AI‑Designed Drug Rentocertib Shows Anti‑Aging Effects in IPF Trial
The drug rentocertib, created by the AI‑driven company Insilico, was originally designed to treat idiopathic pulmonary fibrosis (IPF), a progressive lung‑scarring condition that usually leads to death within a few years. In addition to improving lung volume, the compound was found to lower systemic markers of biological aging across the whole body.
The first AI system mined medical records, blood analyses and scientific publications to pinpoint the
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The drug rentocertib, created by the AI‑driven company Insilico, was originally designed to treat idiopathic pulmonary fibrosis (IPF), a progressive lung‑scarring condition that usually leads to death within a few years. In addition to improving lung volume, the compound was found to lower systemic markers of biological aging across the whole body.
The first AI system mined medical records, blood analyses and scientific publications to pinpoint the
🔗 Read original →
Nature
Integration of proteomic aging clocks in a phase 2a clinical trial supports simultaneous geroprotective assessment
Nature Biotechnology - Six proteomic clocks are applied in a clinical trial to assess anti-aging effects.
We need to translate Russian news post into natural English, format per rules.
First line: short headline under 90 chars, no markdown.
Then blank line, then body split into short paragraphs (2-3 sentences each), separated by blank lines.
Wrap few genuinely important facts — key numbers, percentages, drug/company/gene names, dates — in double asterisks. At most 4-5 per post, never a whole sentence.
Wrap study/journal citations and publication references in single underscores (e.g. Nature Aging, July 2026).
We need to preserve all facts, numbers, names, citations exactly. No added commentary.
We need to identify important facts: dates: 8 September, 13 March, 1 September, maybe also mention of Millennium prize? Not a number. Also maybe mention of "OpenAI", "Levent Alpoge", "Tristan Bakmaster", "Sebastien Bubeck". Those are names; not numbers. Key numbers: maybe "8 September", "13 March", "1 September". Also maybe "thousand" (prize of millennium? Actually "премия тысячелетия" is Millennium Prize, $1 million? Not given). So we can bold dates.
We need at most 4-5 double asterisks. We'll choose: 8 September, 13 March, 1 September, maybe also Navier–Stokes? That's not a number. Could also bold Euler equation? Not needed. We'll keep three dates.
We need to wrap study/journal citations in single underscores. There's no explicit journal citation, but there is mention of "политике данных , обновлённой 13 марта" which is a policy update date, not a citation. There's also "OpenAI заявила , что её исследователи и программы-агенты не видели работ математиков ... до публикации". No journal. There's "В объявлении о решении Навье—Стокса OpenAI рассказала, что 1 сентября поручила агентам искать ответы на открытые задачи". Not a citation. There's no explicit study/journal. So maybe we don't need any underscores. But we could still wrap "политике данных" as not a citation. The rule: wrap study/journal citations and publication references in single underscores. If none, we can skip.
We need to ensure we don't wrap whole sentences in double asterisks. Only key facts.
We need to split into short paragraphs 2-3 sentences each.
Let's craft translation.
First, headline: something like "OpenAI says its models may have been improved by anonymized data from two mathematicians". Under 90 chars.
Check length: "OpenAI says its models may have been improved by anonymized data from two mathematicians" count: let's count roughly: OpenAI(5)+space+ says(4)=9, space+its(3)=13, space+models(6)=20, space+may(3)=24, space+have(4)=29, space+been(5)=35, space+improved(9)=45, space+by(2)=48, space+anonymized(11)=60, space+data(4)=65, space+from(4)=70, space+two(3)=74, space+mathematicians(13)=88. Good under 90.
Now blank line.
Now body paragraphs.…
🔗 Read original →
First line: short headline under 90 chars, no markdown.
Then blank line, then body split into short paragraphs (2-3 sentences each), separated by blank lines.
Wrap few genuinely important facts — key numbers, percentages, drug/company/gene names, dates — in double asterisks. At most 4-5 per post, never a whole sentence.
Wrap study/journal citations and publication references in single underscores (e.g. Nature Aging, July 2026).
We need to preserve all facts, numbers, names, citations exactly. No added commentary.
We need to identify important facts: dates: 8 September, 13 March, 1 September, maybe also mention of Millennium prize? Not a number. Also maybe mention of "OpenAI", "Levent Alpoge", "Tristan Bakmaster", "Sebastien Bubeck". Those are names; not numbers. Key numbers: maybe "8 September", "13 March", "1 September". Also maybe "thousand" (prize of millennium? Actually "премия тысячелетия" is Millennium Prize, $1 million? Not given). So we can bold dates.
We need at most 4-5 double asterisks. We'll choose: 8 September, 13 March, 1 September, maybe also Navier–Stokes? That's not a number. Could also bold Euler equation? Not needed. We'll keep three dates.
We need to wrap study/journal citations in single underscores. There's no explicit journal citation, but there is mention of "политике данных , обновлённой 13 марта" which is a policy update date, not a citation. There's also "OpenAI заявила , что её исследователи и программы-агенты не видели работ математиков ... до публикации". No journal. There's "В объявлении о решении Навье—Стокса OpenAI рассказала, что 1 сентября поручила агентам искать ответы на открытые задачи". Not a citation. There's no explicit study/journal. So maybe we don't need any underscores. But we could still wrap "политике данных" as not a citation. The rule: wrap study/journal citations and publication references in single underscores. If none, we can skip.
We need to ensure we don't wrap whole sentences in double asterisks. Only key facts.
We need to split into short paragraphs 2-3 sentences each.
Let's craft translation.
First, headline: something like "OpenAI says its models may have been improved by anonymized data from two mathematicians". Under 90 chars.
Check length: "OpenAI says its models may have been improved by anonymized data from two mathematicians" count: let's count roughly: OpenAI(5)+space+ says(4)=9, space+its(3)=13, space+models(6)=20, space+may(3)=24, space+have(4)=29, space+been(5)=35, space+improved(9)=45, space+by(2)=48, space+anonymized(11)=60, space+data(4)=65, space+from(4)=70, space+two(3)=74, space+mathematicians(13)=88. Good under 90.
Now blank line.
Now body paragraphs.…
🔗 Read original →
X (formerly Twitter)
OpenAI (@OpenAI) on X
We congratulate Levent Alpöge and Tristan Buckmaster on their remarkable mathematical work.
We (the researchers and the agents) did not see any of their work through any means until they released…
We (the researchers and the agents) did not see any of their work through any means until they released…
Higher infant cash payments linked to slower biological aging at age four
On September 8, Nature Human Behaviour published results from the US Baby’s First Years trial. Families with newborns were randomly assigned to receive either $333 or $20 per month. After four years, 735 children provided saliva samples for analysis.
Researchers measured DNA methylation and calculated the DunedinPACE score, which estimates the pace of aging from epigenetic marks. In the high‑payment group, DunedinPACE was lower by 0.17 standard deviation compared to the low‑payment group. No other epigenetic measures differed between the groups.
The trial enrolled a thousand mothers living below the US poverty line in 2018–2019; 400 received $333 and 600 received $20. Randomization ensured the only systematic difference was the assigned payment amount. By isolating income, the study shows that the early‑life environment can alter a DNA‑based aging biomarker in four‑year‑olds.
🔗 Read original →
On September 8, Nature Human Behaviour published results from the US Baby’s First Years trial. Families with newborns were randomly assigned to receive either $333 or $20 per month. After four years, 735 children provided saliva samples for analysis.
Researchers measured DNA methylation and calculated the DunedinPACE score, which estimates the pace of aging from epigenetic marks. In the high‑payment group, DunedinPACE was lower by 0.17 standard deviation compared to the low‑payment group. No other epigenetic measures differed between the groups.
The trial enrolled a thousand mothers living below the US poverty line in 2018–2019; 400 received $333 and 600 received $20. Randomization ensured the only systematic difference was the assigned payment amount. By isolating income, the study shows that the early‑life environment can alter a DNA‑based aging biomarker in four‑year‑olds.
🔗 Read original →
Nature
Effects of a randomized controlled trial of unconditional cash transfers on epigenetic measures of ageing and cognition in children…
Nature Human Behaviour - Raffington et al. find that providing low-income mothers with cash gifts for the first four years of their children’s lives appears to change the children’s...
We need to translate Russian news post into natural English, format per rules.
First line: short headline under 90 chars, no markdown, no '#'.
Then blank line, then body split into short paragraphs (2-3 sentences each), separated by blank lines.
Wrap few genuinely important facts — key numbers, percentages, drug/company/gene names, dates — in double asterisks. At most 4-5 per post, never a whole sentence.
Wrap study/journal citations and publication references in single underscores (e.g. Nature Aging, July 2026).
We need to preserve facts, numbers, names, citations exactly. No added commentary.
We need to identify important facts: dates: 8 September (OpenAI published article), 166 pages, Lean formalization, 10,000 agents, 88 hours search, 17 hours verification, 1934 Jean Leray, 2000 Clay Mathematics Institute, etc. Also maybe "positive viscosity", "smooth external force", etc. But we need to be selective: at most 4-5 double asterisks.
We need to decide which facts are most important: maybe the date of publication, the 166-page length, the 10k agents, 88 hours, 17 hours verification, the 1934 Leray, 2000 Clay Institute. That's many. We need only 4-5.
We can choose: 8 September, 166 pages, ≈10,000 agents, 88 hours, 17 hours maybe that's 5. Or we could include the Clay Institute year 2000 as important. But we need to limit.
We need to wrap each fact individually with double asterisks, not whole sentences. So we can embed them within sentences.
We also need to wrap study/journal citations in single underscores. There's mention of a preprint by Levanta Alpöge and Tristan Buckmaster? Actually "В препринте Левента Альпёге и Тристана Бакмастера сингулярность строится для уравнения Эйлера, где вязкости нет." That's a citation but not a journal. Could treat as preprint by Levanta Alpöge and Tristan Buckmaster maybe. Also maybe we need to cite the article itself? Not needed.
We need to preserve the content exactly, just translate.
Let's draft translation.
Headline: something like "OpenAI claims proof of Navier–Stokes singularity with viscous fluid". Must be under 90 chars.
Let's count: "OpenAI claims proof of Navier–Stokes singularity with viscous fluid" length ~ 55. Good.
Now blank line.
Now body paragraphs.
Paragraph 1: OpenAI published article on September 8 with claimed proof of singularity in Navier–Stokes equations, released full 166-page text and Lean formalization. The Lean language automatically checks reasoning steps.
We need to embed double asterisks for key numbers: maybe September 8, 166 pages. Also maybe Lean is not a number, but it's a name; we might not need to asterisk. We'll keep numbers.
Paragraph 2: According to the claimed theorem, for any positive viscosity the authors prescribe a smooth external force acting in a limited region of space and time, yielding a smooth three‑dimensional flow with finite kinetic energy that becomes unboundedly fast in finite time. The flow starts from rest, forms a vortex around an axis where fluid spirals inward and moves along the axis; the vortex core radius shrinks faster than its height, so speed grows while the volume shrinks enough to keep energy finite.
We might include positive viscosity maybe not needed. Could include finite kinetic energy but that's descriptive.
Paragraph 3: To avoid a non‑smooth remainder at the core boundary, the authors add short‑wavelength velocity oscillations around the core; the background vortex shear amplifies these waves, and their average momentum transport cancels the remainder. Subsequent corrections and spatial localisation keep the external force smooth even as the maximum speed grows without bound.…
🔗 Read original →
First line: short headline under 90 chars, no markdown, no '#'.
Then blank line, then body split into short paragraphs (2-3 sentences each), separated by blank lines.
Wrap few genuinely important facts — key numbers, percentages, drug/company/gene names, dates — in double asterisks. At most 4-5 per post, never a whole sentence.
Wrap study/journal citations and publication references in single underscores (e.g. Nature Aging, July 2026).
We need to preserve facts, numbers, names, citations exactly. No added commentary.
We need to identify important facts: dates: 8 September (OpenAI published article), 166 pages, Lean formalization, 10,000 agents, 88 hours search, 17 hours verification, 1934 Jean Leray, 2000 Clay Mathematics Institute, etc. Also maybe "positive viscosity", "smooth external force", etc. But we need to be selective: at most 4-5 double asterisks.
We need to decide which facts are most important: maybe the date of publication, the 166-page length, the 10k agents, 88 hours, 17 hours verification, the 1934 Leray, 2000 Clay Institute. That's many. We need only 4-5.
We can choose: 8 September, 166 pages, ≈10,000 agents, 88 hours, 17 hours maybe that's 5. Or we could include the Clay Institute year 2000 as important. But we need to limit.
We need to wrap each fact individually with double asterisks, not whole sentences. So we can embed them within sentences.
We also need to wrap study/journal citations in single underscores. There's mention of a preprint by Levanta Alpöge and Tristan Buckmaster? Actually "В препринте Левента Альпёге и Тристана Бакмастера сингулярность строится для уравнения Эйлера, где вязкости нет." That's a citation but not a journal. Could treat as preprint by Levanta Alpöge and Tristan Buckmaster maybe. Also maybe we need to cite the article itself? Not needed.
We need to preserve the content exactly, just translate.
Let's draft translation.
Headline: something like "OpenAI claims proof of Navier–Stokes singularity with viscous fluid". Must be under 90 chars.
Let's count: "OpenAI claims proof of Navier–Stokes singularity with viscous fluid" length ~ 55. Good.
Now blank line.
Now body paragraphs.
Paragraph 1: OpenAI published article on September 8 with claimed proof of singularity in Navier–Stokes equations, released full 166-page text and Lean formalization. The Lean language automatically checks reasoning steps.
We need to embed double asterisks for key numbers: maybe September 8, 166 pages. Also maybe Lean is not a number, but it's a name; we might not need to asterisk. We'll keep numbers.
Paragraph 2: According to the claimed theorem, for any positive viscosity the authors prescribe a smooth external force acting in a limited region of space and time, yielding a smooth three‑dimensional flow with finite kinetic energy that becomes unboundedly fast in finite time. The flow starts from rest, forms a vortex around an axis where fluid spirals inward and moves along the axis; the vortex core radius shrinks faster than its height, so speed grows while the volume shrinks enough to keep energy finite.
We might include positive viscosity maybe not needed. Could include finite kinetic energy but that's descriptive.
Paragraph 3: To avoid a non‑smooth remainder at the core boundary, the authors add short‑wavelength velocity oscillations around the core; the background vortex shear amplifies these waves, and their average momentum transport cancels the remainder. Subsequent corrections and spatial localisation keep the external force smooth even as the maximum speed grows without bound.…
🔗 Read original →
OpenAI
On the Navier–Stokes Millennium Prize Problem
We’re sharing an AI-generated solution to the Navier–Stokes Millennium Prize Problem, including a writeup and a formal proof in Lean.
Ovarian stiffness increases with age, linked to lower oocyte yield
A preprint published Preprint, September 8 measured ovarian tissue stiffness in 132 participants from fertility clinics. Researchers used shear‑wave elastography, an ultrasound technique that tracks tissue waves to gauge resistance to deformation. They compared the readings with ultrasound signs of tissue remodeling and with outcomes of IVF cycles.
In the first cohort, 16 women aged 33 or younger had an average stiffness of 13.3 kPa, while 16 women aged 37 or older averaged 18.8 kPa. With age, both the maximum value and the variability of the measurements increased. Mouse experiments from 2020 had suggested that old ovaries are about 2.5‑fold stiffer than young ones, and that collagenase can bring the tissue back toward youthful levels.
The age‑related rise in stiffness remained significant after adjusting for anti‑Müllerian hormone (AMH), a marker of follicular reserve, and for body‑mass index. A second cohort of 100 women aged 24‑45 showed the same three stiffness metrics climbing with age. These findings suggest that the ultrasonic measure reflects intrinsic tissue changes rather than hormonal or metabolic confounders.
To validate the ultrasound signal, researchers examined follicular fluid: the older group had lower levels of C6M, a fragment generated when collagen VI breaks down
🔗 Read original →
A preprint published Preprint, September 8 measured ovarian tissue stiffness in 132 participants from fertility clinics. Researchers used shear‑wave elastography, an ultrasound technique that tracks tissue waves to gauge resistance to deformation. They compared the readings with ultrasound signs of tissue remodeling and with outcomes of IVF cycles.
In the first cohort, 16 women aged 33 or younger had an average stiffness of 13.3 kPa, while 16 women aged 37 or older averaged 18.8 kPa. With age, both the maximum value and the variability of the measurements increased. Mouse experiments from 2020 had suggested that old ovaries are about 2.5‑fold stiffer than young ones, and that collagenase can bring the tissue back toward youthful levels.
The age‑related rise in stiffness remained significant after adjusting for anti‑Müllerian hormone (AMH), a marker of follicular reserve, and for body‑mass index. A second cohort of 100 women aged 24‑45 showed the same three stiffness metrics climbing with age. These findings suggest that the ultrasonic measure reflects intrinsic tissue changes rather than hormonal or metabolic confounders.
To validate the ultrasound signal, researchers examined follicular fluid: the older group had lower levels of C6M, a fragment generated when collagen VI breaks down
🔗 Read original →
bioRxiv
Multimodal profiling establishes ovarian fibrosis as a measurable and targetable hallmark of human reproductive aging
ABSTRACT Ovarian aging underpins infertility, systemic morbidity, and mortality in women. Stromal fibrosis is implicated in ovarian aging but has not been defined in the human ovary in situ. We integrated shear wave elastography (SWE), extracellular matrix…
Zebrafish heart repair uses distinct cardiomyocyte layers for growth and regeneration
On September 8, biologists described in eLife a thin layer of cardiomyocytes in zebrafish hearts that helps assemble the muscle wall and coronary vessels during growth.
After injury, other cardiomyocytes rebuild lost tissue; zebrafish hearts can regenerate muscle after ventricular tip removal; surviving cardiomyocytes change state, divide, and replace the lost tissue; the heart consists of several such layers.
Researchers mapped 1,668 cardiomyocytes of adult heart and found a group with active phlda2 gene; these cells lie in a thin layer between outer compact muscle and inner trabeculae.
They created a fish line where phlda2-active cells produce bacterial NTR enzyme and become sensitive to metronidazole; treatment removed about 96.9% of these cells from the ventricle.
In young fish, trabecular muscle area became roughly 54.7% smaller, outer compact layer lost proper organization, and coronary vessels fragmented; after 90 days the vascular pattern remained disrupted.
This layer participates in how the growing heart assembles muscle and vascular network.
In adult fish, ventricular tip was removed six days after treatment start; one week later the wound contained as many gata4-active cells (a marker of dividing cardiomyocytes during repair) as in controls.
By day 30 new muscle covered the injury; vessel density and scar area matched controls; the phlda2‑active layer did not recover even after 60 days, and its cells did not overlap with those activating gata4 during regeneration, indicating that heart growth and adult tissue repair rely on different cardiomyocyte populations.
🔗 Read original →
On September 8, biologists described in eLife a thin layer of cardiomyocytes in zebrafish hearts that helps assemble the muscle wall and coronary vessels during growth.
After injury, other cardiomyocytes rebuild lost tissue; zebrafish hearts can regenerate muscle after ventricular tip removal; surviving cardiomyocytes change state, divide, and replace the lost tissue; the heart consists of several such layers.
Researchers mapped 1,668 cardiomyocytes of adult heart and found a group with active phlda2 gene; these cells lie in a thin layer between outer compact muscle and inner trabeculae.
They created a fish line where phlda2-active cells produce bacterial NTR enzyme and become sensitive to metronidazole; treatment removed about 96.9% of these cells from the ventricle.
In young fish, trabecular muscle area became roughly 54.7% smaller, outer compact layer lost proper organization, and coronary vessels fragmented; after 90 days the vascular pattern remained disrupted.
This layer participates in how the growing heart assembles muscle and vascular network.
In adult fish, ventricular tip was removed six days after treatment start; one week later the wound contained as many gata4-active cells (a marker of dividing cardiomyocytes during repair) as in controls.
By day 30 new muscle covered the injury; vessel density and scar area matched controls; the phlda2‑active layer did not recover even after 60 days, and its cells did not overlap with those activating gata4 during regeneration, indicating that heart growth and adult tissue repair rely on different cardiomyocyte populations.
🔗 Read original →
Nature
Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration
Nature Communications - It is not clear if it is the embryonic origin or anatomical location of cardiomyocytes that restrict their contribution to zebrafish heart regeneration. Here, the authors...
BioPharma APAC Maps Four Longevity Funding Channels in Asia‑Pacific
On September 9, BioPharma APAC released a map of four channels of longevity financing in the Asia‑Pacific region. The map separates funds that pay for therapy development, diagnostics, clinic services, and scientific projects linked to the region but financed or incorporated outside it. Venture‑tracker records show when an investor receives equity after a deal.
Payments from pharmaceutical companies for joint development, research grants, and clinic revenue from examinations go to different recipients and support distinct work, which the author keeps separate. Therapeutic programs in the map draw venture money, public capital, grants, and pharma partnership payments. Biological‑age diagnostics — tests that assess age‑related changes in the body — form a separate line.
Two additional lines cover clinics and services funded
🔗 Read original →
On September 9, BioPharma APAC released a map of four channels of longevity financing in the Asia‑Pacific region. The map separates funds that pay for therapy development, diagnostics, clinic services, and scientific projects linked to the region but financed or incorporated outside it. Venture‑tracker records show when an investor receives equity after a deal.
Payments from pharmaceutical companies for joint development, research grants, and clinic revenue from examinations go to different recipients and support distinct work, which the author keeps separate. Therapeutic programs in the map draw venture money, public capital, grants, and pharma partnership payments. Biological‑age diagnostics — tests that assess age‑related changes in the body — form a separate line.
Two additional lines cover clinics and services funded
🔗 Read original →
Nature
Recommendations for biomarker data collection in clinical trials by longevity biotechnology companies
npj Aging - Recommendations for biomarker data collection in clinical trials by longevity biotechnology companies
Radical Numerics launches Omnii for personalized mRNA cancer vaccine target selection
On September 8, Radical Numerics unveiled Omnii, a post‑trained model designed to pick targets for personalized mRNA cancer vaccines. The system takes a tumor’s mutational profile and the patient’s MHC variants, then selects vaccine targets and builds an mRNA cassette sequence.
Omnii first predicts whether a mutant peptide will be presented by the patient’s MHC class I molecules on the tumor cell surface. It then estimates the peptide’s immunogenicity, i.e., whether a T‑cell will recognize the presented fragment and mount a response. Only peptides that pass both presentation and immunogenicity checks can be included in the vaccine cassette.
In head‑to‑head comparisons, Omnii achieved an AUROC 0.939 for MHC class I presentation, outperforming BigMHC‑EL’s 0.933. For immunogenicity prediction, the model scored AUROC 0.750, compared with 0.558 for BigMHC‑IM.
In a simulation where 100 candidate peptides were evaluated, only 6% were truly immunogenic and the cassette had five slots. Omnii selected an average of 1.3 immunogenic targets per cassette, while BigMHC‑IM managed just 0.7.
After target selection, Omnii outputs the mRNA sequence encoding the chosen neoantigens. The model is currently available in research preview, and Radical Numerics is seeking partners in cancer immunology and vaccine development.
🔗 Read original →
On September 8, Radical Numerics unveiled Omnii, a post‑trained model designed to pick targets for personalized mRNA cancer vaccines. The system takes a tumor’s mutational profile and the patient’s MHC variants, then selects vaccine targets and builds an mRNA cassette sequence.
Omnii first predicts whether a mutant peptide will be presented by the patient’s MHC class I molecules on the tumor cell surface. It then estimates the peptide’s immunogenicity, i.e., whether a T‑cell will recognize the presented fragment and mount a response. Only peptides that pass both presentation and immunogenicity checks can be included in the vaccine cassette.
In head‑to‑head comparisons, Omnii achieved an AUROC 0.939 for MHC class I presentation, outperforming BigMHC‑EL’s 0.933. For immunogenicity prediction, the model scored AUROC 0.750, compared with 0.558 for BigMHC‑IM.
In a simulation where 100 candidate peptides were evaluated, only 6% were truly immunogenic and the cassette had five slots. Omnii selected an average of 1.3 immunogenic targets per cassette, while BigMHC‑IM managed just 0.7.
After target selection, Omnii outputs the mRNA sequence encoding the chosen neoantigens. The model is currently available in research preview, and Radical Numerics is seeking partners in cancer immunology and vaccine development.
🔗 Read original →
PubMed Central (PMC)
Artificial intelligence in peptide cancer vaccine design: from neoantigen discovery to immunogenicity prediction
Peptide-based cancer vaccines represent a promising immunotherapeutic strategy aimed at inducing tumor-specific immune responses through the targeting of tumor-associated antigens and neoantigens. Recent advances in next-generation sequencing and ...
IRIS RNA model predicts developmental signals to improve stem cell differentiation
The IRIS model uses RNA profiles to infer which developmental signals acted on a cell. It was described in Nature Methods, September 8 after being trained on human stem cells exposed to known combinations of six developmental signals and then tested on single‑cell data from mouse embryos.
An RNA profile records which genes are currently active, giving a snapshot of the cell’s state. A benchmark of 400 models on cell atlases showed that merely expanding collections of RNA profiles quickly ceases to improve predictive power.
IRIS first learns from cells with known signal combinations, then searches the RNA profile for the trace of a signaling pathway—the chain through which a cell responds to an external cue. Researchers cultured human embryonic stem cells, applied defined signal mixes at different stages, and measured single‑cell RNA after each condition to teach IRIS to recognize these traces.
When applied to mouse embryo data, IRIS recovered the expected order of signal combinations in lineages that give rise to the foregut and heart muscle. It then predicted heightened activity of WNT and BMP in the prospective respiratory mesenchyme surrounding the lung bud.
In mouse foregut culture, activating WNT expanded the domain where the respiratory mesenchymal markers Tbx4 and Foxf1 are expressed, while a WNT inhibitor erased Tbx4 expression. Guided by this finding, the authors added WNT stimulation on the fourth day of differentiation of human stem cells and maintained it, which raised TBX4 levels and kept intermediate WNT activity to preserve FOXF1.
🔗 Read original →
The IRIS model uses RNA profiles to infer which developmental signals acted on a cell. It was described in Nature Methods, September 8 after being trained on human stem cells exposed to known combinations of six developmental signals and then tested on single‑cell data from mouse embryos.
An RNA profile records which genes are currently active, giving a snapshot of the cell’s state. A benchmark of 400 models on cell atlases showed that merely expanding collections of RNA profiles quickly ceases to improve predictive power.
IRIS first learns from cells with known signal combinations, then searches the RNA profile for the trace of a signaling pathway—the chain through which a cell responds to an external cue. Researchers cultured human embryonic stem cells, applied defined signal mixes at different stages, and measured single‑cell RNA after each condition to teach IRIS to recognize these traces.
When applied to mouse embryo data, IRIS recovered the expected order of signal combinations in lineages that give rise to the foregut and heart muscle. It then predicted heightened activity of WNT and BMP in the prospective respiratory mesenchyme surrounding the lung bud.
In mouse foregut culture, activating WNT expanded the domain where the respiratory mesenchymal markers Tbx4 and Foxf1 are expressed, while a WNT inhibitor erased Tbx4 expression. Guided by this finding, the authors added WNT stimulation on the fourth day of differentiation of human stem cells and maintained it, which raised TBX4 levels and kept intermediate WNT activity to preserve FOXF1.
🔗 Read original →
OmniSyn builds 2.7‑billion‑entry virtual library for human protein drug design
A preprint describing OmniSyn was posted on bioRxiv, September 6. The computational model takes a protein’s amino‑acid sequence and proposes a candidate molecule together with a step‑by‑step synthesis plan that uses purchasable chemical fragments and reaction types. Unlike many structure‑based methods, OmniSyn relies solely on the sequence, selecting from over 220 000 fragments and 115 common reaction types during training.
The model was tested on 35 proteins not seen during training. For these targets OmniSyn identified exact matches to known active molecules in 0.255% of cases, compared with 0.028% for the next‑best method. When the candidates were analogues of known molecules, the retrosynthesis tool AiZynthFinder found a viable route for 71.92% of them.
For 21 306 human protein sequences OmniSyn generated 2.7 billion target‑molecule entries, each containing a synthetic route and scoring metrics for candidate selection. In a test on 200 proteins, the interaction score distinguished the true target from random proteins (7.64 vs 4.47) and the docking score showed better binding (−6.88 vs −6.20 kcal mol⁻¹).
The library stores, for every protein sequence, a virtual candidate, its synthesis plan
🔗 Read original →
A preprint describing OmniSyn was posted on bioRxiv, September 6. The computational model takes a protein’s amino‑acid sequence and proposes a candidate molecule together with a step‑by‑step synthesis plan that uses purchasable chemical fragments and reaction types. Unlike many structure‑based methods, OmniSyn relies solely on the sequence, selecting from over 220 000 fragments and 115 common reaction types during training.
The model was tested on 35 proteins not seen during training. For these targets OmniSyn identified exact matches to known active molecules in 0.255% of cases, compared with 0.028% for the next‑best method. When the candidates were analogues of known molecules, the retrosynthesis tool AiZynthFinder found a viable route for 71.92% of them.
For 21 306 human protein sequences OmniSyn generated 2.7 billion target‑molecule entries, each containing a synthetic route and scoring metrics for candidate selection. In a test on 200 proteins, the interaction score distinguished the true target from random proteins (7.64 vs 4.47) and the docking score showed better binding (−6.88 vs −6.20 kcal mol⁻¹).
The library stores, for every protein sequence, a virtual candidate, its synthesis plan
🔗 Read original →
bioRxiv
OmniSyn unifies target-aware molecular generation and optimization within a synthesis-native LLM framework across the human proteome
Designing target-specific bioactive molecules with actionable synthesis routes for the human proteome holds enormous potential for expanding therapeutic discovery, but remains a challenge. Existing target-aware generative models often depend on protein structures…
Lipid nanoparticle with cerium oxide, CasRx plasmid, and D4F peptide reduces kidney injury
The authors described a lipid nanoparticle on 6 September that contains three parts: cerium oxide to scavenge reactive oxygen species, a plasmid expressing the CasRx protein guided by a short RNA to target STING transcripts, and the peptide D4F that directs the particle to kidney macrophages. In kidney organoids and a mouse model of transient blood‑flow occlusion, this construct lowered macrophage inflammation, tubular damage, and markers of kidney dysfunction.
Cerium oxide bound excess ROS, the plasmid drove CasRx production that cleaved STING RNA, and D4F facilitated particle accumulation in kidneys and binding to macrophages. In activated mouse macrophages the full construct decreased the proportion of cells showing a fluorescent ROS signal from 71.9% to 24.5%; a second guide RNA gave a similar reduction, while mutating the STING target site partially restored signal levels, confirming the effect depended on CasRx‑STING targeting.
Medium taken from macrophages treated with the nanoparticle reduced death, ROS signaling, and inflammatory gene activity in nearby tubular cells, even though the particles themselves did not reach the tubules, indicating that altered macrophage state can be transmitted via secreted factors. In kidney organoids, D4F increased the fraction of particles‑labeled cells from 9.65% to 27.5%.
In the mouse ischemia‑reperfusion model, two intravenous doses were given two hours before vessel occlusion and 30 minutes after blood flow returned; kidneys were evaluated after one day. Animals receiving the full construct showed the lowest tubular injury, creatinine, and blood urea nitrogen among all groups, with gene‑protein analysis revealing suppressed inflammatory pathways and enhanced oxidative‑stress defense and tissue‑repair programs.
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The authors described a lipid nanoparticle on 6 September that contains three parts: cerium oxide to scavenge reactive oxygen species, a plasmid expressing the CasRx protein guided by a short RNA to target STING transcripts, and the peptide D4F that directs the particle to kidney macrophages. In kidney organoids and a mouse model of transient blood‑flow occlusion, this construct lowered macrophage inflammation, tubular damage, and markers of kidney dysfunction.
Cerium oxide bound excess ROS, the plasmid drove CasRx production that cleaved STING RNA, and D4F facilitated particle accumulation in kidneys and binding to macrophages. In activated mouse macrophages the full construct decreased the proportion of cells showing a fluorescent ROS signal from 71.9% to 24.5%; a second guide RNA gave a similar reduction, while mutating the STING target site partially restored signal levels, confirming the effect depended on CasRx‑STING targeting.
Medium taken from macrophages treated with the nanoparticle reduced death, ROS signaling, and inflammatory gene activity in nearby tubular cells, even though the particles themselves did not reach the tubules, indicating that altered macrophage state can be transmitted via secreted factors. In kidney organoids, D4F increased the fraction of particles‑labeled cells from 9.65% to 27.5%.
In the mouse ischemia‑reperfusion model, two intravenous doses were given two hours before vessel occlusion and 30 minutes after blood flow returned; kidneys were evaluated after one day. Animals receiving the full construct showed the lowest tubular injury, creatinine, and blood urea nitrogen among all groups, with gene‑protein analysis revealing suppressed inflammatory pathways and enhanced oxidative‑stress defense and tissue‑repair programs.
🔗 Read original →
PubMed Central (PMC)
D4F‐Functionalized Ceria Nanozyme‐CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury
Acute kidney injury (AKI) is sustained by reciprocal amplification of oxidative stress, innate immune signaling, and maladaptive immune–parenchymal crosstalk. Here, we developed a lipid nanoparticle containing a ceria nanozyme and a STING‐targeting ...
Stiff hydrogel boosts early bone formation via PIEZO1 mechanosensor in mice
In mouse experiments, a stiff water‑saturated hydrogel enhanced early bone formation through the mechanosensor PIEZO1. On 6 September, Advanced Science, September 6 published an article showing how a material placed in a bone defect alters cell behavior.
In normal mice with a 1‑mm femoral defect and hind‑limb unloading, a 15% GelMA hydrogel gave more new trabecular bone and collagen by day 7 than a 5% GelMA. This early time point involved five mice per group in the key comparisons.
Cells in the damaged bone contact the matrix, and the authors tested whether matrix stiffness steers cells toward bone or fat programs. Mouse mesenchymal stem cells cultured on gels with 2 and 25 kPa stiffness showed stronger osteogenic markers on the stiffer gel and more lipid droplets on the softer gel under adipogenic induction.
PIEZO1 is a membrane channel that admits calcium when deformed. Blocking mechanosensitive channels with GsMTx4 weakened the stiff‑gel effect, and deleting Piezo1 in mesenchymal progenitors abolished the bone‑program boost on stiff gel.
The authors traced the path from calcium to the gene Stc2, showing that CaMKII inhibition lowered active SP1 and STC2 levels; SP1 binds the Stc2 promoter to drive its transcription. Mutating the promoter reduced SP1 binding and reporter activity, supporting this link.
Even when PIEZO1 was pharmacologically inhibited, adding secreted STC2 shifted cells toward osteogenesis. In a separate experiment, a soft 5% GelMA supplemented with STC2 enhanced early bone‑formation signs in the defect.
In mice lacking Piezo1 in mesenchymal progenitors, neither soft nor stiff gels increased bone formation, and the difference between 5% and 15% GelMA disappeared; these controls were performed without hind‑limb unloading.
🔗 Read original →
In mouse experiments, a stiff water‑saturated hydrogel enhanced early bone formation through the mechanosensor PIEZO1. On 6 September, Advanced Science, September 6 published an article showing how a material placed in a bone defect alters cell behavior.
In normal mice with a 1‑mm femoral defect and hind‑limb unloading, a 15% GelMA hydrogel gave more new trabecular bone and collagen by day 7 than a 5% GelMA. This early time point involved five mice per group in the key comparisons.
Cells in the damaged bone contact the matrix, and the authors tested whether matrix stiffness steers cells toward bone or fat programs. Mouse mesenchymal stem cells cultured on gels with 2 and 25 kPa stiffness showed stronger osteogenic markers on the stiffer gel and more lipid droplets on the softer gel under adipogenic induction.
PIEZO1 is a membrane channel that admits calcium when deformed. Blocking mechanosensitive channels with GsMTx4 weakened the stiff‑gel effect, and deleting Piezo1 in mesenchymal progenitors abolished the bone‑program boost on stiff gel.
The authors traced the path from calcium to the gene Stc2, showing that CaMKII inhibition lowered active SP1 and STC2 levels; SP1 binds the Stc2 promoter to drive its transcription. Mutating the promoter reduced SP1 binding and reporter activity, supporting this link.
Even when PIEZO1 was pharmacologically inhibited, adding secreted STC2 shifted cells toward osteogenesis. In a separate experiment, a soft 5% GelMA supplemented with STC2 enhanced early bone‑formation signs in the defect.
In mice lacking Piezo1 in mesenchymal progenitors, neither soft nor stiff gels increased bone formation, and the difference between 5% and 15% GelMA disappeared; these controls were performed without hind‑limb unloading.
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PubMed Central (PMC)
Matrix Stiffness Orchestrates Mesenchymal Stem Cell Lineage Commitment Toward Osteogenesis and Adipogenesis Through the PIEZO1/SP1/STC2…
Mesenchymal stem cells (MSCs) are critical for bone regeneration, and their osteogenic and adipogenic lineage balance is intricately regulated by cellular mechanotransduction. Through single‐cell RNA sequencing reanalysis of the public dataset ...
Hakken model selects three biomedical hypotheses for lab testing
Hakken constructs a map of biomedical entities from publications, linking each pair with a relation type and the time it appeared in the literature. The model compares this structure to article fragments where the entities are mentioned separately and scores hypotheses that are absent from the authors’ working knowledge base. For each candidate it provides a short chain of known facts that explains the high score.
Experts focused on aging, taking 1,386 aging‑related genes; among 959,805 gene pairs Hakken identified 1,543,297 hypotheses above a set threshold. Known interactions were removed, and an automatic selection of the top three candidates per entity left 2,804 hypotheses for further consideration.
Biologists chose three hypotheses with model scores above 0.8 and sent them to an independent contract laboratory. In these experiments a “link” means functional regulation of gene expression: after a cellular intervention the level of messenger RNA (mRNA) or the corresponding protein changes.
For the TP53–BAMBI pair, the drug Nutlin‑3 raised the p53 protein encoded by TP53, and BAMBI mRNA increased by 16% after 24 hours and by 38% after 48 hours.
For the RAF1–TNF pair, the RAF1 inhibitor GW5074 produced a small, repeatable rise in TNF mRNA at 24 hours, while the amount of TNF secreted into the medium stayed below the detection limit.
The third hypothesis, SOAT1–STAT3, received no support: stimulating SOAT1 did not alter STAT3 mRNA or protein levels.
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Hakken constructs a map of biomedical entities from publications, linking each pair with a relation type and the time it appeared in the literature. The model compares this structure to article fragments where the entities are mentioned separately and scores hypotheses that are absent from the authors’ working knowledge base. For each candidate it provides a short chain of known facts that explains the high score.
Experts focused on aging, taking 1,386 aging‑related genes; among 959,805 gene pairs Hakken identified 1,543,297 hypotheses above a set threshold. Known interactions were removed, and an automatic selection of the top three candidates per entity left 2,804 hypotheses for further consideration.
Biologists chose three hypotheses with model scores above 0.8 and sent them to an independent contract laboratory. In these experiments a “link” means functional regulation of gene expression: after a cellular intervention the level of messenger RNA (mRNA) or the corresponding protein changes.
For the TP53–BAMBI pair, the drug Nutlin‑3 raised the p53 protein encoded by TP53, and BAMBI mRNA increased by 16% after 24 hours and by 38% after 48 hours.
For the RAF1–TNF pair, the RAF1 inhibitor GW5074 produced a small, repeatable rise in TNF mRNA at 24 hours, while the amount of TNF secreted into the medium stayed below the detection limit.
The third hypothesis, SOAT1–STAT3, received no support: stimulating SOAT1 did not alter STAT3 mRNA or protein levels.
🔗 Read original →
SpringerLink
Link prediction for hypothesis generation: an active curriculum learning infused temporal graph-based approach
Artificial Intelligence Review - Over the last few years Literature-based Discovery (LBD) has regained popularity as a means to enhance the scientific research process. The resurgent interest has...
Jim Greenwood urges longevity movement to partner with biotech groups to shape FDA policy
On September 9, Jim Greenwood told the Alliance for Longevity Initiatives (A4LI) that the longevity movement should work with biotech associations such as BIO and the Alliance for Regenerative Medicine to influence FDA rules. He proposed forming a political action committee (PAC) to repeatedly engage elected officials on a single issue and bringing family members of people with dementia and other age‑related diseases to congressional meetings.
Greenwood served 12 years in the U.S. House of Representatives. He was president and CEO of the Biotechnology Innovation Organization (BIO) from 2005–2020, a period during which BIO’s membership grew to more than >1,000 companies.
He identified the next reauthorization of the Prescription Drug User Fee Act (PDUFA) as a practical window for action, saying A4LI should formulate its requirements in advance and channel them through the associations that already sit at the FDA table. “A4LI will not be sitting at that table… it should work closely with those who are, because they can convey its demands to the FDA,” Greenwood said.
Greenwood tied this political strategy to the likely path of aging‑biology interventions, noting they will first demonstrate efficacy in individual age‑related diseases that already have an approval and reimbursement pathway. In his view, A4LI can simultaneously discuss future drug rules with Congress and the
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On September 9, Jim Greenwood told the Alliance for Longevity Initiatives (A4LI) that the longevity movement should work with biotech associations such as BIO and the Alliance for Regenerative Medicine to influence FDA rules. He proposed forming a political action committee (PAC) to repeatedly engage elected officials on a single issue and bringing family members of people with dementia and other age‑related diseases to congressional meetings.
Greenwood served 12 years in the U.S. House of Representatives. He was president and CEO of the Biotechnology Innovation Organization (BIO) from 2005–2020, a period during which BIO’s membership grew to more than >1,000 companies.
He identified the next reauthorization of the Prescription Drug User Fee Act (PDUFA) as a practical window for action, saying A4LI should formulate its requirements in advance and channel them through the associations that already sit at the FDA table. “A4LI will not be sitting at that table… it should work closely with those who are, because they can convey its demands to the FDA,” Greenwood said.
Greenwood tied this political strategy to the likely path of aging‑biology interventions, noting they will first demonstrate efficacy in individual age‑related diseases that already have an approval and reimbursement pathway. In his view, A4LI can simultaneously discuss future drug rules with Congress and the
🔗 Read original →
U.S. Food and Drug Administration
PDUFA VIII: Fiscal Years 2028 – 2032
Information related to FDA’s preparation for the seventh reauthorization of PDUFA.
Nature reports chromosomal damage and mosaic editing in human embryos after base editor PCSK9 tweak
On Nature, September 9, 2026
On September 9, 2026, researchers published a study describing experiments on early human embryos targeting the PCSK9 and HBG genes with the adenine base editor ABE8e-V106W introduced at fertilization. The editor modified all PCSK9 alleles and permitted some embryos to reach the blastocyst stage, yielding embryonic stem cell lines with edited PCSK9.
The paper also notes a rare chromosome break at the target site, chromosomal abnormalities, and mosaic off‑target edits—different cells within the same embryo displayed distinct changes. While standard CRISPR/Cas9 creates double‑strand breaks that in early human embryos are associated with large deletions and loss of chromosomal segments, the adenine base editor produces a single‑strand nick and chemically alters a single DNA base.
PCSK9 and HBG were selected because they have been extensively studied in somatic cell editing, allowing the team to monitor how the embryo repairs such damage. After validating guide RNAs in cellular models, the editor was applied to human zygotes; delivering the editor protein together with its guide RNA enabled some embryos to develop to the blastocyst stage and produce PCSK9‑edited stem cell lines.
mRNA that encodes the editor frequently arrested development at early divisions, a effect the authors attribute to the deaminase activity of the editor independent of the guide RNA. A June 2026 review of the preprint had found no large deletions or chromosomal anomalies after editing, but the September article describes a different damage profile: a rare chromosome break at the target site, chromosomal anomalies, and mosaic off‑target edits near the targets and elsewhere in the genome.
When assessing safety, researchers examine the whole embryonic genome, chromosome status, and whether edits are uniform across cells. The authors conclude that the genomic and developmental consequences currently preclude clinical application of this approach in reproduction.
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On Nature, September 9, 2026
On September 9, 2026, researchers published a study describing experiments on early human embryos targeting the PCSK9 and HBG genes with the adenine base editor ABE8e-V106W introduced at fertilization. The editor modified all PCSK9 alleles and permitted some embryos to reach the blastocyst stage, yielding embryonic stem cell lines with edited PCSK9.
The paper also notes a rare chromosome break at the target site, chromosomal abnormalities, and mosaic off‑target edits—different cells within the same embryo displayed distinct changes. While standard CRISPR/Cas9 creates double‑strand breaks that in early human embryos are associated with large deletions and loss of chromosomal segments, the adenine base editor produces a single‑strand nick and chemically alters a single DNA base.
PCSK9 and HBG were selected because they have been extensively studied in somatic cell editing, allowing the team to monitor how the embryo repairs such damage. After validating guide RNAs in cellular models, the editor was applied to human zygotes; delivering the editor protein together with its guide RNA enabled some embryos to develop to the blastocyst stage and produce PCSK9‑edited stem cell lines.
mRNA that encodes the editor frequently arrested development at early divisions, a effect the authors attribute to the deaminase activity of the editor independent of the guide RNA. A June 2026 review of the preprint had found no large deletions or chromosomal anomalies after editing, but the September article describes a different damage profile: a rare chromosome break at the target site, chromosomal anomalies, and mosaic off‑target edits near the targets and elsewhere in the genome.
When assessing safety, researchers examine the whole embryonic genome, chromosome status, and whether edits are uniform across cells. The authors conclude that the genomic and developmental consequences currently preclude clinical application of this approach in reproduction.
🔗 Read original →
Nature
Highly efficient base editing at PCSK9 and normal human embryo development
Nature - Highly efficient base editing at PCSK9 and normal human embryo development
Anthropic's Hubinger Says AI Extinction Risk Over 10% in Next Decade
On September 9, Evan Hubinger, head of AI alignment at Anthropic, replied to a thread by former colleague Jacob Cockson. He agreed with Cockson’s warning about a race toward self‑improving superintelligence and said Anthropic currently lacks a plan to align such a system with human interests.
The same day Jacob Cockson announced his departure from Anthropic. In his thread he described the situation as a race to self‑improving superintelligence, urged researchers to pursue alternative development conditions, and suggested a temporary halt on scaling model capabilities might be needed to avert a global race.
In his reply Hubinger added his personal assessment, stating that he believes the probability of AI causing human extinction in the next ten years is >10%. He said Anthropic is doing
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On September 9, Evan Hubinger, head of AI alignment at Anthropic, replied to a thread by former colleague Jacob Cockson. He agreed with Cockson’s warning about a race toward self‑improving superintelligence and said Anthropic currently lacks a plan to align such a system with human interests.
The same day Jacob Cockson announced his departure from Anthropic. In his thread he described the situation as a race to self‑improving superintelligence, urged researchers to pursue alternative development conditions, and suggested a temporary halt on scaling model capabilities might be needed to avert a global race.
In his reply Hubinger added his personal assessment, stating that he believes the probability of AI causing human extinction in the next ten years is >10%. He said Anthropic is doing
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X (formerly Twitter)
Evan Hubinger (@EvanHub) on X
Jacob is correct here—we really do earnestly believe AI could kill all humans! I personally think it is >10% within the next decade. I believe Anthropic is trying its best, but we do not yet ha…
AI Agent Calibrates Six‑Qubit Chip, Improves Four of Forty Measurements
GPT‑5.6 Sol performed calibration of four qubits on a new MIT chip on September 8. Researchers intervened in only 4 of 40 target measurements to improve results. The agent, guided by OpenAI’s description of graduate student Beatrice Yankelevich’s work, used the Codex system to control measurements on a separate chip with six superconducting qubits.
Calibration sets the chip before experiments: the outcome of one measurement becomes the
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GPT‑5.6 Sol performed calibration of four qubits on a new MIT chip on September 8. Researchers intervened in only 4 of 40 target measurements to improve results. The agent, guided by OpenAI’s description of graduate student Beatrice Yankelevich’s work, used the Codex system to control measurements on a separate chip with six superconducting qubits.
Calibration sets the chip before experiments: the outcome of one measurement becomes the
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