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Category: biotech/medical – Page 160

DNA as a quantum system in evolution

Time may be viewed as an emergent consequence of increasing information entropy. I explore a toy quantum‑information model in which DNA is treated as an open quantum system. In this framework, weak, time‑dependent perturbations (potentially arising from thermal fluctuations, ionic microfields, metabolic noise, or electromagnetic signals) bias the micro‑timing of events during replication and repair. These slight timing shifts can influence the fate of transient electronic and protonic configurations (including short‑lived tautomeric states driven by proton‑transfer tunnelling), subtly altering mutation probabilities. To test this idea, I map nucleotides in the Mycobacterium tuberculosis genome to constrained qubit states and quantify informational structure using Shannon and von Neumann entropies and coding to non‑coding correlation metrics. Simulations of Hamiltonian dynamics under physiologically plausible perturbations show that real genomic segments exhibit distinctive dynamical signatures compared with controls. I also examine a variant in which a weak, slowly varying external signal is introduced as a background “beat” against which DNA dynamics can be compared. Because a Doppler shift in electromagnetic waves encodes the flow of time through the relative motion of source and observer, a cosmic microwave background (CMB) with a tiny frequency drift provides a conceptual clock and a source of informational entropy: it feeds a time‑correlated input into the DNA quantum system, allowing the molecule to sample cosmic time and translate it into a biological scale by modulating tunnelling probabilities and thus mutation patterns. This CMB‑inspired drive is simply a convenient illustration; the model does not rely on it, and other sources of weakly structured entropy could be tested. Across simulations, sequence‑dependent responses to both intrinsic and structured perturbations generate testable predictions: changing the structure or timing of these weak perturbations should produce reproducible shifts in mutation spectra. This framework connects cellular ageing and evolution to the flow of cosmic time and suggests experiments to probe DNA’s sensitivity to time‑dependent perturbations.

Citation: Garcia NA (2026) DNA as a quantum system in evolution. PLoS One 21: e0344520. https://doi.org/10.1371/journal.pone.

Editor: Yang Jack Lu, Beijing Technology and Business University, CHINA.

Could a gut microbe influence muscle strength?

The trillions of microbes living in the human gut are increasingly recognized as important partners in human health. Scientists have linked the gut microbiome to several aspects of health, from metabolism and immunity to mental health.

A recent study suggests that these microbes may also influence an important aspect of fitness—muscle strength.

Muscle strength is a crucial feature of health for many reasons. It supports our joints and keeps our bones healthy, boosts athletic performance and even plays a role in metabolic health.

Quantitative Measurement of Glycosylated ⍺-Dystroglycan as a Biomarker for Disease Severity in Limb-Girdle Muscular Dystrophy Type 2I/R9

Background and ObjectivesLimb-girdle muscular dystrophy type 2I (LGMD2I/R9) is caused by biallelic variants in the gene for Fukutin-related protein (FKRP), an enzyme required for proper glycosylation of α-dystroglycan (⍺DG), a critical structural protein…

Cuproptosis in cancer: emerging mechanism and therapeutic opportunities

Cuproptosis mechanism in cancer!

As a copper-dependent regulated form of cell death, cuproptosis is critically important for developing targeted cancer therapies and overcoming drug resistance.

A multidimensional framework deciphers the physiological regulation of copper homeostasis, including hepatocentric organ-level regulation, organelle-specific cellular storage and transport, and iron– copper–zinc ion crosstalk.

Cuproptosis is mainly regulated by core cuproptosis proteins, mitochondrial respiratory function, and cellular copper homeostasis.

By depleting glutathione (GSH), alleviating hypoxia, modulating immunity, and enabling multimodal synergy, innovative copper-based nanomaterials enhance copper ion delivery and cytotoxicity, resulting in potent antitumor effects. sciencenewshighlights ScienceMission https://sciencemission.com/Cuproptosis-in-cancer

Cuproptosis is a mitochondria-and copper-dependent regulated form of cell death that has attracted growing interest as a therapeutic strategy in oncology. Its core mechanism involves the aggregation of lipoylated proteins in the tricarboxylic acid cycle to trigger proteotoxic stress and the destabilization of iron–sulfur cluster proteins, leading to mitochondrial dysfunction. These two effects synergize to initiate this regulated form of cell death. Recent studies have expanded this framework, revealing multilayered regulation through the core proteins of cuproptosis, mitochondrial respiratory function, and cellular copper homeostasis. Translational efforts have led to the development of copper-based therapeutics, including ionophores and nanomaterials. The utilization of smart-responsive nanomaterials also offers improved precision in tumor delivery and resistance circumvention.

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3 Billionaires Are (Quietly) Deciding Our Future

Max Tegmark explains why the race to superintelligence is not inevitable, why most people don’t want it, and what we can do about it. He covers the three superpowers of AI, why tool AI can solve our biggest problems without replacing us, and the case for regulating AI like we regulate drugs and airplanes.

00:00 The Race.
00:25 Superintelligence.
01:48 The cage.
03:03 Three superpowers.
05:16 Sandwiches.
11:14 Consciousness.
13:04 Life 3.

Produced by:
https://zeino.tv/

Predicting cardiovascular events from routine mammograms using machine learning

Background Cardiovascular risk is underassessed in women. Many women undergo screening mammography in midlife when the risk of cardiovascular disease rises. Mammographic features such as breast arterial calcification and tissue density are associated with cardiovascular risk. We developed and tested a deep learning algorithm for cardiovascular risk prediction based on routine mammography images.

Methods Lifepool is a cohort of women with at least one screening mammogram linked to hospitalisation and death databases. A deep learning model based on DeepSurv architecture was developed to predict major cardiovascular events from mammography images. Model performance was compared against standard risk prediction models using the concordance index, comparative to the Harrells C-statistic.

Results There were 49 196 women included, with a median follow-up of 8.8 years (IQR 7.7–10.6), among whom 3,392 experienced a first major cardiovascular event. The DeepSurv model using mammography features and participant age had a concordance index of 0.72 (95% CI 0.71 to 0.73), with similar performance to modern models containing age and clinical variables including the New Zealand ‘PREDICT’ tool and the American Heart Association ‘PREVENT’ equations.

Mitochondria power immunity against cancer

Dendritic cells are innate immune cells that regulate the quality, magnitude, and duration of antitumor responses.

Conventional type 1 dendritic cells (cDC1s) are crucial in this capacity but are paradoxically rare and functionally impaired in most solid tumors. This is a major barrier to effective immunotherapy. The molecular underpinnings of cDC1 dysfunction within the tumor microenvironment are poorly understood.

In a new Science study, researchers report that mitochondrial fitness is important for cDC1 function. They also demonstrate the therapeutic rescue of cDC1 function within the tumor microenvironment in mice, which provides a framework for metabolically reprogramming dendritic cells to restore antitumor immunity.

Learn more in a new Science Perspective.

A subset of dendritic cells relies on mitochondrial fitness to trigger antitumor responses in mice.

Irene S. Molina and Malay Haldar Authors Info & Affiliations

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The scientist using AI to hunt for antibiotics just about everywhere

When he was just a teenager trying to decide what to do with his life, César de la Fuente compiled a list of the world’s biggest problems. He ranked them inversely by how much money governments were spending to solve them. Antimicrobial resistance topped the list.

Twenty years on, the problem has not gone away. If anything, it’s gotten worse. Infections caused by bacteria, fungi, and viruses that have evolved ways to evade treatments are now associated with more than 4 million deaths per year, and a recent analysis, published in the Lancet, predicts that number could surge past 8 million by 2050. In a July 2025 essay in Physical Review Letters, de la Fuente, now a bioengineer and computational biologist, and synthetic biologist James Collins warned of a looming “postantibiotic” era in which infections from drug-resistant strains of common bacteria like Escherichia coli or Staphylococcus aureus, which can often still be treated by our current arsenal of medications, become fatal. “The antibiotic discovery pipeline remains perilously thin,” they wrote, “impeded by high development costs, lengthy timelines, and low returns on investment.”

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