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Comment by Dr. Krishna Kumari Challa on January 7, 2026 at 2:23pm

Yet from the viewpoint of classical mechanics, compartmentalization and reaction selection—the "constraints" imposed at a system's boundaries—should have no cost at all, as they are treated as fixed external conditions that do not contribute to entropy production.
Researchers now developed a method to calculate these overlooked costs to rank the pathways. This allows researchers to assess their biological efficiency—valuable information for evolutionary studies exploring how life emerged on our planet.
devised a general method to estimate the thermodynamic costs of metabolic processes systematically. In their framework, the cell is imagined as a system crossed by a constant flow, where, for instance, one molecule (a nutrient) enters and another (a product or waste) exits.

Given the underlying chemistry, one can generate all chemically possible pathways that convert the input into the output. Each pathway has its own "thermodynamic cost." Instead of calculating energy in the classical sense, the method estimates how improbable it would be—in a world driven solely by spontaneous chemistry—to see the network (the set of molecules and reactions that convert input to output) behave in exactly that way.

This improbability has two components. The first is the maintenance cost, meaning how unlikely it is to sustain a constant flow through a certain pathway. The second is the restriction cost, which measures how unlikely it is to block all the alternative reactions in the network while keeping only the pathway of interest active.

The calculated improbability represents the cost of that process, which can then be used to classify metabolic pathways according to how "expensive" it is for the cell to keep one pathway active and silence the others.
Part 2

Comment by Dr. Krishna Kumari Challa on January 7, 2026 at 2:21pm

The (metabolic) 'cost of life': New method quantifies hidden energy costs of maintaining metabolic pathways
A new thermodynamic framework quantifies the hidden energetic costs required to maintain specific metabolic pathways and suppress alternatives, beyond direct metabolic energy use. This method ranks pathways by their maintenance and restriction costs, revealing that nature often selects the least dissipative routes, providing insights into the evolution and selection of metabolic processes.

There are "costs of life" that mechanical physics cannot calculate. A clear example is the energy required to keep specific biochemical processes active—such as those that make up photosynthesis, although the examples are countless—while preventing alternative processes from occurring.

In mechanics, no displacement implies zero work, and, put simply, there is no energetic cost for keeping things from happening. Yet careful stochastic thermodynamic calculations show that these costs do exist—and they are often quite significant.

A paper published in the Journal of Statistical Mechanics: Theory and Experiment (JSTAT) proposes a way to calculate these costs from a thermodynamic perspective and thus to offer a new tool for understanding the selection and evolution of metabolic pathways at the root of life.

When, in an ancient ocean, a handful of organic molecules formed an external boundary—the first cell membrane—a sharp distinction between an inside and an outside appeared for the first time.

From that moment on, that primordial system had to invest energy to maintain this compartmentalization and to select, among the many chemical reactions that could occur, only a few metabolic pathways capable of exploiting valuable substances taken from the "outside" and transforming them into new products. Life was born together with this effort of compartmentalization and choice.

Metabolic processes have a direct energetic cost, but they also require an "extra cost" to keep steering chemical flows into a preferred pathway rather than letting them disperse into all physically possible alternatives.

Part 1

Comment by Dr. Krishna Kumari Challa on January 7, 2026 at 2:06pm

Cohort groups included 13,957 children conceived via assisted reproductive technology and 55,828 children conceived naturally after 1:4 matching by maternal age, neonatal sex, and birth month.

Asthma, allergic rhinitis, and atopic dermatitis were analyzed and reported individually, allowing a child to receive one, two, or all three diagnoses during follow-up. Mean follow-up for asthma measured 7.99 years in the assisted reproductive technology group and 8.41 years in the control group, with allergic rhinitis at 5.79 and 6.34 years, and atopic dermatitis at 7.34 and 7.62 years.
Intracytoplasmic sperm injection use showed no statistically significant differences in risk estimates across the three outcomes. Adjusted hazard ratios measured 1.04 for asthma, 0.99 for allergic rhinitis, and 1.04 for atopic dermatitis.

Fresh embryo transfer carried a higher allergic rhinitis risk than frozen embryo transfer, with an adjusted hazard ratio of 1.12. Asthma showed no statistically significant difference between fresh and frozen embryo transfer, with an adjusted hazard ratio of 0.96, and atopic dermatitis showed no statistically significant difference, with an adjusted hazard ratio of 1.01.

Interaction testing showed no statistically significant interaction between intracytoplasmic sperm injection and embryo type for asthma, allergic rhinitis, or atopic dermatitis.
Researchers conclude that children conceived via assisted reproductive technology had a higher risk of developing asthma, allergic rhinitis, or atopic dermatitis than children conceived naturally. Findings supported an association between assisted reproductive technology conception and later atopic disease development across the outcomes evaluated.

Yao-Chi Hsieh et al, Atopic Disease Development in Offspring Conceived via Assisted Reproductive Technology, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.51690

Part 2

Comment by Dr. Krishna Kumari Challa on January 7, 2026 at 2:05pm

Assisted reproductive technology associated with higher risk of childhood atopic diseases

Researchers  report higher risks of atopic disease among children conceived via assisted reproductive technology compared to those conceived naturally.

Assisted reproductive technology use has increased, with estimates placing assisted reproductive technology at 1% to 4% of births, especially in high-income societies, alongside wider use of embryo transfer.

Atopic disease covers three conditions; asthma, allergic rhinitis, and atopic dermatitis. Atopic diseases are believed to be influenced by genetic factors and environmental triggers, with developmental origins of health and disease theory proposing that fetal-stage factors can program changes in organ and tissue structure and function.

In the study, "Atopic Disease Development in Offspring Conceived via Assisted Reproductive Technology," published in JAMA Network Open, researchers conducted a retrospective, population-based cohort analysis to investigate whether conception via assisted reproductive technology was associated with atopic disease development in offspring.

Data came from a pool of 23.5 million people in Taiwan through Taiwan's National Health Insurance Research Database, Assisted Reproduction Database, and the Maternal and Child Health Database.

Assisted reproductive technology included procedures such as in vitro fertilization and embryo transfer, intracytoplasmic sperm injection, gamete intrafallopian transfer, zygote intrafallopian transfer, and tubal embryo transfer.

Part 1

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 9:28am

Tumor bacteria linked to immunotherapy resistance in head and neck cancer

Researchers have discovered that bacteria inside cancerous tumors may be key to understanding why immunotherapy works for some patients but not others.
Elevated bacterial levels within head and neck squamous cell carcinoma tumors suppress immune responses and contribute to resistance against immunotherapy. These bacteria attract neutrophils, which can inhibit the immune activity required for effective treatment. Reducing tumor bacteria with antibiotics may enhance immunotherapy efficacy, suggesting new avenues for patient selection and targeted interventions.

These studies shift the focus of immunotherapy resistance research beyond tumor genetics to unexpected factors like the tumor microbiome.

By identifying bacteria as a key barrier to treatment, we're opening the door to new strategies for patient selection and targeted antibiotic therapies, potentially improving outcomes for those who don't benefit from immunotherapy, the researchers say.

The research confirmed that patients with high tumor bacteria levels had poorer outcomes with immunotherapy compared to standard chemoradiotherapy.

Together, the two studies showed that elevated bacteria levels in tumors attract neutrophils, white blood cells that fight infection. While neutrophils are essential for combating bacterial infections, in cancer they can suppress the immune system needed for immunotherapy to work effectively.

These findings lay the foundation for future research on why bacteria are attracted to tumors and how to modify them to improve treatment.

1. Tumor ecosystem and microbiome features associated with efficacy and resistance to avelumab plus chemoradiotherapy in head and neck cancer, Nature Cancer (2025). DOI: 10.1038/s43018-025-01068-0

2. Nature Cancer (2025). www.nature.com/articles/s43018-025-01067-1

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 9:12am

Two 'survival modes' and why they matter
The researchers identified two archetypes of growth arrest that can both lead to persistence, but for very different reasons:

Regulated growth arrest: a protected dormant state. In this mode, bacteria intentionally slow down and enter a stable, defended condition. These cells are harder to kill because many antibiotics rely on bacterial growth to be effective.

Disrupted growth arrest: survival through breakdown. In the second mode, bacteria enter a dysregulated and disrupted state. This is not a planned shutdown, but a loss of normal cellular control. These bacteria show a broad impairment in membrane homeostasis, a core function needed to maintain the integrity of the cell. That weakness could become a key treatment target.
Antibiotic persistence plays a role in recurring infections across a wide range of settings, from chronic urinary tract infections to infections tied to medical implants. Yet despite intense research, scientists have struggled to agree on a single mechanism explaining why persister cells survive. Different experiments have produced conflicting results about what persisters look like and how they behave.

This study offers an explanation: researchers may have been observing different types of growth-arrested bacteria without recognizing they were distinct.

By separating persistence into two different physiological states, the findings suggest a future where treatments could be tailored, targeting dormant persisters one way, and disrupted persisters another.
How the researchers saw what others missed
The team combined mathematical modeling with several high-resolution experimental tools, including:

Transcriptomics, to measure how bacterial gene expression shifts under stress
Microcalorimetry, to track metabolic changes through tiny heat signals
Microfluidics, allowing scientists to observe single bacterial cells under controlled conditions
Together, these approaches revealed clear biological signatures distinguishing regulated growth arrest from disrupted growth arrest, along with the specific vulnerabilities of the disrupted state.

Adi Rotem et al, Differentiation between regulated and disrupted growth-arrests allows tailoring of effective treatments for antibiotic persistence, Science Advances (2026). DOI: 10.1126/sciadv.adt6577. www.science.org/doi/10.1126/sciadv.adt6577

Part 2

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 9:10am

Bacteria reveal second 'shutdown mode' for surviving antibiotic treatment
Bacteria can survive antibiotic treatment through two distinct growth-arrest states: a regulated, protective dormancy and a disrupted, dysregulated arrest marked by impaired membrane stability. This duality explains conflicting observations of antibiotic persistence and suggests that targeting each state differently could improve treatment effectiveness and reduce infection relapse.

A new study reveals that bacteria can survive antibiotic treatment through two fundamentally different "shutdown modes," not just the classic idea of dormancy. The paper is published in the journal Science Advances.

The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results.

By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.

For years, persistence has largely been blamed on bacteria that shut down and lie dormant, essentially going into a kind of sleep that protects them from antibiotics designed to target active growth. But new research reveals that this explanation tells only part of the story.

The study shows that high survival under antibiotics can originate from two fundamentally different growth-arrest states, and they are not just variations of the same "sleeping" behavior. One is a controlled, regulated shutdown, the classic dormancy model. The other is something entirely different: a disrupted, dysregulated arrest, where bacteria survive not by protective calm but by entering a malfunctioning state with distinct vulnerabilities.

Part 1

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 9:05am

Two white-blooded fish, two paths: Icefish and noodlefish independently lose red blood cell function

Both Antarctic icefish and Asian noodlefish independently evolved to lack hemoglobin and red blood cells, resulting in white blood. Icefish survive in cold, oxygen-rich waters by dissolving oxygen directly in their blood, while noodlefish, living in warmer waters, lost myoglobin and have nonfunctional hemoglobin genes, likely aided by their short, juvenile-like life span. These findings highlight distinct evolutionary paths to similar physiological outcomes.

 Yu-Long Li et al, Independent evolutionary deterioration of the oxygen-transport system in Asian noodlefishes and Antarctic icefishes, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.050

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 9:02am

Evidence of upright walking found in 7-million-year-old Sahelanthropus fossils

Analysis of Sahelanthropus tchadensis fossils using 3D methods identified features unique to bipedal hominins, including a femoral tubercle, femoral antetorsion, and gluteal muscle attachments. These findings indicate that this seven-million-year-old species was adapted for upright walking, making it the earliest known bipedal hominin.

The analysis revealed three features that point to bipedalism in Sahelanthropus:

The presence of a femoral tubercle, which provides attachment for the iliofemoral ligament linking the pelvis to the femur and has so far been identified only in hominins

A natural twist, specifically within the range of hominins, in the femur—or femoral antetorsion—that helps legs to point forward, thereby aiding walking.

The presence, drawn from the 3D analysis, of gluteal, or butt, muscles similar to those in early hominins that keep hips stable and aid in standing, walking, and running.

Scott Williams, Earliest evidence of hominin bipedalism in Sahelanthropus tchadensis, Science Advances (2026). DOI: 10.1126/sciadv.adv0130. www.science.org/doi/10.1126/sciadv.adv0130

Comment by Dr. Krishna Kumari Challa on January 3, 2026 at 8:56am

Ancient African bedrock reveals the violent beginnings of life on our blue planet

Ancient bedrock from the Makhonjwa Mountains reveals that early Earth featured extensive oceans, intense volcanic activity, and a hostile atmosphere rich in methane and CO2 but lacking oxygen. Life began as anaerobic microbes near undersea vents, thriving despite frequent volcanic eruptions, earthquakes, and asteroid impacts. Plate tectonics and a stable climate enabled Earth to remain habitable and blue.

The Oldest Rocks on Earth | Columbia University Press

Ancient African bedrock reveals the violent beginnings of life on o...

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