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Category: biotech/medical – Page 26

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].

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.

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.

Why Nobody’s Talking about Neuralink’s Progress

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Neura Pod is a series covering topics related to Neuralink, Inc. Topics such as brain-machine interfaces, brain injuries, and artificial intelligence will be explored. Host Ryan Tanaka synthesizes information, shares the latest updates, and conducts interviews to easily learn about Neuralink and its future.

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‘Lock-and-key’ chemistry keeps cancer drugs inactive until they reach tumor sites

Many therapeutic molecules used in cancer treatments are highly toxic, often harming healthy tissues and causing significant side effects. This creates a critical need for strategies that localize their toxic activity to tumors. What if cancer drugs could stay dormant until they reach cancer cells? A new study by Syracuse University researchers demonstrates a promising chemistry-based strategy that could do just that.

Xiaoran Hu, assistant professor of chemistry in the College of Arts & Sciences (A&S), and his team introduced a prototyping “lock-and-key” system that holds therapeutic drugs in an inactive, caged form until a separate chemical trigger releases them at a specific site. The study was published in Angewandte Chemie International Edition. It introduces a new platform to control when and where chemical bonds break inside living systems.

“We are developing a broadly applicable tool that has the potential to regulate the activity of different types of therapeutics,” Hu says. “Think of this as a tool, like a hammer, that could be used on different nails.”

Is The Brain an Analog Computer? Consciousness as Dynamic Brainwave Organization | Earl Miller

Professor Earl Miller discusses, Mind-Body Solution podcast.

Earl K. Miller is the Picower Professor of Neuroscience at the Massachusetts Institute of Technology. He has faculty positions in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences. He holds degrees from Kent State University (B.A.) and Princeton University (M.A., Ph.D.) as well as an honorary Doctor of Science from Kent State University.

For decades, neuroscience treated the brain like a digital machine — storing information in synaptic connections and sustaining activity like a switch flipped on. But what if that model is incomplete?

In this conversation, I sit down with Earl Miller, MIT professor and head of the Miller Lab, to explore a growing shift in cognitive neuroscience: the brain may compute using dynamic electrical waves.

We discuss how oscillations coordinate millions of neurons, how waves interact with spikes in a two-way system, why large-scale brain organization may depend on rhythmic patterns, and what this means for artificial intelligence.

Continue reading “Is The Brain an Analog Computer? Consciousness as Dynamic Brainwave Organization | Earl Miller” | >

Abstract: Emily Gutierrez-Morton

Yanchang Wang and colleagues (Florida State University) show that in yeast, polo-like kinase Cdc5 promotes the phosphorylation of SUMO protease Ulp2, reducing its affinity for SUMO chains and thereby facilitating polySUMOylation.

Genetics CellCycle

1Infectious Diseases Division, Department of Medicine and.

2Division of Plastic and Reconstructive Surgery, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.

3Department of Mathematics, Dartmouth College, Hanover, New Hampshire, USA.

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