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Cost-Effectiveness of Thrombectomy With or Without Alteplase in Large Vessel Occlusion StrokeA Meta-Analysis Considering Time-to-Treatment

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A neuropeptide regulates cell non-autonomous protein homeostasis

FLP-17’s role in stress resistance aligns with its established functions. FLP-17 belongs to an evolutionarily conserved class, FMRF-amide/RF-amide neuropeptides, that plays important roles in energy balance and reproduction across phyla.34,35 In C. elegans, FLP-17 is secreted from a pair of sensory neurons (BAG) in response to low oxygen and high carbon dioxide, which can be caused by unfavorable food conditions or pathogens.36,37 FLP-17 then acts through specific neurons to inhibit egg laying and initiate an aversion behavior until the animal has reached more favorable conditions.30,36 Interestingly, unfavorable food conditions and pathogens also threaten organismal protein homeostasis.33,38 Therefore, we speculate that FLP-17 evolved to simultaneously protect the animal from proteotoxic stress while facilitating a behavioral program to help the animal navigate to more favorable conditions.

To coordinate adaptive behavioral and metabolic responses, FLP-17 primarily signals through the GPCR EGL-6 in specific neurons.30,31 Therefore, we tested whether EGL-6 also mediates FLP-17’s role in UPRER activation and found that FLP-17-induced activation of the UPRER and ER stress resistance is partially dependent on EGL-6. Egl-6 expression is predominantly neuronal, evidenced by transcriptional reporters and single-cell RNA-seq datasets.30,39 However, low levels of egl-6 expression were detected in intestine-specific translation of ribosome-affinity purification, which may better reflect protein levels.40 This suggests that FLP-17 may signal either through an intermediate cell type (such as a neuron) or directly to the intestine to activate UPRER.30,39 Furthermore, the partial dependence, combined with persistent stress gene activation in egl-6 (lof) backgrounds (Figure 5 E), indicates that additional unidentified receptors and mechanisms likely contribute to FLP-17 phenotypes.

Although FLP-17 was sufficient to activate the UPRER, it was not required for cell non-autonomous activation of the UPRER by glial:: xbp-1s, as flp-17 null mutants did not suppress glial:: xbp-1s phenotypes. This likely reflects neuropeptide network redundancy. Supporting this hypothesis, flp-17 (lof)) resulted in modest upregulation of stress response genes (Figure S3G) and a slight increase in hsp-4p::GFP in the glial:: xbp-1s animals (Figure 2D), suggesting compensatory activation of stress signaling pathways when FLP-17 is absent. This compensation could occur through multiple mechanisms. First, glial:: xbp-1s may induce multiple neuropeptides that provide functionally redundant UPRER activation. While no other candidate from our neuropeptidomics screen was individually sufficient to induce UPRER, we cannot exclude compensation by peptides not detected in our analysis, such as insulin-like peptides.

This Physicist (Unexpectedly) Derived Gravity from Information

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What if gravity is just entropy in disguise? Professor Erik Verlinde joins me to argue that gravity isn’t a fundamental force—it’s thermodynamic, emerging from quantum information the way gas pressure emerges from molecules bouncing around. We explore why spacetime may be stitched together by entanglement, and how dark energy and dark matter both pop out automatically without extra particles or parameters. Verlinde explains why the cosmological constant problem is a red herring, and why there may be no final theory of physics. When asked where the universe comes from, his answer is one word: chaos.

SUPPORT: Support me on Substack: https://curtjaimungal.substack.com/su… me on Crypto: https://commerce.coinbase.com/checkou… Support me on PayPal: https://www.paypal.com/donate?hosted_… JOIN MY SUBSTACK (Personal Writings): https://curtjaimungal.substack.com LISTEN ON SPOTIFY: https://open.spotify.com/show/4gL14b9… TIMESTAMPS:

  • 00:00:00 — Thermodynamic Gravity and Information
  • 00:06:35 — Beyond Effective Field Theory
  • 00:13:08 — Turtles All The Way Down
  • 00:25:41 — Entropy as a Force
  • 00:36:31 — Entanglement and Spatial Connectivity
  • 00:47:31 — Deriving Inertia and F=ma
  • 00:56:41 — De Sitter Space Challenges
  • 01:02:01 — Dark Matter and Milgram
  • 01:11:51 — The Emergence of Time
  • 01:21:01 — Statistical Gravity Fluctuations
  • 01:27:01 — Quantum Computational Complexity
  • 01:36:01 — Physics Intuition and Mentorship
  • 01:47:31 — Beauty, Garbage, and Chaos

LINKS MENTIONED: Papers, books, websites:

Videos:

  • • A 2 Hour Deep Dive into Entropy
  • • The Mathematics of String Theory [Graduate…
  • • The Debate That Divides Physics: Is the Un…
  • • The Physicist Who Found Quantum Theory’s U…
  • • Retrocausality & The Transactional Interpr…
  • • The Physicist Who Proved Entropy = Gravity
  • • The Physicist Who Says Time Doesn’t Exist
  • • The Most Astonishing Theory of Black Holes
  • • The (Simple) Theory That Explains Everythi…
  • • The Crisis in String Theory is Worse Than…
  • • Dark Dimensions: NEW THEORY Unifying Dark…
  • • MIT Scientist’s Discovery: “Black Holes Mi…
  • • The Woman Who Broke Gravity | Claudia de Rham
  • • Solving the Problem of Consciousness | Ste…
  • • Frederic Schuller: The Physicist Who Deriv…
  • • The Loop Quantum Gravity Debacle: Carlo Ro…
  • • An (Elementary) Introduction to Quantum Co…
  • • Can Physics Explain Its Own Laws?
  • • The Nobel Laureate Who (Also) Says Quantum…
  • • This Cosmologist Discovered Something Stra…
  • • Michael Levin: Consciousness, Biology, Uni…

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TIMESTAMPS: 00:00:00 — Thermodynamic Gravity and Information 00:06:35 — Beyond Effective Field Theory 00:13:08 — Turtles All The Way Down 00:25:41 — Entropy as a Force 00:36:31 — Entanglement and Spatial Connectivity 00:47:31 — Deriving Inertia and F=ma 00:56:41 — De Sitter Space Challenges 01:02:01 — Dark Matter and Milgram 01:11:51 — The Emergence of Time 01:21:01 — Statistical Gravity Fluctuations 01:27:01 — Quantum Computational Complexity 01:36:01 — Physics Intuition and Mentorship 01:47:31 — Beauty, Garbage, and Chaos.

Continue reading “This Physicist (Unexpectedly) Derived Gravity from Information” | >

Deep Dive: The Agentic AI Economy

The Moat: The moat is no longer how smart your AI is; it’s what your AI is allowed to touch. An agent that has “Write Access” to a company’s internal financial system or a medical record database is 100x more valuable than a “smart” chatbot that can only read public websites. Connectivity is the new Intellectual Property.

In the agentic economy, the most valuable human skill isn’t “coding” or “writing”—it is Agentic Orchestration.

The agentic economy thrives on Data Flywheels. As an agent performs a task (e.g., “Review this legal contract”), it gets human feedback (“This clause was too aggressive”). That feedback isn’t just a correction; it’s training data that makes the agent more valuable for the next task. This creates a winner-take-all dynamic for whoever has the most active agents in a specific niche.

We are moving toward an outcome-based economy. However, the real “gold rush” isn’t in building the smartest AI; it’s in building the safest and most connected AI—the one that humans trust enough to give the “keys” to their bank accounts, their calendars, and their businesses.

Universal Bridge Theorem

We proved that our Universe was made from AI Algorithm.

What if spacetime itself is the result of a gigantic self-learning quantum neural network? 🤯🌌

A new framework called the Universal Bridge Theorem (UBT) proposes a deep equivalence between:

🧠 Neural network training.
and.
🌌 The evolution of spacetime geometry.

The proposal combines:

4-octyl itaconate inhibits cytokine-mediated inflammation via alkylation of TYK2 and JAK1

Li et al. discovered that 4-octyl itaconate (4-OI) directly covalently modifies TYK2 and JAK1 to inhibit the type I interferon response. Endogenous metabolite itaconate in sepsis is a JAK inhibitor. In the mouse, in vivo experiments, intraperitoneal injection of 4-octyl itaconate could alleviate multi-organ damage caused by sepsis.

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