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Since January 2025, ResearchHub has deployed over $1.5M in research funding to scientists worldwide. We just redesigned our funding page to make it even easier for funders and researchers to connect. Take a look ↓ researchhub.com/fund
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In the largest spectroscopy meta-analysis of depression, 1,180 patients against 1,066 controls, the glutamate-plus-glutamine signal in medial frontal cortex was lower, not higher: -0.38. Glutamate alone showed no difference.
Glutamate dysregulation is a key driver of issues such as anxiety, anhedonia, bipolar disorders, headaches, autism spectrum disorder, TBIs, irritability, inability to focus etc Here's what you need to know. Thread🧵
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Moriguchi et al., Glutamatergic neurometabolite levels in major depressive disorder: a systematic review and meta-analysis of proton magnetic resonance spectroscopy studies, Molecular Psychiatry 2019, Keio University, CAMH Toronto and Yokohama City University (open access; 49 studies; the decrease reached significance only in medicated patients). doi.org/10.1038/s41380-018-0…
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Stool pooled from 3 severely depressed men, given to antibiotic-depleted rats, produced anhedonia (p=0.022) and anxiety-like behavior (p=0.029). Ten years on, the largest human trial, n=60, missed its primary endpoint.
Scientists transferred gut bacteria from depressed people to rats. The rats then developed behaviors characteristic of depression (anhedonia and anxiety-like behavior).
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Kelly et al., Transferring the blues: Depression-associated gut microbiota induces neurobehavioural changes in the rat, Journal of Psychiatric Research 2016, APC Microbiome Institute, University College Cork (28 rats, 13 given depressed-donor microbiota; the human trial is Li et al., Cell Host and Microbe, July 2026, remission 43.3% vs 26.7%, p=0.176). doi.org/10.1016/j.jpsychires…
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ResearchHub retweeted
Should we use @ginkgo’s autonomous lab to test if Claude’s gene editor actually works ? Lmk what you think
Today we announced the Claude-led discovery of a molecular machine that we suspect could represent a new gene editing mechanism. Its precise function, biotechnological utility (if any), or level of significance is not yet clear, but at minimum it is work I would have been proud to do as a PhD student. The work was done mostly, though not entirely, by Claude: our life sciences team suggested a broad area of research, Claude read through the literature and a bunch of genome data and discovered something interesting, then Claude proposed experiments to verify the discovery and our team carried them out. It’s easy to dismiss this as a one-off or curiosity, but we’ve repeatedly seen a pattern where AI performance in new intellectual domains goes from weak to superhuman in a matter of a few years. In 2023 models struggled to do math at the level of an average high-school student. In 2024 they started to do well on math competitions for the best high-schoolers in the country, in 2025 they started to solve minor open problems, in early 2026 more significant open problems, and in late 2026 they are beginning to solve the top few open problems in all of mathematics. We believe AI for biology is on a similar exponential trend. The main difference between biology and mathematics, of course, is that math can be done purely theoretically, while biology requires experimentation. Some have used this to draw the conclusion that AI’s utility in biology will be limited. We think this is wrong. As we’ve demonstrated today, humans can collaborate with AI to perform the experiments, validate key results in a few weeks and, if necessary, work with the AI to iterate on what they find. Eventually it may even be possible for Claude itself to safely perform the experiments by autonomously controlling lab equipment, with appropriate safeguards in place, but we aren’t doing that today (our lab is also a BSL1/BSL2 facility that doesn't handle materials dangerous to humans). More broadly, biomedical advancement has many stages — from fundamental biology discoveries, to translational research, to drug discovery, clinical trials, and finally the actual delivery of medicines and health care to patients. We are also interested in these later stages, but even simply accelerating the first stage of fundamental biological discoveries has the potential to speed up and broaden the entire pipeline. Improving our understanding of biology and sharpening biologists’ tools can drive forward all of the later stages, for example by identifying new drug targets, finding new therapeutic modalities, allowing for more precise measurement, and speeding up the experimental loop which itself further accelerates our understanding of biology. This will not in itself speed up clinical trial times, but if it succeeds it could greatly increase the number of promising candidates that go into the pipeline — an increase in throughput even though latency remains. In Machines of Loving Grace, I wrote about AI’s potential to ā€œcure most diseases in 5-10 yearsā€ — a goal that sounds impossible, but one I believe is just barely possible if AI is applied to every stage of the pipeline. The first step is showing that AI can first help with, and then drive, biological discoveries. Claude’s discovery is the latest in a line of related prior work that goes back decades, beginning with systems like CRISPR, and continuing with discoveries like the bridge recombinase and VIPR in the past few years. Recently, there has been heightened interest in systems based on reverse transcriptase (RT) enzymes, the enzyme underlying the system Claude identified. And most recently, a Stanford team working independently described a novel RT system with an associated non-coding array that is in some ways similar to the one Claude found, though they are distinct systems that evolved independently from each other. I believe that we’re at the very beginning of finding such systems and developing them into powerful tools for biotechnology. I’m proud of the resources Anthropic has invested in accelerating the public benefits of AI through the life sciences, and we’re aiming both to grow our life sciences team and to work with other scientists to extend this approach to a broad range of problems. If you have a proposal for a research collaboration or are interested in joining our life sciences team, please reach out.
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The Athanatos Foundation has launched a new funding pool on ResearchHub, committing up to $23K to independent replication studies investigating the reported effects of epothilone B on anesthetic sensitivity. 🧵
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What this RFP funds Researchers are invited to propose the strongest replication possible, including: → Rodent replication (up to $15K) → Tetrahymena replication (up to $5K) → One high-value extension or data audit (up to $3K) Positive, negative, and inconclusive results are all valuable.
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Researchers in anesthesiology and related fields are encouraged to submit proposals. Community members can also contribute directly to the funding pool. Submit a proposal or fund the research ↓ researchhub.com/grant/32943/…
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198,953 $RSC has been burned to date from activities on ResearchHub. Come fund more science. Science šŸ¤ Crypto
The first burn under RIP-23 has been completed. šŸ”„ • Amount burned: 71,229.48 $RSC • Source wallet: 0x7F57d306a9422ee8175aDc25898B1b2EBF1010cb • Destination (null) address: 0x000000000000000000000000000000000000dEaD •Date: 08/25/2025 This inaugural burn includes all $RSC the ResearchHub Foundation has collected from transaction fees so far. From now on: • Every week, 100% of the $RSC collected in platform transaction fees will be sent to the null address. • Burns will take place at the start of each week. • All activity is verifiable onchain. This milestone strengthens ResearchHub Foundation’s commitment to neutral, community-aligned protocol governance under RIP-23. Link to onchain transaction šŸ‘‡
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Across 38 randomized trials, text reminders improved health behaviors by 0.29 SD. Opt-out defaults raise uptake by about 0.68 SD over opt-in. A new Annual Review sorts such tools by phase: motivation, follow-through, habit.
ā€¼ļøNew Paper Alertā€¼ļøWhat does it take to change behavior? In a fresh Annual Review article, @JGVoelkel, @AngelaDuckw and I argue it's helpful to consider 3 phases of change: 1ļøāƒ£ building motivation 2ļøāƒ£ following-through 3ļøāƒ£ forming durable habits 🧩KEY TAKEAWAY: At each phase, different obstacles to change arise that need to be met with evidence-based, tailored solutions. For instance, at the follow-through phase, forgetting can disrupt change. But forgetting can be combatted by reminders or feedback. Impatience can also disrupt follow-through, but it can be addressed in part by making change more fun or providing access to commitment devices. These are not the only obstacles to follow-through, however, and different obstacles arise at the motivation and habit forming phases, which are best tackled with entirely different solutions. Table 1 from our paper (reprinted below) offers a summary of common obstacles to change and evidence-based solutions. ⭐Our review focuses on solutions supported by *high quality evidence*, particularly from field experiments with objective behavioral outcomes (e.g., grades, gym visits, hours spent volunteering). šŸ‘€Take a look at our new piece in the Annual Review of Psychology: tinyurl.com/change-annualrev… Huge thanks to our excellent editor @EliJFinkel. We're very grateful for support from @Wharton, @BehaviorChange, @Penn and @Cornell, which made this work possible.
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Voelkel, Milkman and Duckworth, Behavior Change, Annual Review of Psychology (Review in Advance 2026, vol. 78, 2027), Cornell, Wharton and Penn (narrative review; effect sizes are cited from prior RCTs and meta-analyses, which the authors call rough benchmarks). doi.org/10.1146/annurev-psyc…
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In male rats, 3 weeks of methylene blue raised pituitary dopamine, cut D-2 receptor number and partly blocked estradiol-driven pituitary growth. The same group found methylene blue alone left blood prolactin unchanged (abstract).
Methylene blue lowered blood prolactin by 65%, nearly tripled pituitary dopamine, and partially prevented estradiol-induced pituitary enlargement in rats. After 21 days, male rats given methylene blue had 65% lower blood prolactin than controls: 1.7 vs. 4.9 ng/mL. Dopamine in the anterior pituitary was 2.7 times higher. In rats treated with estradiol, methylene blue also partially prevented pituitary enlargement and reduced prolactin buildup inside the gland. The dopamine increase occurred without a detectable increase in dopamine synthesis. DOI: 10.1016/S0304-3940(01)01752-9.
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Nedvidkova et al., The role of dopamine in methylene blue-mediated inhibition of estradiol benzoate-induced anterior pituitary hyperplasia in rats, Neuroscience Letters 2001, Institute of Endocrinology, Prague (male rats; paywalled, abstract read; the blood-prolactin null is from the same group's 1993 Physiol Res paper, PMID 8218149). pubmed.ncbi.nlm.nih.gov/1134…
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Heavier loads (80%+ of 1RM) improved strength in 6 systematic reviews (n=6,574). For muscle size, 8 reviews (n=5,340) found load made no difference. 10+ sets a week drove hypertrophy (ACSM overview of 137 reviews).
Resistance training works—and it doesn’t need to be complicatedšŸ‹ļø ACSM’s review of 137 systematic reviews; train regularly, progressively, and with sufficient effort. Volume matters for hypertrophy; heavier loads favor strength Consistency > complexity pubmed.ncbi.nlm.nih.gov/4184…
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Currier et al., American College of Sports Medicine Position Stand: Resistance Training Prescription for Muscle Function, Hypertrophy, and Physical Performance in Healthy Adults: An Overview of Reviews, Medicine & Science in Sports & Exercise 2026, McMaster University (137 systematic reviews, over 30,000 participants; vote-count synthesis, no pooled effect sizes; free full text via PMC). doi.org/10.1249/MSS.00000000…
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Lead was quantified in 23 of 25 protein bars. 18 topped the Prop 65 warning level (0.5 µg/day); 1 topped FDA's 2.2 µg/day children's level; 0 topped its 8.8 µg/day level for women of childbearing age. Company screen, 1 bar each.
25/25 protein bars tested positive for heavy metals: - Aloha Chocolate Chip Cookie Dough - Aloha Peanut Butter Cup - Kreatures of Habit Daily Bar Choc PB Banger - Laird Superfood Double Chocolate Peanut Butter - Clif Bar Chocolate Brownie - GoMacro MacroBar Sweet Awakening - Jacob's Protein Bar Chocolate - Prima Cacao Ancestral Protein Bar - Santa Cruz Paleo Chocolate - RXBAR Peanut Butter Chocolate - GoMacro MacroBar Smooth Sanctuary - Lineage Protein Bar Chocolate - Built Puff Brownie Batter - Barebells Creamy Crisp - Blueprint Macadamia White Cocoa Butter - David Peanut Butter Chocolate Chunk - Perfect Bar Dark Chocolate Chip Peanut Butter - PROMIX Protein Puff Bar Blueberry - RXBAR Chocolate Sea Salt - KIND Breakfast Protein Dark Chocolate Cocoa - Clif Bar Crunchy Peanut Butter - Kirkland Chocolate Chunks Cookie Dough - Kirkland Protein Bar Chocolate Brownie - Rise Almond Honey Lead: found in 23/25 (18 exceeded the Prop 65 limit, 1 exceeded FDA's limit) Cadmium: found in all 25 (2 exceeded Prop 65) Mercury: found in 2/25 (both exceeded the Prop 65) Arsenic: found in 20/25 Full results on Oasis
Community note
The claim that all 25 bars "tested positive for heavy metals" refers to trace detections common in foods; per their data most were below FDA lead benchmarks and Prop 65 uses extremely low warning thresholds unrelated to acute safety. oasishealth.app/science/25-pro… fda.gov/food/environme… oag.ca.gov/prop65/faqs-vi…
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Oasis, Heavy Metals in Retail Protein Bars: A Twenty-Five Product Screen, September 2026 (company report, not journal peer-reviewed; ICP-MS per AOAC 2015.01 at an unnamed accredited lab; one unit of one lot per product; Prop 65 MADL is a California warning threshold, not a harm threshold). oasishealth.app/science/25-p…
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How well a model matched a drug's transcriptome told you almost nothing about whether it got the mechanism right: median Spearman 0.052. 12 models plus 3 baselines; a plain linear-regression baseline led on mechanism fidelity.
A single-cell model can predict a transcriptome almost perfectly and still get the drug response backwards. That is a serious problem if we want ā€œvirtual cellsā€ to do more than reconstruct gene-expression profiles. Let introduce scDrugPerturb-Bench, a mechanism-aware benchmark for single-cell drug perturbation models. Instead of asking only: Does the predicted transcriptome resemble the measured one? it asks: Did the model recover the biological response that actually matters? The benchmark brings together 2.5 million cells, 181 datasets, 101 drugs and 423 literature-curated drug-response cases, with experimentally supported directional changes for 717 key genes across different cellular contexts. The authors then evaluated 12 perturbation-prediction models, simple baselines and multiple single-cell foundation-model representations. The result is uncomfortable: expression similarity was only weakly aligned with mechanism fidelity. A prediction could look convincing at the whole-transcriptome level while getting key genes, pathway direction or mechanism specificity wrong. One example makes the problem tangible. For a drug perturbation in human iPSC-derived microglia, the predicted profiles achieved very low reconstruction error, yet 0 of 8 annotated key genes changed in the correct direction. The transcriptome looked right. The biology was backwards. To capture this distinction, the authors introduce a Mechanism Fidelity Score that tests whether predictions preserve key-gene direction, effect size, gene-set coherence, mechanism specificity and pathway-level polarity - not just global expression similarity. The hard-negative experiments are perhaps even more revealing. Some models could generate plausible-looking perturbation responses by exploiting generic transcriptional programmes or overall perturbation strength, without recovering the specific drug-response signature. This matters far beyond benchmarking. If virtual-cell models are eventually used to prioritize compounds, infer mechanisms or design experiments, then a biologically wrong prediction does not become useful simply because its transcriptome correlation is high. Prediction quality depends on what we choose to measure. Reconstructing expression is one task. Recovering mechanism is another. And for biological AI, those two should not be treated as the same thing.
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Li et al., A mechanism-annotated benchmark reveals limited fidelity to drug-response signatures in single-cell perturbation models, bioRxiv preprint, August 2026 (not peer reviewed), Harbin Institute of Technology Shenzhen and MindFlow.ai. biorxiv.org/content/10.64898…
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