Scientists have revealed a downscaled, lab-sized, high-energy ultrafast laser to the size of a matchhead, enabling futuristic technologies.
Abstract Despite substantial progress in identifying neural correlates of consciousness, no unified quantitative framework currently derives a formally specified order parameter for conscious-state organisation from established neurophysiological principles, or links thalamocortical coordination dynamics to measurable state transitions across pharmacological, pathological, and perturbational conditions through a single computational formalism. We propose a neurocomputational theoretical framework in which conscious states are associated with metastable regimes of large-scale thalamocortical coordination operating near critical dynamical boundaries. The framework is formalised through a dynamic coordination functional Φ(t), defined as a surface integral over the thalamocortical interface and directly operationalisable from high-density EEG as a weighted combination of gamma-band power spectral density, thalamocortical coherence, and theta-gamma phase-amplitude coupling. The thalamic reticular nucleus (TRN) is identified as the anatomical implementation of the control parameter governing proximity to the critical point, grounded in a Wilson-Cowan model of TRN inhibitory gating whose bifurcation structure is characterised computationally. Numerical simulation of the linearised field equation on the thalamocortical boundary demonstrates internal consistency: the simulated system produces power-law recovery dynamics tau_rec proportional to | θ — θ _c|^v with nu consistent with model A universality class [0.5, 1.5], and a Kuramoto mean-field derivation establishes that Φ(t) emerges as the natural order parameter of coupled thalamocortical oscillators rather than being postulated. The joint (|Φ(t)|, Var[|Φ(t)|]) phase space correctly separates simulated waking, anaesthetic, ictal, and minimally conscious regimes without parameter fitting to empirical data. All simulation code is publicly available. Six quantitatively specific, independently falsifiable predictions are derived across five experimental domains: power-law Gamma Dip scaling in near-threshold EEG with a specific exponent range; causal disruption of thalamocortical coherence by selective TRN silencing; opposite EEG scaling exponent deviations in ASD versus schizophrenia; systematic Φ_est collapse under propofol anaesthesia correlated with PCI; Φ_est as a real-time consciousness biomarker in disorders of consciousness; and clinical validity of Φ_est in disorders of consciousness and ictal state discrimination by the metastability index. Each prediction is stated with quantitative thresholds and a pre-specified falsification criterion. The framework provides: the first anatomically specified and formally derived order parameter for conscious-state organisation directly operationalisable from passive EEG; a mechanistically grounded identification of the TRN as the dynamical control parameter, testable by a single optogenetic experiment; and a computationally validated, pre-registerable programme of six falsifiable predictions defining a tractable empirical agenda. Φ_est would constitute a candidate real-time consciousness biomarker if the framework’s predictions are confirmed in purpose-designed experiments.
High-density electrophysiology devices allow neuroscientists to observe spikes from large populations of neurons, and optogenetics allows them to drive or suppress those spikes. We show that a single device can combine these two capabilities, providing a high-resolution means to both read and write neural activity in the living brain.
If Scientists Already PROVED We’re In A Simulation?
Bell’s theorem. Maldacena’s holographic proof. Wheeler’s participatory universe.
Three independent bodies of peer-reviewed physics — all pointing at the same unsettling answer.
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Bell’s theorem. Maldacena’s holographic proof. Wheeler’s participatory universe.
Three independent bodies of peer-reviewed physics — all pointing at the same unsettling answer.
What if the simulation hypothesis isn’t a thought experiment? What if the physics we already have — quantum entanglement, the holographic principle, the measurement problem — is the proof?
In this video, Harvard theoretical physicist Lisa Randall walks through the three experiments and mathematical proofs that, taken together, describe a universe that functions in every measurable way like a simulation. Not as metaphor. As structure.
We cover:
→ Alain Aspect’s 1982 Bell test experiment and what it actually proved about local reality.
→ The Bekenstein-Hawking holographic bound — why information scales with surface area, not volume.
→ Maldacena’s AdS/CFT correspondence — the proof that a 3D universe is dual to a 2D information system.
→ Wheeler’s delayed choice experiment and the participatory universe.
→ What the fine-tuning problem looks like inside a simulation framework.
→ Why you — the observer — are not peripheral to the physics. You are part of the mechanism.
This is Episode 1 of The Proof Series — a weekly deep-dive into peer-reviewed science that challenges everything you think you know about reality.
New episode every Thursday.
— Lisa Randall is a theoretical physicist and professor at Harvard University, author of Warped Passages and Dark Matter and the Dinosaurs, and one of the most cited physicists alive.
#SimulationTheory #QuantumPhysics #HolographicUniverse.
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3. TIMESTAMPS / CHAPTERS
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00:00 — The proof nobody is talking about.
01:10 — What \
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Scientists say that they’ve just detected a massive cloud of gas some 3 billion lightyears in diameter, floating in space roughly 7 billion light years away from us. This is pretty cool, but the problem is that our current models of the universe say that it (and other massive structures like it) just shouldn’t exist. Let’s take a look.
Paper: https://arxiv.org/abs/2604.
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Findings may warrant exploration of the hormones as glioblastoma treatment.
In a new National Institutes of Health (NIH)-funded study, scientists at Cleveland Clinic discovered that hormones associated with male development may play a key role in limiting the growth of brain tumors in men. The research team found that the loss of androgen hormones, such as testosterone, in a preclinical model of glioblastoma drove tumor growth by inducing local inflammation and triggering the production of stress hormones. In an analysis of data from more than 1,300 men with glioblastoma, the authors found that supplemental testosterone was significantly associated with improved survival, which was consistent with their preclinical experiments.
“This outcome is a welcome surprise and may potentially offer a lead for new treatments for a kind of cancer that is deadlier in men,” said Anthony Letai, M.D., Ph.D., director of NIH’s National Cancer Institute (NCI).