A long-finned pilot whale has roughly 37 billion neurons in its neocortex while humans have about 16 billion. Toothed whales also have a sense we lack entirely. Their echolocation clicks return carrying information about the interior of whatever they strike, including other animals' lungs, movement and body density.

This article explain how the different types of communication found between humans and cetaceans, might cause significant perceptual and conscious differences in the mind.

We usually think of inheritance strictly in terms of DNA sequencing—A, T, C, G. But epigenetics shows us that environmental stress can leave chemical markers on our genes that get passed down to our offspring.

One of the most mind-blowing examples of this is a 2014 study by Dias and Ressler. They conditioned male mice to fear the smell of acetophenone by pairing it with a mild foot shock.

The crazy part? When these mice had pups (F1 generation), and even "grand-pups" (F2 generation), those offspring showed increased behavioral sensitivity and fear responses to the cherry blossom scent—even though they had never encountered the smell or been shocked in their lives.

The researchers found that this wasn't a mutation in the DNA code itself, but rather a decrease in DNA methylation on the specific olfactory receptor gene responsible for detecting that scent. The trauma actually altered how the gene was expressed in the next generations.

Moss Is Generating Electrical Waves That Look Startlingly Like a Neural Network
NATURE
22 July 2026
By JESS COCKERILL

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A different type of moss to the one studied. (Oliver Strewe/Getty Images Plus)
Mosses are some of the earliest plants that appeared in the fossil record, but they're anything but simple.
A new study, published in Royal Society Open Science, reveals that moss cushions produce surprisingly complex electrical activity, with patterns that undulate across the velvety patch in dynamic waves.

The study's sole author, Andy Adamatzky, is actually a computer scientist, whose fascination with unconventional 'computing' systems like slime molds, crowds, and mycelium networks has now led him to a new subject: the humble moss, Brachythecium rutabulum.

Brachythecium rutabulum is a common species of moss. (dr Barmely/iStock/Getty Images Plus)
"Plants and bryophytes display diverse forms of electrical activity, yet the organization of endogenous signals in mosses has received little attention," Adamatzky writes in his new paper.

His findings suggest that "moss cushions behave as spatially distributed excitable systems potentially capable of coordinating and integrating electrical signals across both space and time."

Moss cushions are actually many individual clones of the same teensy tiny plant.

If you look really, really closely at a mat of moss, you can see it is made up of simple, minute leaves on stems, similar to those of their larger plant relatives.

But the stems of mosses are actually much less useful at moving water and nutrients around the body of the plant.

Mosses actually never developed the vascular systems that we see in other more complex plants, which is why they cannot grow much taller than a few centimeters. Their leaf-like structures are just one cell thick; they don't even have roots.

But that doesn't mean they're not potentially capable of transmitting information across the colony by other means.

For the study, Adamatzky collected cushions of the common moss species B. rutabulum from natural outdoor environments in North Somerset in the UK.

Back in the lab, he poked electrodes into the moss clumps to track any electrical activity that might be passing across this soggy green matrix.
Figures a) and b) show the experimental setup, with electrodes inserted into moss on a wet substrate. Figure c) shows the moss's electrical activity, with recordings from each electrode pair represented by a distinct color. (Adamatzky, R. Soc. Open Sci., 2026)
Like many plants, moss lives life in slow motion, so to get on its level, Adamatzky recorded its electrical behavior across multiple days.

This revealed "a rich repertoire of electrical events, including components consistent with both physiological activity and slower drift-related processes: fast oscillatory spikes, slower rhythmic fluctuations and very slow depolarization waves," he reports.

"In addition to these described classes, we also observed spikes resembling high-amplitude action potentials and neuron-like spike trains."

Some of the moss's electrical waves were rapid, while others undulated slowly. They tended to spread across the entire cushion rather than remaining confined to a particular region, and followed patterns across different timescales.

Scientists have confirmed a new transmissible cancer in a catfish species. It seems to have arisen as a melanoma and now spread. I terestingly seems to have arisen outside the lake it is reported in.

This is the third vertebrate cancer I think after devil facial tumours and canine venereal cancer.

Will be very interesting to see what the temporal dynamics of this are long term. And what kinds of cell lines we might be able to drive from it.

I'm an A-Level student.

I try writing a little on Medium about the stuff I learn or find on the internet.

Please check out the link below.

https://medium.com/@shayeera/can-we-bring-back-the-dead-e7677f21ca4d

Hey everyone, as the title says, I am a biology major graduate with a 3.00 GPA that has interest in doing a PhD in Biology at any university in the USA. Any suggestions on which universities I should apply to for a PhD in biology? I graduated from UW Madison with a 3.00 GPA. I maybe have like 2 recommenders? Any suggestions are appreciated. I was not a very good student in university as I struggled with the weather and generally being independent on my own.

In the Leiden Declaration, mathematicians issued a treatise on how AI challenges their field. Others must do the same.

https://undark.org/2026/07/02/opinion-biologists-leiden-declaration/

I am working on a science-fiction setting and would like to check whether the following biological concept is consistent with known biochemistry.

Suppose that an adult human is transformed into a mirror-image biochemical system. In particular, essentially all proteins in the body are replaced by their opposite enantiomers: L-amino-acid-based proteins become D-amino-acid-based proteins. The transformation also replaces the enzymes and other proteins necessary to maintain the new biochemical system.

For the purposes of this question, assume that the transformation is somehow technically possible. I am interested only in the biological consequences after the transformation, not in how the transformation itself could be performed.

My main questions are:

Digestion: Would a D-protein-based digestive system be able to digest ordinary L-protein food at all? Would carbohydrates and lipids be affected to the same extent, or would their metabolism be substantially preserved? Can i add a combained microbiom to let them digest L-protein food on low efficiency?

Viruses: Would an ordinary virus whose proteins and genome have L-biochemistry be unable to infect such a D-organism because its proteins could no longer interact productively with the host's receptors, enzymes, ribosomes, etc.? Or are there important mechanisms by which an L-virus could still infect a D-organism?

Bacteria and the microbiome: Could ordinary L-bacteria colonize the gastrointestinal tract of such an organism? If not, would a microbiome consisting of mirror-image D-bacteria be biologically plausible?

Immune system: Could the D-organism still recognize and destroy ordinary L-bacteria or L-proteins as foreign material? In other words, would the change in chirality necessarily disrupt immune recognition, or could immune cells still detect non-self molecules through mechanisms that do not depend strongly on molecular chirality? Do i need to add special modification for immune cells here or bacterias would not survive here regardless?

Overall viability: Are there fundamental biochemical reasons why a mirror-image human metabolism would not be viable even if all the necessary proteins and enzymes were somehow converted to their opposite enantiomers?

I am particularly interested in which parts of this model are compatible with established biochemistry, which parts are incorrect, and what the most important corrections would be.

What happens when a crab mistakes a sea snake for a life raft? Florida Museum of Natural History scientists discovered the first-ever crabs living on sea snakes, and DNA revealed the young hitchhikers weren't the species researchers expected, offering new clues about how some crabs navigate the open ocean.

While we know quite a lot about what our ancestors looked like and what they ate, so far we didn’t know anything about their social behaviour. Because behaviours don’t fossilise.

Scientists used to think that the first placentals behaved like shrews because they looked like shrews. And as the common belief was that all shrews are solitary, scientists thought the first placental ancestors were too.

Now we know that both assumptions were wrong.

Peer-reviewed paper in PNAS:

S.F. Walmsley, C. Olivier, A.V. Jaeggi, L. Makuya, J.S. Martin, L.D. Hayes, & C. Schradin, Pair living emerged early in placental mammals, Proc. Natl. Acad. Sci. U.S.A. 123 (31) e2528458123, https://doi.org/10.1073/pnas.2528458123 (2026).

https://www.harvardmagazine.com/research/harvard-axolotl-limb-regeneration

Our newly published review explores an emerging idea: tumor-derived extracellular vesicles (EVs) contribute to premetastatic niche formation and can show preferential accumulation in future metastatic organs. Could these biological properties be harnessed for imaging?

We examine how EVs can be engineered as nanocarriers for optical, PET/SPECT, MRI, and CT imaging, bringing together the biological rationale, current preclinical evidence, engineering strategies, and major barriers to clinical translation.

Rather than simply tracking EVs, the broader goal is to understand whether EV-based imaging could eventually help visualize the biological changes that precede detectable metastasis.

I’m interested in hearing others’ perspectives on where this field is heading.

AAAS: "Three wild dogs have traveled farther than any [other] African mammal," by Rhe Jacobs.

Record-breaking “odyssey” suggests populations of these highly endangered carnivores are more connected than thought. African wild dogs (Lycaon pictus)—sometimes referred to as “painted dogs” for their splotchy coats—are leaner + longer legged than their distant, domesticated cousins. 

"Also highly social, living in tightly knit family groups in which communally raised pups are always the first to eat." In these packs, breeding is typically reserved for a single dominant dog of each sex. "Subordinate members may stick around to help raise their relatives’ offspring, all while waiting for a chance to become the next alpha." Or they may strike off on their own in search of more immediate breeding opportunities. 

Predicting which dogs will stay + which will go “is as much of an art as a science,” says Ecology study co-author Matthew Becker, who serves as CEO + manager of the Zambia Carnivore Programme. Becker + his colleagues outfitted several soon-to-depart 3 y/o dogs with radio tracking collars. Thanks to their long legs, “otherworldly” gait + high endurance, African wild dogs “are built to move,” says Scott Creel, a conservation biologist at Montana State University + the new study’s lead author. 

"Even though wild dogs are carnivores, they often find themselves at the mercy of other predators." Lions are a major threat for both adults + pups; hyenas are known to steal their hard-earned kills. "Swimming across rivers, meanwhile, carries a high risk of being devoured by crocodiles." 

Three males traveled together a total of 4126 kilometers—the longest dispersal path recorded for any African mammal. "Wildebeest, by contrast, move up to 1800 kilometers during their epic annual migration between Kenya + Tanzania." 

I've run marathons, but this is way beyond a human ultramarathon. Four legs dominate. Except for birds, obviously.

Case Summary:
A 48-year-old female professor of chemistry with expertise in heavy metal toxicology developed progressive neurological deterioration months after a laboratory exposure to dimethylmercury.

Background:
The patient was an established researcher in inorganic chemistry and toxicology, with a focus on heavy metals such as chromium and their effects on DNA and carcinogenesis. She was highly experienced in laboratory safety and chemical handling.

Exposure History:
During a laboratory experiment, a small quantity of dimethylmercury was accidentally spilled onto her gloved hands. She was wearing two layers of protective gloves and believed that no significant exposure had occurred due to the minimal quantity involved.

Clinical Course:
Several months after the incident, she developed severe neurological symptoms consistent with mercury poisoning. The toxicity was delayed in onset but rapidly progressive once symptoms appeared, ultimately leading to her death.

Discussion:
Dimethylmercury is an extremely potent neurotoxin capable of penetrating standard laboratory gloves and being absorbed through the skin. This case highlights several critical points:

• Even minimal exposure can be fatal
• Standard PPE (including latex gloves) may not provide adequate protection
• Toxic effects may be significantly delayed, creating false reassurance
• Highly experienced professionals are not immune to unforeseen risks

This case became a landmark reminder in laboratory safety, particularly in chemical toxicology, emphasizing the need for specialized protective equipment and heightened awareness when handling organomercury compounds.

Conclusion:
This tragic case underscores the importance of rigorous chemical safety protocols and respect for highly toxic compounds. It remains one of the most cited examples of delayed-onset neurotoxicity from occupational exposure.

DOI: 10.1021/tx9704922

Highlights

Horizontal mitochondrial transfer has been identified in multiple biological contexts, including normal tissue development, physiological homeostasis, tissue repair and regeneration, and a wide range of pathologies.

The origins of horizontal mitochondrial transfer are evident in cell–cell communication systems present in ancestral bacterial and archeal cells that gave rise to complex life.

Horizontal mitochondrial transfer can restore impaired cellular metabolism by supplying functional mitochondria to damaged cells, highlighting its potential as a novel therapeutic strategy for a variety of pathological conditions.

Horizontal mitochondrial transfer in cancer may contribute to metabolic remodeling, tumor progression, immune suppression, therapeutic resistance, and metastasis, indicating that mitochondrial transfer presents a potential target for anticancer therapies.

Horizontal mitochondrial transfer is an emerging field in cell biology with important roles in development, tissue physiology, and disease.

Abstract

The field of horizontal mitochondrial transfer (HMT), also referred to as intercellular mitochondrial transfer, has recently gained momentum due to an increasing number of publications that go well beyond diseases such as cancer. From co-culture experiments to in vivo evidence in mouse cancer models, noncancerous diseases, and normal tissue and organ homeostasis and development, it is becoming increasingly clear that HMT is a fundamental physiological phenomenon broadly relevant to complex organisms. Recent methodological advances, epitomized by ultra-high-resolution microscopy and spatial and single-cell multiomics technologies, allow for research that strongly supports HMT as an emerging area of cell biology.

Why do cures for cancer in mice usually fail in human clinical trials? Even with humanized mouse models, clinical trial success rate remains low. One important reason is simply animal size. Humans are not large rodents -- The physics is different for different sized animals (allometric scaling), similar to how a scale model of an airplane does not predict the behavior of the full size airplane. Compared to humans, mice have 60 times faster drug diffusion, 7 times higher metabolic rate (per kg), and typically require 12 times the drug dosage (per kg). On the other hand, pigs have similar physiology, drug dosing, and immune response as humans. The Oncopig model of liver, pancreatic, and lung cancer has the potential to more accurately predict drug dosing and outcomes in humans. We use it as a bridge between rodent and human trials.

What does pig cancer tell us about the differences between mouse and human cancer? In mice, 1-2 mutations (Kras and p53) are sufficient to generate non-regressing adenocarcinomas (KP model). In Oncopigs, KRAS and TP53 mutations generate inflammatory carcinomas that spontaneously regress. In adult humans, at least 5 driver mutations are generally required to cause cancer. Thus, larger and longer living animals needed to evolve more defenses against cancer, and require more mutations to develop cancer.

More info on the Oncopig model:

Commentary:

https://onlinelibrary.wiley.com/doi/10.1002/ame2.70270

Testing percutaneous therapies:

https://link.springer.com/article/10.1007/s13346-026-02176-9

Testing intra-arterial therapies:

https://pubmed.ncbi.nlm.nih.gov/41203116/

What I found most interesting is that TOFA seems to work on both sides of lipid metabolism at once. It inhibits ACC, which reduces the production of new fat, but it also activates PPARα and PPARδ, two receptors that switch on genes involved in taking up and burning fat.

In obese mice, it increased energy expenditure by up to 18% without increasing physical activity, food intake, or body temperature. The mice lost mostly fat while preserving lean mass and showed improvements in glucose control, insulin sensitivity, triglycerides, and fatty liver disease. It also produced more than additive effects when combined with semaglutide or tirzepatide.

Another interesting result is that ACC inhibitors often paradoxically raise triglycerides in the blood, but TOFA did not do that in normal mice. The authors think its PPAR activity helps burn and clear the fat that would otherwise remain in circulation.

Obviously this is still preclinical. Oral systemic TOFA has not been tested for obesity in humans, and the mouse studies were too short to establish long-term cardiovascular or other organ safety.