication provides a formula, a constant Jacobian, and three points that can be verified separately. If new coordinates are added to this map and left unchanged, the counterexample works in any number of variables starting from three. The two-dimensional case of the Jacobian conjecture remains open.

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Deep Origin has retrospectively ranked TCIP3 as the top molecule among 17 molecular glues - compounds that bring two proteins together. TCIP3 connects BCL6 with p300/CBP - enzymes that help the cell turn on genes. In lymphoma cells, this binding triggers programs that stop growth and kill the cell. Deep Origin checked if its calculation matched the molecule that the laboratory had already identified as a leader. On July 20, an article by researchers from Stanford, MD Anderson, and Deep Origin about TCIP3 was published in Cell. In some cases of diffuse large B-cell lymphoma, BCL6 keeps genes turned off that slow down cell division and trigger cell death. TCIP3 binds to BCL6 with one part and to p300/CBP with another, bringing these enzymes to the DNA regions controlled by BCL6. TCIP3 brings p300/CBP to the genes that BCL6 keeps turned off. The enzymes acetylate BCL6 and the proteins that DNA is wound around in these regions. After this, BCL6 is less able to keep genes turned off, and the cell turns on programs that stop growth and apoptosis - controlled cell death. An open preprint by the authors in 2025 showed this mechanism in cell lines. In a 72-hour test on lymphoma cells, TCIP3 suppressed their growth with an IC50 of around 0.8 nanomoles per liter: half of the maximum suppression was achieved at a concentration of less than one billionth of a mole. Control compounds with the same chemical linker that could not bind to either BCL6 or p300/CBP were more than a thousand times weaker in toxicity to these cells. Thus, the authors showed that the effect requires the triple assembly of BCL6-TCIP3-p300/CBP. In the July 20 announcement, Deep Origin described its calculation. The company built a triple complex for each of the 17 compounds, simulated the movement of these assemblies, and calculated the stress of the chemical linker between the two parts of the molecule. This linker affects whether the proteins can maintain the necessary mutual arrangement. In Deep Origin's ranking, TCIP3 was first in a retrospective calculation: its laboratory activity had already been measured before this analysis. In the international CASP competition, teams submit predictions of protein structures that experimenters have already measured but have not yet disclosed. A similar test for Deep Origin would look like this: the calculation ranks previously unmeasured compounds, the laboratory synthesizes several candidates from the top of the list, and then measures their activity. Only Deep Origin reports on the almost complete disappearance of tumors in mice with xenografts - transplanted human tumors. The open preprint from 2025 calls TCIP3 a tool molecule and says that the authors did not study its efficacy in a live mouse model of this lymphoma at that time; the full text of the Cell version from July 20 is not available. Even successful ranking of a new series will show a prediction for a chosen laboratory system, and the connection between cellular and animal models and the result in patients will require other data.

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Retro obtained a transplant from six adult donors' cells, which twice restored human hematopoiesis in mice and preserved a DNA methylation age of around five years. On July 17, the Retro team posted an unrevised preprint on donor cells aged 18–60 years. After the second transplant, 18 of 23 immunodeficient mice had more than 1% human cells in their bone marrow; Horvath clocks estimated the age of isolated human hematopoietic cells with the CD45 marker at 5.28 ± 1.45 years. Blood stem cells constantly replenish erythrocytes, platelets, and immune cells. After transplantation, they should settle in the bone marrow and produce all these lines for a long time. With age, this becomes more difficult. Reprogramming an adult cell into an induced pluripotent stem cell, or iPSC, resets many DNA methylation age marks and lengthens telomeres. For transplantation, such a cell needs to be converted into a blood stem cell and tested in a living organism. Resetting age marks does not eliminate all damage: in serially cloned mice, by the 58th generation, cloning success sharply decreased due to accumulated genomic errors. In 2024, the Elizabeth Ng group obtained iPSC-derived cells that engrafted in the bone marrow of mice for a long time and produced several blood lines. In April, Retro described the path from iPSC to hematopoietic stem cell transplantation. The new preprint checks two things: whether such cells can re-engraft in the bone marrow and maintain a young DNA methylation age pattern. The team obtained iPSC-derived hematopoietic stem cells, iHSC, in 15 days and introduced them into immunodeficient NBSGW mice. In such animals, human transplants can engraft in the bone marrow. After 20 weeks, the bone marrow of recipient mice from three donor lines was transplanted into other mice. In the second cycle, 18 of 23 animals had more than 1% human cells in their bone marrow; these cells again formed erythrocytes and several types of immune cells. In the first transplant, each mouse received five million iHSC, while control animals received from 50,000 cord blood cells to one million adult hematopoietic stem cells. This design shows that cultured cells can restore blood at this dose but does not compare the potency of one iHSC to a conventional transplant. During 15 days of iHSC differentiation, the pluripotency program was turned off and the hematopoietic program was turned on, but their methylation pattern still differed from that of adult blood stem cells. After living in the mouse bone marrow, it became closer to the adult profile. Methylation was studied in a mixture of isolated human cells with the CD45 marker. Therefore, the adult profile may indicate both cell maturation in the bone marrow and the growth of a subset of cells that initially engrafted better. The methylation pattern answered two different questions: did the cells become similar to adult blood stem cells and did they preserve a young age according to DNA methylation marks? Horvath clocks translate the methylation pattern into an age estimate. After the second transplant, they gave 5.28 ± 1.45 years. In this mouse model, cells from adult donors acquired signs of adult hematopoietic transplants and preserved a young age according to DNA methylation marks.

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The White House is proposing to test the rules for awarding scientific grants with an experiment. On July 21, the White House Office of Science and Technology Policy released a report, Science: A New Golden Age, and a memorandum on research and development budget priorities for fiscal year 2028. Agency heads with research and development budget authority of at least $3 billion in fiscal year 2026 must submit an action plan to the Office of Science and Technology Policy and the White House Office of Management and Budget within 90 days. The agencies should consider these priorities in their fiscal year 2028 budget requests. The US federal government spends around $200 billion on research and development each year. The report proposes to test the rules by which the state selects recipients of scientific funding. To do this, the memorandum suggests that agencies develop metascience - research on how agencies select applications, review them, award grants, and obtain results. It proposes linking data on applications, reviewer evaluations, grant decisions, and subsequent outcomes in one system. This would allow for testing a different selection method on parts of the federal research portfolio and comparing it to the usual method based on subsequent outcomes. The proposals include portable fellowships that remain with the researcher when moving to another organization, and rapid grants for preliminary and exploratory work. A rapid grant requires only a few pages of application, and a decision should be made in less than a month. A "golden ticket" would allow a technical reviewer of an agency to recommend an unusual application that an expert panel did not support. New mechanisms, including the "golden ticket", the memorandum proposes to study, pilot, and evaluate. AI for science can quickly propose a molecular target, material, or explanation of a biological process. A laboratory then conducts an experiment and checks the prediction. The journal Science has already warned that AI can produce more science than people can check. The report proposes combining models with open data, robotized laboratories, and reproducibility packages - sets of data, code, and analysis conditions with which another laboratory or program can reproduce the result. The Genesis Mission is a federal AI for science program that combines data, computing, and research equipment. In March, Argonne presented more than a dozen Genesis projects, including AI for enzyme research and a network of autonomous laboratories. On July 22, the White House announced more than $5 billion in federal commitments and 278 selected projects in the Genesis Mission. Among the tasks of Genesis is to "help Americans live longer and healthier". To do this, the Department of Health, the Department of Energy, and the Department of War of the USA plan to combine data on molecules, genes, organism signs, treatment, and real clinical practice to search for new applications of existing drugs and to bring new therapies to patients faster.

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In four patients with complete cervical spinal cord injuries, no tumors were found after transplantation of neural cell precursors over 2-4 years. The results of the first trial of such transplantation in humans were published in Nature Medicine. Four men were administered two million cells each, 14-28 days after injury; the goal of the first phase is to test the safety of the procedure. In complete cervical spinal cord injuries, signals from the brain do not pass to the body below the injury. In double neural bypass, implants read the desire to move an arm and, with electrical stimulation of muscles and spinal cord, bypass this gap. Here, surgeons introduced cells directly into the damaged spinal cord segment. The transplant consisted of neural precursors - cells from which neurons and cells covering nerve fibers with a protective sheath - myelin, can develop. They were grown from iPSC - reprogrammed donor umbilical cord blood cells, which can again transform into different tissues. One cell line allows for the pre-manufacture of identical batches for several patients. Before transplantation, the laboratory checked the cells for genetic changes and pushed them to a more mature state to reduce the risk of excessive growth. Then, patients took tacrolimus for nine months - a drug that suppresses the immune system and prevents the body from rejecting the donor cells. Over the first year, doctors recorded 84 undesirable events: two moderate surgical complications and 22 mild or moderate reactions related to tacrolimus. MRI and positron emission tomography (PET), which shows tissue metabolism, did not reveal signs of tumor growth at the transplantation site. Over 2-4 years of observation, none of the four patients experienced severe reactions related to the cell product, and neurological functions did not worsen. In all participants, scores on movement and self-care scales increased over the year. Two patients developed voluntary movements below the injury. These improvements cannot be attributed to the transplantation without comparison with similar patients who did not receive cells. In the first months after injury, some functions return on their own. The next study should distinguish between natural recovery and the effect of cells. The current work answered a different question: can a uniform cell product be prepared, introduced into the damaged spinal cord, and patients be observed for several years without signs of tumor growth.

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On July 17, Irina Conboy's group published a study on DMA, a combination of dichloroacetate, metformin, and navitoclax. The treatment began at approximately 18 months of age. In the nine mice receiving DMA, the median lifespan was 1002 days, while in the nine control mice, it was 815 days. After damage or other stress, some cells stop dividing, remain in tissue, and release inflammatory signals; these cells are called senescent. Navitoclax blocks BCL-XL, a protein that helps both senescent cells and platelets survive. Platelets help stop bleeding by forming a clot, and the same protein is necessary for the survival of both senescent cells and platelets. 18 hours after administering 50 mg of navitoclax per kilogram of body weight, the number of platelets was approximately one-quarter of the control. The authors reduced the navitoclax dose to 5 mg per kilogram and added metformin and dichloroacetate. Metformin inhibits complex I in mitochondria, one of the links in energy production. Dichloroacetate helps direct pyruvate, a product of glucose breakdown, into mitochondria. The authors tested the hypothesis that senescent and cancer cells are worse at switching between ways of obtaining energy, so the two drugs would create a burden for them and increase their sensitivity to a low dose of navitoclax. In cultures, DMA almost reduced ATP, the molecule that transports energy within cells, to background levels in senescent cells of connective tissue and MCF-7, a line of breast cancer cells. Healthy connective tissue cells maintained their ATP level. Exogenously added ATP partially restored the viability of senescent cells. Partial restoration of viability supports the connection between the decline in ATP and cell death. In human neural precursor cells, viability did not decrease. In human muscle cells, it decreased by approximately 20%, and in liver cells, by 5%. From these cultures, it is impossible to understand which cells DMA affects in mouse organs. The median lifespan in the DMA group was 187 days longer, and the average total lifespan was 12% longer. A separate analysis of males and females did not allow confidently distinguishing the effect of DMA from random fluctuations: there were three to six animals in each subgroup. In the survival experiment, the authors tested the effect of the entire DMA mixture. Control mice received a solution without drugs; there were no separate groups for each component in the experiment. The mice were observed until natural death, unlike the Immorta Bio study, where survival was measured after a toxic regimen of doxorubicin in young mice. In this group, the authors did not measure the number of senescent cells in organs. One protein marker does not provide such a map: the SenNet atlas showed that the set of senescence markers changes with cell type and cause of aging. The survival data relates to the DMA mixture as a whole. After DMA, the number of platelets was approximately 70% of the control; the authors were unable to distinguish the difference from random fluctuations. This short test only measured the number of platelets. In several animal models of pulmonary hypertension, elevated pressure in the lung vessels, ABT-263 was accompanied by the loss of cells lining the vessels and bearing signs of senescence, as well as worsening of lung vessel function. In the DMA study, the authors did not measure which cells the mixture affects in mouse organs and how this affects their function.

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Alcor announced that it began training local European deployment teams for cryopreservation on July 21. Alcor reported that preparation has been declared for brain and whole-body cryopreservation. The organization does not disclose the countries, the number of trainees, the date of the first independent deployments, and the measured response time. After the cessation of blood circulation, the brain stops receiving blood, oxygen, and glucose; neuronal damage increases within minutes. DART is Alcor's deployment team: when a member's life is expected to end, it can be on standby at the bedside, and in the event of sudden death, it must arrive at the patient as soon as possible. After confirming legal death, the team performs primary stabilization and organizes transportation to a storage facility. In its July bulletin, Alcor reported that its DART team is already deploying to organization members worldwide and that it has begun training local teams in Europe. For sudden cases, a team from the US has to cross the Atlantic. Alcor expects that locally trained specialists will reduce this delay. In April, Alcor gathered more than thirty specialists from the US, Canada, and Europe in Arizona for four days of training, practice, and drills. According to Alcor's internal rules, an active DART member undergoes annual recertification: confirms a minimum number of actual deployments and passes an exam. European teams, according to Alcor's statement, will be trained to the same standards and goals. In its May bulletin, Alcor reported on James Arrowood's trip to Europe and meetings with potential partners. In July, the organization announced that it was already training local teams. On the Alcor Europe page, the legal structure, headquarters, and long-term storage are described as future projects after securing funding. Training local DART teams relates to the earliest part of the procedure - the time from legal death to primary stabilization.

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A team led by David Liu, with the help of AI, strengthened proteases so that laboratory evolution could find new functions. On July 22, a study by David Liu's team was published in Nature. ProteinMPNN redesigned three proteases, and automated laboratory evolution taught them to cut new protein targets. The best variant against ataxin-2 turned out to be more than 79 times more selective than the variant grown from a natural enzyme. To teach a ferment to cut a new target, mutations must change protein recognition and preserve its three-dimensional shape. Often, a new useful mutation makes the protein less stable: it folds worse, and selection weeds it out along with the new function. Liu's team decided to strengthen the protease before selection. ProteinMPNN received three-dimensional structures of proteases of botulinum neurotoxin and modified areas away from the catalytic center. One of the proteases had 74 variants, 58 of which preserved activity, and 22 gave more soluble protein. AI created a reserve of stability, and the experiment checked which new functions this reserve allowed to survive. Then the authors launched PACE - a system of continuous evolution with bacteriophages. The phage multiplied only when the protease cut a given peptide; in a day, the system went through dozens of generations of mutations and selection. On the most difficult of the three new targets, a working ferment appeared in all four lines started from the redesigned variant D3, and in two out of four lines from the natural protease. When the authors transferred the found mutations between proteins, mutations from D3 often lost function in the natural protease. Mutations from the natural start, on the other hand, worked in D3. The same amino acid substitution behaves differently in a different protein background. This is consistent with the fact that D3 carries part of the useful but destabilizing mutations. In the final campaign, the protease was tuned to ataxin-2 - a protein associated with the risk of lateral amyotrophic sclerosis - and selection was carried out for cleavage of SNAP25, its natural target. The best variant from D3 had a ratio of ataxin-2 cleavage to SNAP25 cleavage more than 79 times higher than the best variant from the natural start. In a culture of human HEK293T cells, it gave more target product and fewer side fragments. In a May study by the same laboratory, ProteinMPNN stabilized an already evolved DNA editor PE8. In the new article, the model acts earlier: it prepares the starting ferment from which selection then obtains variants with a new function. The authors tested three related proteases, bacterial selection, and HEK293T cells. For treatment, delivery of the ferment to motoneurons, testing of the immune response, safety, and effect in animals will be required.

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Repligen is acquiring BioLife for $1.5 billion and adding cell therapy storage to its business. On July 22, Repligen and BioLife Solutions announced an agreement where BioLife shareholders will receive 64% of the deal's value in Repligen stock and 36% in cash. The companies are expecting the deal to close in the fourth quarter of 2026, following a BioLife shareholder vote and regulatory approvals. Cell therapy comes to the patient as a living material, and cells need to be processed, stored, transported, and prepared for administration in a way that ensures their survival. BioLife sells media for freezing and storing cells, as well as tools for their processing. Its CryoStor is a solution in which cell products are frozen and stored. According to the companies' statement, the CryoStor line is used in 18 approved cell therapies and in most sponsored cell product trials in the US. Repligen is acquiring a supplier of consumables for the stage at which cell products are frozen, stored, and transported. Among commercial therapies using BioLife products, BioSpace names Carvykti, Yescarta, and Breyanzi. Repligen already sells biopharmaceutical companies filters, liquid systems, chromatography equipment, and analytical instruments. After the deal closes, BioLife will add cell preservation means to this lineup; the company expects new types of therapies, including cell therapies, to account for around a quarter of its revenue. The $1.5 billion is an estimate of BioLife's entire business, not just the CryoStor medium. Repligen also forecasts $20 million in savings in the first year after the deal and $30 million in the second. These amounts are contingent on the deal closing and the companies' integration.

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MIT has directed the growth of vascular branches through magnetic stretching in a model of a human vessel. In a collagen gel, researchers changed the force and direction of stretching on the vessel wall. With weak stretching, more branches formed, while strong stretching caused individual branches to grow longer. Engineered tissue requires a network of thin vessels for cells to receive oxygen and nutrients. Large channels can be printed, but capillaries must sprout from cells and connect into a functioning network. Their shape is currently difficult to control with the same precision. On July 14, MIT released a breakdown of the research, published in PNAS on July 6. In the collagen gel, the team created a hollow channel and lined it with human endothelial cells - the cells that form the inner lining of blood vessels. Near the channel, they placed a small magnet; an external drive moved it and stretched the gel on the vessel wall for one hour a day for three days. The force of stretching changed the number and length of branches, and the direction of stretching changed their route. With stretching at 5% of the gel's width, more branches formed. At 15%, there were fewer, but individual branches were longer. When the researchers changed the direction of the magnet's movement along three axes, the branches turned to follow the stretching; some became L-shaped. Within some branches, a channel connected to the original vessel was preserved, which the authors verified using a fluorescent dye. This control currently only works on the early growth of branches in a model of a single vessel. The authors have not yet assembled a complete vascular network. The next test is to obtain a dense network from these branches that can supply complex tissue for a long time and connect to the bloodstream after transplantation. The researchers also tested the cells' response to stretching. When they suppressed PIEZO1 - a gene that encodes a stretch-sensitive ion channel - fewer branches formed. However, stretching still maintained the barrier function of the vessel wall, as other mechanisms also participate in the cells' response to force.

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US federal agencies searched for active scientific grants by keywords before terminating funding. Agreements with federal agencies, attached to a court petition, describe the general procedure: first, grants were found by words and themes, then some of them were selected for termination of funding. In individual cases, artificial intelligence tools were used when compiling lists. On July 15, the plaintiffs in the case of Thakur v. Trump filed a petition in federal court and attached agreements with agencies. The National Science Foundation, the National Foundation for the Humanities, the Department of Defense and Transportation, and the US National Institutes of Health described in them how they selected grants for consideration for termination. "Search terms, keywords or phrases" highlighted grants for review. According to the text of the agreements, then projects that expressed or allegedly expressed positions not supported by the administration were selected from the list. The agencies applied general criteria and standard letters, rather than separately checking whether each grant recipient had met the conditions. The same agreements state that the recipients did not violate the terms of funding. At the National Institutes of Health and the Department of Health, the list of themes was expanded: from projects on diversity, equality, and inclusion to gender, vaccine skepticism, and COVID-19. The lists included "health equity", "structural racism", and "sexual orientation". The materials do not explain what data the AI tools processed and how their results influenced the decisions. The agencies only indicated that AI could participate in preparing the lists provided to it. The Associated Press reported on July 21 that the case concerns more than a thousand grants from the University of California. The plaintiffs estimate the previously awarded funding at approximately $2 billion. A hearing on the petition is scheduled for October 20, and the court has not yet decided whether this procedure is lawful. This differs from the White House plan to experimentally test the rules for issuing new grants, where it is proposed to compare the method of selecting applications with research results. The Thakur agreements describe the review of already issued grants by thematic words and the alleged position of the project. For long-term biomedicine research, continuity is important: a team is hired for a grant, participants are recruited, and experiments are conducted for years. The materials do not allow us to establish the consequences for each laboratory, but the described procedure creates a risk for such programs: the funding of an already started study may be revised without a separate assessment of whether the laboratory has met the conditions of the grant. This applies to aging research as one of the long-term biomedical areas; individual gerontology programs are not named in the documents.

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On July 22, Haowei Man's team published an article in Nature about ContactSeek. The method combines AlphaFold3 predictions for the protein-RNA-DNA complex with sequencing data and suggests amino acid substitutions for more selective DNA editors. A base editor changes one DNA letter without a double-strand break. A guide RNA leads it to the desired sequence, a CRISPR protein holds the complex on the DNA, and an attached enzyme performs the chemical substitution. Similar sequences sometimes also hold this complex, and then the editor changes letters outside the chosen target. Usually, engineers screen amino acid substitutions in the protein and measure the result. ContactSeek starts with the error traces of the original editor: the authors found genome-wide sites where it came together with the guide RNA and submitted the target and these site sequences to AlphaFold3. The model built complex variants from protein, RNA, and DNA. Here, AlphaFold3 builds a map of likely contacts within the complex. ContactSeek compares the differences between the target and off-target sites with the sequencing signal. This is how the program identifies amino acids whose contacts with RNA or DNA change along with the frequency of off-target edits and suggests substitutions for cellular experiments. The authors tested this route on the adenine editor Cas9 and the cytosine editor Cas12a in HEK293T cells. The ABE8e-DD variant had a total guide-dependent off-target editing signal 99.2% lower than the original ABE8e: on the ABEsite16 target, the comparison covered 270 off-target sites. For the cytosine editor variant on Cas12a, the signal decreased by 82.1-95.1% for four guide RNAs. The authors also measured target editing, off-target RNA changes, and editing without guide RNA. Base editors have already reached patients: in personalized therapy, the KJ Malton editor was delivered to the liver with lipid nanoparticles, and after a year, clinical improvement was noted in a child without serious side effects. ContactSeek has been tested only in HEK293T cells, so its variants still need to be tested for delivery to tissues and in long-term observations. ProteinMPNN helped obtain prime editor variants that accumulated better in cells. ContactSeek solves a different problem: it narrows down the list of places where the editor can trigger outside the target. The contact map turns a broad screening of amino acid substitutions into specific hypotheses for experimentation.

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User LessWrong bits suggested that people will start making plans for future anti-aging therapy before it appears. On July 20, bits published an essay on when radical life extension will enter people's personal plans. This refers to increasing healthy and overall life beyond what current medicine and habits provide. In the essay, bits asks when a person will decide that they will be able to take advantage of future therapy. Then the planning horizon changes: decisions about retirement, savings, children, and career depend on the new understanding of how much time is left. To explain this, bits uses the concept of Turkish-American economist Timur Kuran - preference falsification. A person may want to live significantly longer, but publicly repeat the usual norm as long as such a desire seems like a strange fantasy. When future therapy seems plausible, people start talking about it openly, and it becomes easier for the next person to do the same. This model is based on two assumptions: many people already want a long life, but hide this desire; a change in norms will allow them to speak out. In the essay, this is an explanatory hypothesis, not a measurement of public opinion: the author does not provide data on the scale of hidden demand or the speed of the cascade. In his scenario, the cascade can be triggered by signals that are easy to see and retell: a recognized scientific result of rejuvenation in humans, a notable discovery using AI, a new therapy in the public eye, or a regulator's permission to measure aging in clinical trials. Such signals make future therapy a subject of ordinary conversation. Then, bits suggests, demand for research, money, and political decisions change. In a comment to the essay, Dagon suggests a different sequence. "The strongest factor in expected lifespan - measured or at least claimed life extension or significant health extension in old age," he writes. A wide audience, in his opinion, will change expectations after a result; early supporters are able to believe earlier and be wrong about the timing. The dispute concerns the order of events. According to bits' model, public expectation is able to gather support for future research. According to Dagon's model, a visible result appears first, which people trust. If people start changing plans before such a result, bits' hypothesis will gain support. If expectations shift after results, Dagon will be proven right.

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