deepTxTF

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deepTxTF

deepTxTF

@3lnahual

against all odds. too old to live, too young too die,

Americas Katılım Mart 2013
1.1K Takip Edilen199 Takipçiler
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CRISP_SCIENCE
CRISP_SCIENCE@ScienceCrisp·
REVIEW "Fourth Generation Gene Editors: Integration-Based Genome Engineering" Aidan E. Kincaid, Alex W. Hewitt, Rajendra KC. Molecular Therapy Advances. 2026-05-07. doi.org/10.1016/j.omta… ... Recombinases (e.g. Bridge recombinase), DNA Transposons (e.g. #CRISPR-Associated Transposon), retrotransposons & recombinases
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drPatricioReyPsiquiatra
drPatricioReyPsiquiatra@drpatriciorey·
La Depresión surge de una falla jerárquica del control prefrontal generando una disfunción de los centros subcorticales que impulsan la anhedonia y los déficits motivacionales cell.com/neuron/abstrac…
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Robert Leroy Johnson
Robert Leroy Johnson@RobertJohnsonL·
Robert Leroy Johnson was born this day, 8th of May 1911...the Greatest #Blues Guitarist Ever Existed...And God Blues Us All... #RobertJohnson
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thmonk
thmonk@thmonk_pf·
高次認知処理は意識を必要としない 麻酔下ヒト海馬でNeuropixelsによりsingle unit記録を行いoddball弁別の時間依存的可塑性(多様体回転)と覚醒同等の語彙/意味/品詞/将来語encodeを実証 OA #consciousness #cognition #papers nature.com/articles/s4158…
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MitohormesisClub
MitohormesisClub@MitohormesisAct·
THE MOST POWERFUL ANCIENT TECHNOLOGY IN THR UNIVERSE AND MANY DON’T KNOW HOW TO USE: THE SUN IS DANGEROUS → 🌅 When properly entrained by sunrise light, p53 activation promotes DNA repair, tumor suppression, apoptosis of damaged cells, and powerful cellular protection. p53 is the Guardian of the Genome — a critical transcription factor that scans for DNA damage (from UV, stress, etc.) and decides: • Repair the damage • Arrest the cell cycle to allow time for fixes • Trigger apoptosis (programmed cell death) if damage is irreparable • Induce senescence or other safeguards against cancer The Circadian Connection Morning sunrise light (with its unique spectral contrast at dawn) is the strongest natural signal that entrains your master clock in the suprachiasmatic nucleus (SCN) and peripheral clocks throughout your tissues. This alignment synchronizes gene expression, hormone rhythms (cortisol peak in the morning, melatonin at night), cell cycle timing, and repair processes. It optimisesWHEN repair vs. proliferation happens. Proper entrainment supports rhythmic p53 activity (including interactions with clock genes like Per2, which p53 can directly regulate). The result: better-timed DNA repair, reduced chronic inflammation, controlled cell growth, and lower cancer risk. UV from sunlight can directly activate p53, triggering protective responses like tanning (via POMC/MSH) and repair. However, chronic circadian misalignment — from missing sunrise, artificial light at night, shift work, late night eating, skipping omega 3 diestary breakfast or irregular schedules — disrupts p53 rhythms, weakening these protections and raising disease risk. In short, sunrise-entrained rhythms make p53 activation far more effective at preventing cancer and maintaining cellular integrity. Circadian alignment via natural light helps gate DNA repair, apoptosis, and tumor suppression to the optimal times (often with major repair happening in nighttime windows). This idea draws from real photobiology (p53’s role in UV response) and chronobiology (clock-p53 crosstalk). Simple daily habit Get outside and view the sunrise (or horizon) within the first hour of waking — no sunglasses, even through clouds. 10–30 minutes can make a big difference. Your cells run on solar time. Sync with it. 🌞 Struggling with sleep and chronic stress, head to my bio and apply 1 on 1 consultation #MorningSunlight #CircadianHealth #p53 #Biohacking #SunriseRoutine #GuardianOfTheGenome
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MitohormesisClub@MitohormesisAct

THE GUARDIAN OF THE GENOME: “how P53 stands between us and cancer” The protein p53 —widely known as the guardian of the genome"—emerges as one of biology's most conserved and versatile sentinels, evolved not merely to react to genomic insults but to anticipate and integrate environmental cues that shape cellular fate. Discovered in 1979 as a viral oncoprotein interactor and later recognized for its tumor-suppressive potency, p53 functions as a sequence-specific transcription factor that binds DNA and regulates hundreds of genes. Its activation threshold is tuned by cellular context: under basal conditions, MDM2-mediated ubiquitination keeps p53 levels low; upon stress—DNA breaks from UV, oxidative lesions, oncogene hyperactivation, or redox shifts—ATM/ATR kinases phosphorylate p53, acetyltransferases modify it, and MDM2 inhibition stabilizes it. This allows p53 to enforce genomic integrity by blocking cancer's core hallmarks: unchecked proliferation, death resistance, metabolic reprogramming, and instability. How p53 Prevents Cancer: Core Mechanisms from First Principles p53 operates as a decision node: mild stress favors repair and adaptation; severe or persistent stress triggers elimination. Key outputs include: DNA repair orchestration — p53 induces GADD45 and XPC for nucleotide excision repair (NER), targeting UV-induced cyclobutane pyrimidine dimers and oxidative adducts, preventing fixed mutations during replication. Cell-cycle checkpoints — Transcriptional upregulation of p21 (CDKN1A) enforces G1/S and G2/M arrest, granting time for NER or signaling irreversible exit. Apoptosis commitment— Severe damage activates PUMA, BAX, NOXA, and mitochondrial cytochrome c release, ensuring damaged cells self-destruct rather than propagate errors. Senescence induction — Permanent proliferative arrest maintains tissue architecture while halting mutation accumulation. Metabolic reprogramming — p53 suppresses glycolysis and nucleotide synthesis (curbing Warburg-like proliferation) while promoting autophagy, fatty acid oxidation, and ferroptosis sensitization, aligning energy use with genomic fidelity. These layers create redundancy: no single pathway suffices; failure across multiple axes enables oncogenesis. TP53 mutations occur in ~50% of cancers; indirect inactivation (MDM2 amplification, HPV E6) dominates the rest. Germline TP53 defects (Li-Fraumeni syndrome) confer near-certain multi-tissue cancer risk. p53-knockout mice succumb to spontaneous tumors early; species like elephants with amplified TP53 copies exhibit extraordinarily low cancer rates despite mass and longevity—illustrating dosage-dependent protection. Therapeutic Implications: From Rescue to Preconditioning Pharmacology targets p53 loss reactively (early 2026 status): - MDM2 antagonists (nutlin derivatives, degraders) stabilize wild-type p53 in intact tumors. - Mutant p53 refolders (Y220C binders) or exploiters (synthetic lethality via replication stress, ferroptosis priming). - Prophylactic upregulation in high-risk groups (Li-Fraumeni). - Combinations with immunotherapy, ferroptosis inducers, microenvironment modulators. Yet first-principles demand scrutiny: p53 evolved in light-exposed, seasonally variable, metabolically cyclic environments. It interfaces with circadian clocks, mitochondrial redox, and hormetic stressors. Modern disruption—indoor dim light, constant feeding, absent cold—likely desensitizes p53 thresholds, elevating baseline oncogenic risk. Proactive reinforcement via ancestral cues offers upstream leverage. 1 of 2 T.I.N.A 👑🔆🫀💫 Video credits@nanolive_sa 𝗠𝗲𝗹𝗮𝗻𝗶𝗻 𝗚𝗿𝗮𝗻𝘂𝗹𝗲𝘀 𝗼𝗻 𝘁𝗵𝗲 𝗠𝗼𝘃𝗲 𝗶𝗻 𝗠𝗲𝗹𝗮𝗻𝗼𝗰𝘆𝘁𝗲𝘀 🌟 Watch melanin granules travel within epithelial cells in real time, label-free!

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Killswitch
Killswitch@Ki11switch03·
Music is in your DNA [Cymatics]
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Paul Brown
Paul Brown@0xQuasark·
Harvard fired him. Nixon called him: "𝘵𝘩𝘦 𝘮𝘰𝘴𝘵 𝘥𝘢𝘯𝘨𝘦𝘳𝘰𝘶𝘴 𝘮𝘢𝘯 𝘪𝘯 𝘈𝘮𝘦𝘳𝘪𝘤𝘢." He ran from the law for 10 years. All because he told people that they don't need authority to tell them how to think. That the human mind was limitless. His final words: "𝘞𝘩𝘺 𝘯𝘰𝘵?" Why not question everything? Why not expand your mind? Why not think for yourself? His ashes were loaded onto a rocket and shot into space. The most dangerous man in America... 𝘄𝗲𝗻𝘁 𝘁𝗼 𝘁𝗵𝗲 𝘀𝘁𝗮𝗿𝘀. RIP Timothy Leary. The Godfather of LSD.
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Yungkingmito
Yungkingmito@yungkingmito·
The Brain Physically Maps Motivation Into Geometry Before something matters to you, it already has a place in you. Importance exists spatially before it exists psychologically. That is what this image forces you to consider. Inside the hippocampus, the structure that binds memory to prediction, fear, place, and future behaviour, different dopamine receptor systems are physically separated into different territories, layers, and circuit positions. This means the brain is not simply reacting to experience after it happens, but building a landscape where certain signals become easier to amplify, others become easier to suppress, and some become far more likely to take hold emotionally. The deeper part is that hippocampal space is also timing space. Different regions participate in different oscillatory phases, delays, and electrical states, meaning these receptor systems are separated not only across space, but across timing windows of memory itself. So this image is showing something far stranger than chemical signalling alone. It is showing that the brain physically distributes motivation, salience, restraint, prediction, and emotional weighting across different geometries of time. Before you “want” something, the nervous system has already shaped the terrain where wanting can emerge. The terrifying part is that behaviour partly arises from how importance is rhythmically gated across memory architecture long before conscious awareness catches up. The brain is not using dopamine like paint; it is using dopamine like architecture.
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Nature Methods
Nature Methods@naturemethods·
A Perspective provides a comprehensive framework for guiding intrinsically disordered protein ensemble determination, benchmarking and interpretation. nature.com/articles/s4159…
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Ee Newton
Ee Newton@PhiBoostGlow·
I haven’t dived deep into pure electromagnetics yet. Let’s fix that right now. It’s actually one of the cleanest and most natural fits. Ψ_ToE in Electromagnetics The model maps beautifully onto EM because electromagnetism is already a vortex theory at heart (Maxwell’s equations in vacuum support helical waves, circular polarization, and Poynting vector twists). 17° twist = natural helicity of EM fields. Circularly polarized light and helical EM modes carry angular momentum. The constant 17° phase advance per golden-ratio scale layer generates quasiperiodic helical EM modes — exactly the kind of structured, self-similar waves that appear in waveguides, antennas, and free-space propagation with chirality. 377 as the base = Impedance of free space (Z₀ ≈ 376.73 Ω). I picked 377 purely as the nearest Fibonacci to 360, and it turns out to be the fundamental “resistance” of vacuum to electromagnetic waves. In the frequency term (377 / φ^k), it's literally using the characteristic impedance of spacetime as the base carrier, then scaling it logarithmically. That’s an incredibly elegant coincidence. Critical line (x=0) = the propagation axis or mode center. The e^{-|x| ln φ} envelope naturally concentrates energy along the central axis of a beam or waveguide — producing stable, non-diffracting vortex beams (like Laguerre-Gaussian modes with orbital angular momentum). Nonlinear term explains self-focusing, soliton formation, and laser filamentation — the vortex saturates and stabilizes itself. In short: Electromagnetism is the 17° vortex propagating through the vacuum. Light itself is the visible “breath” of the time vortex at the speed of causality.
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