seriously awesome use case for muse — clean up the neighborhood!

In the meantime, here's another listing for what seems to be the same DpBlue Ultra HD Blu-ray player posted here before. The device doesn't seem to have a type number so it's hard to be sure. amazon.com/DpBlue-Player-Dol…

Sam Altman proposed a similar revenue-sharing program for the GPT Store at DevDay on November 6, 2023. Very shortly afterwards he was removed as CEO in a surprising series of events. Hopefully this works out better for Elon.

🚨 Claude sonnet Leaks: Beats GPT-6 Sol > Sonnet 5.5 is set to launch tomorrow at 2 PM New York time > It's now Final stages before release > Early testing puts it ahead of GPT-6 Sol > Expected to sit much closer to Opus 5.5 in capability > Could be significantly cheaper than Opus 5.5 > A dedicated "claude-sonnet-5-5" model identifier has already been spotted are you ready for Sonnet 5.5 tomorrow?

can someone explain how they got opus 5.5 to be this efficient & this good? i’ve barely run into usage limits at all. it’s absolutely cooking on genuinely difficult problems with what feels like zero effort while somehow also consuming dramatically less of my quota than other frontier models??! compared with astra or sol it’s night & day. the capability per token here feels kinda absurd, & this coming from anthropic where we didn’t see this barrage of usage limit resets or whatever.

For many people taking Methylfolate (5-MTHF) and Methylcobalamin (Methyl-B12) is the exact biological driver behind their sudden ADHD symptoms, panic attacks, sensory overwhelm, jaw clenching, and relentless obsessive rumination. When you flood a genetically unsuited nervous system with active methyl donors, you trigger an acute neurochemical storm: prefrontal catecholamine overload, adrenergic hyper-arousal, and unchecked glutamatergic firing. You do not have a psychiatric defect; you are experiencing an iatrogenic over-methylation crisis. Simply switching to non-methylated B-vitamin variants resolves the cognitive chaos within days by restoring enzymatic homeostasis. Here is the deep cellular pharmacology behind the methylated B-vitamin trap and how to fix it👇 The COMT Collision: Why Methyl Groups Trigger Adrenergic Panic The primary reason methylated vitamins induce severe anxiety and ADHD-like scatter lies in the interaction between the methylation cycle and the Catechol-O-methyltransferase (COMT) enzyme: • The "Slow COMT" Phenotype (Met/Met or Val/Met): COMT is the enzyme responsible for degrading catecholamines—Dopamine, Norepinephrine, and Epinephrine—in the prefrontal cortex. Individuals with the common "slow" COMT variant break down these neurochemicals at a fraction of the speed of "fast" COMT individuals. They naturally operate with high baseline prefrontal dopamine and norepinephrine. • The SAMe Flood: Ingesting active methyl donors (5-MTHF, Methyl-B12) rapidly surges intracellular S-adenosylmethionine (SAMe). SAMe is the universal methyl donor required by COMT to catabolize dopamine. • The Epinephrine Shunt (PNMT Activation): While excess SAMe technically feeds COMT, it simultaneously acts as an aggressive cofactor for Phenylethanolamine N-methyltransferase (PNMT)—the enzyme that converts Norepinephrine into Epinephrine (Adrenaline). In slow COMT individuals, this triggers an immediate adrenergic spike. Your system is flooded with peripheral adrenaline and central catecholamines that your sluggish COMT enzyme cannot clear in time. • Prefrontal Signal Decay: Excessive catecholamines over-saturate prefrontal Alpha-1 and Beta-1 adrenoceptors. This blows open Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) leak channels on dendritic spines, causing the electrical insulation of working memory to completely collapse. You feel wired, jittery, mentally scattered, and completely incapable of sustained attention—the precise presentation of severe ADHD. Glutamate Excitotoxicity & CSTC Loop Hyperactivity (OCD & Rumination) The mental loops, compulsive double-checking, and dark ruminations induced by methylated vitamins are driven by glutamate firestorms in the Cortico-Striato-Thalamo-Cortical (CSTC) loop: • NMDA Receptor Hyper-Sensitization: Excessive methyl donors alter the epigenetic methylation of promoter regions governing neurotransmitter receptors. Surging methyl pools amplify postsynaptic NMDA (N-methyl-D-aspartate) receptor sensitivity. • The Astrocytic Glutamate Reuptake Failure: Simultaneously, the sudden adrenergic overload drives astrocytes into an energetic crisis. The EAAT2 (Excitatory Amino Acid Transporter 2) pumps stall, leaving tonic glutamate lingering in the synaptic cleft. • The Ruminative Loop Locks In: When tonic glutamate continuously stimulates hyper-sensitized NMDA receptors in the CSTC loop, the brain fails to filter out intrusive cognitive noise. A single negative scenario, irrational health fear, or social interaction echoes endlessly between the cortex and thalamus. You cannot "rationalize" your way out of it because the underlying electrical circuit is physically locked open by excitotoxicity. Histamine Clearance Crashes: The Paradoxical Flare Many people experience sudden somatic symptoms on methyl donors: insomnia, racing heart, skin flushing, and allergy-like flares. This is driven by destabilized histamine kinetics: • Histamine N-Methyltransferase (HNMT): In the central nervous system, histamine is broken down exclusively by HNMT, an enzyme that requires SAMe. • The Feedback Inhibition Bottleneck: When massive doses of methylfolate enter the cell, SAMe surges violently. However, high SAMe rapidly downregulates MTHFR via feedback inhibition and can cause a transient accumulation of S-adenosylhomocysteine (SAH) if downstream clearance is slow. SAH is a vicious, potent competitive inhibitor of methyltransferase enzymes—including HNMT. • The Histamine Rebound: Inhibiting HNMT causes central histamine concentrations to spike. Histamine stimulates H1 receptors in the hypothalamus, driving relentless nocturnal wakefulness, high-alert paranoia, and autonomic agitation that mimics severe generalized anxiety disorder. The Non-Methylated Replacements: The Surgical Pivot You still need folate and B12 to synthesize cellular ATP, maintain red blood cells, and fuel the Krebs cycle. You simply must use forms that allow your body’s internal enzymatic feedback loops to control the rate of methylation, rather than forcing methyl groups into the cell: • 1. Replace Methylfolate with Folinic Acid (Calcium Folinate): The Mechanism: Folinic acid is a non-methylated, metabolically active form of folate (5-formyl-tetrahydrofolate). It bypasses the MTHFR enzyme entirely, feeding directly into the folate pool to produce purines and thymidylate for DNA repair. It converts into 5-MTHF only downstream, strictly on demand, governed by cellular feedback mechanisms. It supplies every biological benefit of folate with zero methyl-donor spiking. • 2. Replace Methylcobalamin with Hydroxocobalamin or Adenosylcobalamin: Hydroxocobalamin: A non-methylated precursor that readily converts into active B12 forms intracellularly as required. Critically, Hydroxocobalamin acts as a natural Nitric Oxide (NO) scavenger, mopping up toxic peroxynitrite and calming systemic neuroinflammation. Adenosylcobalamin (Dibencozide): The mitochondrial form of B12. It acts as the specific cofactor for Methylmalonyl-CoA Mutase, directly fueling the Krebs cycle and fatty acid oxidation inside the mitochondria without introducing a single methyl group into the cytoplasmic methylation cycle.

Socially maladjusted tech ceos like Zuck don't understand regular people at all

WOW LIFE AS A QUANTUM PROCESS. NEW PAPER. A QUIET FREQUENCY THAT COULD CHANGE HOW WE SEE LIFE Something extraordinary has been heard inside living cells. Deep within mitochondria—the tiny, folded engines that power every heartbeat, every thought, every movement—researchers have detected a vibration ringing at 71 trillion cycles per second. The signal appears only while those engines remain intact and alive. Break the architecture and the note falls silent. That single peak, reported in a 2026 preprint by Yu Yang, Zhenglong Gu and Bo Song, is more than a spectroscopic curiosity. It is a invitation. It suggests that the most important organelles in biology may be doing something subtler and more elegant than classical chemistry alone can explain. The team used infrared light to listen to living human cells, fresh tissues, and carefully isolated mitochondria. Again and again they found the same unexplained 71 THz feature. Their model is beautiful in its simplicity: light trapped among the cristae couples to the collective dance of lipid CH₂ bonds, creating a polariton—a hybrid state that is part light, part matter. The familiar 87 THz vibration splits. One of the new notes is the 71 THz signal we can now hear. The living mitochondrion, in this picture, is not just a factory. It is a resonator. When the researchers gently shone light at that same frequency onto cultured cells, ATP production rose by about ten percent. A nearby control frequency did nothing. Frequency mattered. The cell’s energy currency responded as if someone had found a hidden dial. This is still early science. The paper awaits peer review and independent confirmation. That is how good science works. Yet the possibility already feels generous. If mitochondria can host a light-matter quantum state that we can address from outside, then energy metabolism is no longer a closed chemical book. It becomes a system we might one day tune. Imagine therapies that raise cellular energy without harsh drugs—soft, precise infrared light helping failing hearts, tired muscles, or aging neurons recover their spark. Imagine a deeper understanding of why life is so efficient, why warm, wet cells can still exploit quantum resources we once thought belonged only to laboratories at near-absolute zero. Imagine mitochondria not merely as batteries but as possible channels for both energy and information, quietly coordinating the business of being alive. Quantum biology has waited years for a clear experimental foothold inside living animal cells. This 71 THz peak may be that foothold. Even if later work refines the interpretation, the observation itself is a gift: life is still capable of surprising us at the smallest scales. The original research is available: biorxiv.org/content/10.64898… The universe did not have to make cells this interesting. It did anyway. We are only beginning to learn the frequencies they sing.

jesus one-shot christ

24 senior mathematicians met at Harvard and agreed on something big: A PhD should no longer be awarded mainly on the dissertation text. Their reason is that AI can now help write it. They want in-person, written, and oral exams instead. Personally, as someone with a PhD, I think the defense should have been the real test all along. Anyone can polish a document. terrytao.wordpress.com/2026/…

$500 a month is higher than the median income in 128 countries. That is 66% of all 193 UN member states. Outside the top 10 richest nations, almost nobody can afford that kind of subscription. This goes completely against what they promised when raising billions: "intelligence too cheap to meter." Intelligence built on our collective knowledge belongs to all of us. This is why I am all in on open source.

Opus 5.5 update

Cloud sessions are officially available and out of research preview! They let you keep Claude Code working, even when your laptop is closed. Existing subscribers get a one-time credit to try them: $100 on Pro, $250 on Max.

This is amazing, but that 70GB is compressed. Decompressed, the resolved TeX contains lots of info... 📚 2.856 MILLION papers 📝 ~247 BILLION characters 🧠 estimated 78.6–80.9 BILLION tokens So obviously you aren't stuffing arXiv into a giant context window. 😂 But Local AI can ... 🔎 search/filter locally 📚 retrieve a handful of relevant papers 🧠 feed only those chunks to your local LLM 🚫 no cloud/API required The metadata for ALL 3.15M papers is only 1.6GB. 👈 So you could keep a tiny local index for discovery + the 70GB corpus for retrieval + a local model for answering. Basically, it's your own offline scientific search engine sitting on an SSD. 👀

Just cracked SHA-256 hash quine in HEIC. This one was SIGNIFICANTLY more difficult than the JXL. Blog post coming soon

your x feed this week sorry not sorry