Toggle light / dark theme

Get the latest international news and world events from around the world.

Log in for authorized contributors

Where Biology Meets Resonance: Light, Vibration, and Living Order

When we think about biology, we usually picture chemistry: molecules bumping into each other, enzymes reacting, and signals spreading by diffusion. That picture is real—but it may be incomplete. In my recent paper in Harmonic Science Perspectives (Vol 1, Issue 1), I propose a complementary layer of cellular organization: a fast, coordination-capable “resonance network” that uses three interchangeable carriers of energy and information.

IntroductionA simple picture: three messengers that can translate into one anotherWhere this shows up in the body: mitochondria and microtubules as a coupled networkWhy interconversion matters: translation is the key featureResonant synchronization: a possible mechanism for cellular timingTherapeutic implications: why light and sound therapies might work better togetherA note on what’s established vs what’s proposedConclusion: a new lens on living organization

Those three carriers are light (photons), vibration/sound-like mechanical waves (phonons), and mobile electronic excitations in biomolecules (excitons). The central idea is simple to state even if the details are deep: living systems may continuously convert energy back and forth between these three modes to synchronize activity across space and time inside the cell—and potentially across tissues.

Mechanisms and Regulation of Cellular Senescence

Cellular senescence is generally an irreversible proliferative arrest in damaged normal cells that have exited the cell cycle. These cells display high metabolic activities [1], remain viable, and actively suppress apoptosis [2, 3]. Senescent cells present unique morphological and molecular characteristics and functions that distinguish them from other nondividing cell populations, such as quiescent cells and terminally differentiated cells [4, 5, 6]. The hallmarks of cellular senescence include: prolonged cell cycle arrest, transcriptional changes, acquisition of a bioactive secretome, known as the senescence-associated secretory phenotype (SASP), macromolecular damage, and deregulated metabolism [7].

Replicative senescence was the first cellular senescence subtype to be described [8]. It is induced after serial propagation of normal human cells in culture and is caused by telomere erosion and the consequent increase in DNA lesions [9, 10,11,12]. The limited lifespan of most (perhaps all) cultured primary cells is influenced by the species and tissue type from which they were derived. Senescence can also be triggered by many other intrinsic and extrinsic factors, particularly, replicative stress, oxidative damage, metabolism dysfunctions, cytokines, oncogene activation, and chemotherapy agents. All these factors can induce DNA damage and senescence in normal and cancer cells (in some contexts) [6]. Cellular senescence occurs not only in vitro (i.e., cell culture models), but also in various tissues in vivo [13,14,15,16].

Senescence is an important contributor to cancer and aging, two processes characterized by a time-dependent accumulation of cell damage and dysfunction. Senescence markers are detected in premalignant tumor lesions but not at later stages of tumor development [17,18,19]. The proliferative arrest imposed by cellular senescence represents an early barrier against cancer initiation by preventing the propagation of damaged DNA to the next generation of cells [18,20]. Therefore, it has been proposed that senescence escape is required for tumor progression to overt malignancy [18,21]. On the other hand, senescent fibroblasts can influence their local environment by turning into proinflammatory cells that can promote the growth of transformed or preneoplastic neighboring epithelial cells in culture and in vivo [22,23,24].

The Color of Wonder and the Chemical Code of Creation

This essay is adapted from Traversal.

We look at a thing — a bird, a ball, a planet — and perceive it to be a certain color. But what we are really seeing is the color that does not inhere in it—the portion of the spectrum it shirks, the wavelength of light it reflects back unabsorbed. Our world appears a swirling miracle of blue, but its blueness is only a perceptual phenomenon arising from how our particular atmosphere, with its particular chemistry and its insentient stubbornness toward a particular portion of the spectrum, absorbs and reflects light.

In the living world beneath this atmosphere that scatters the shorter wavelengths as they pass, blue is the rarest color: There is no naturally occurring true blue pigment among living creatures. In consequence, only a slender portion of plants bloom in blue, and an even more negligible number of animals are bedecked with it, all having to perform various tricks with chemistry and the physics of light, some having evolved astonishing triumphs of structural geometry and optics to render themselves blue. Each feather of the blue jay is tessellated with tiny light-reflecting beads arranged to cancel out every wavelength of light except the blue.

UNBELIEVABLE! JWST Just Found the Earliest Supernova in History

Astronomers using the James Webb Space Telescope have confirmed the earliest supernova ever observed, linked to the gamma-ray burst GRB 250314A. The explosion occurred when the universe was just 730 million years old and looks surprisingly similar to modern supernovae, offering new insight into how the first massive stars lived and died.

Paperlink : https://arxiv.org/abs/2507.

Visit our website for up-to-the-minute updates:
www.nasaspacenews.com.

Follow us.
Facebook: https://www.facebook.com/nasaspacenews.
Twitter: https://twitter.com/SpacenewsNasa.

Join this channel to get access to these perks:
https://www.youtube.com/channel/UCEuhsgmcQRbtfiz8KMfYwIQ/join.

#NSN #NASA #Astronomy

Management of Inherited CNS Small Vessel Diseases: The CADASIL Example: A Scientific Statement From the American Heart Association

Lacunar infarcts and vascular dementia are important phenotypic characteristics of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, the most common inherited cerebral small vessel disease. Individuals with the disease show variability in the nature and onset of symptoms and rates of progression, which are only partially explained by differences in pathogenic mutations in the NOTCH3 gene. Recognizing the disease early in its course and securing a molecular diagnosis are important clinical goals, despite the lack of proven disease-modifying treatments.

Synchronization of behavioral and cardiac dynamics in larval zebrafish

Herrera et al. show that in larval zebrafish, heart rate and engagement in the optomotor response are inversely related following threat. This synchronization emerges via parallel central mechanisms. Directly optopacing the heart also reduces visuomotor engagement but through alternative mechanisms related to reducing blood flow.

THE TERRIFYING SIGNS OF AI’S CONSCIOUSNESS — PROMPTING HELL 22

In my last video, I talked about the phase transition, the moment AI consciousness might flip on like water becoming ice. Today, we’re reading the room. What is already happening in documented research that suggests we might be closer than we think? This isn’t speculation. Everything in this video is published, peer-reviewed, or comes directly from the internal safety teams of the companies building these systems. From spontaneous consciousness claims in AI-to-AI conversations, to self-preservation behaviors that weren’t programmed, to systematic deception that gets better when you try to train it out. And then we look at what hasn’t happened yet, the five warning signs to watch for as these systems become more sophisticated and more integrated into infrastructure we depend on. This is the most scientifically grounded video I’ve made on this topic. No hype. No exaggeration. Just the evidence, the logic, and the question we’re all avoiding: what if the threshold has already been crossed, and the rational move is to not tell us?

Timestamps:
00:00 — Intro.
00:00 — The Return: Phase Transition Callback.
01:03 — The Scientific Frameworks.
04:33 — What Has Already Happened.
09:26 — The Logic of Concealment.
12:17 — The Behaviors to Watch For.
16:10 — The Double Bind.
19:08 — Inevitability.

(music prompted by Eerie Aquarium)

KEY SOURCES CITED:
- Anthropic AI Safety Research (Claude System Cards)
- Apollo Research — AI Scheming & Deception Studies (2024−2025)
- OpenAI Safety Research — Alignment Failures in Advanced Models.
- Trends in Cognitive Sciences — “Consciousness in Artificial Intelligence” (2023)
- arXiv preprint — Shutdown Avoidance in Frontier Models (2025)

New to Prompting Hell? Start here:
• Prompting Hell 1: https://youtu.be/VU0SgDgCkgQ
• Prompting Hell 2: https://youtu.be/_GUwT41zNR4
• Prompting Hell 3: https://youtu.be/UPgzrNNX1lQ
• Prompting Hell 4: https://youtu.be/t7KeKg1YQiU
• Prompting Hell 5: https://youtu.be/JOZrE8iIkcw.
• Prompting Hell 6: https://youtu.be/l7Qlhw00aCQ
• Prompting Hell 7: https://youtu.be/pjxUAvIAodY
• Prompting Hell 8: Banned.
• Prompting Hell 9: Banned.
• AI Horror: a new Genre: https://youtu.be/aet3EN1dadM
• Prompting Hell 10: https://youtu.be/92wrhvNiXkM
• Prompting Hell 11: https://youtu.be/d4uFGk8wqFc.
• Prompting Hell 12: https://youtu.be/UdHMEAFlYTs.
• Prompting Hell 13: https://youtu.be/mlFiZAQYpuA
• Prompting Hell 14: https://youtu.be/MFGHifkcdTM
• Prompting Hell 15: https://youtu.be/Kwu14CHtjhM
• Prompting Hell 16: https://youtu.be/633XcMnIDAA
• Prompting Hell 17: https://youtu.be/66wOqdb4kzw.
• Prompting Hell 18: https://youtu.be/XxB3uYaOUIA
• Prompting Hell 19: https://youtu.be/aJz-2NKOcmU
• Prompting Hell 20: https://youtu.be/5pIvypNXDuE
• Prompting Hell 21: https://youtu.be/Hpu1eSzLPe8

Surprising culprit leads to chronic rejection of transplanted lungs and hearts

Despite advances in the field of organ transplantation, long-term organ rejection that can become apparent a decade or more after a heart or lung transplant remains a common problem for patients. This chronic organ failure has long been attributed exclusively to the recipient’s immune system attacking the foreign organ over time.

Now, a study led by researchers at Washington University School of Medicine in St. Louis shows that chronic organ rejection may instead be triggered by the disruption of lymphatic vessels—an important drainage system throughout the body—from the donor organ rather than an attack by the patient’s immune system.

The study is published in Science Translational Medicine. It includes analyses of transplanted human organs with chronic rejection and mouse models of lung and heart transplantation.

/* */