Beloved Pharaoh. Born: June 3rd., 2003 – Died: June 19th., 2017. A very special dog that will never be forgotten.
Dogs live in the present – they just are! Dogs make the best of each moment uncluttered by the sorts of complex fears and feelings that we humans have. They don’t judge, they simply take the world around them at face value. Yet they have been part of man’s world for an unimaginable time, at least 30,000 years. That makes the domesticated dog the longest animal companion to man, by far!
As man’s companion, protector and helper, history suggests that dogs were critically important in man achieving success as a hunter-gatherer. Dogs ‘teaching’ man to be so successful a hunter enabled evolution, some 20,000 years later, to farming, thence the long journey to modern man. But in the last, say 100 years, that farming spirit has become corrupted to the point where we see the planet’s plant and mineral resources as infinite. Mankind is close to the edge of extinction, literally and spiritually.
Dogs know better, much better! Time again for man to learn from dogs!
Meet Lola: a loving rescue pup who knew something was wrong when it mattered most.
Back in 2025, team members at National Mill Dog Rescue saved Lola from a commercial breeding facility where she’d spent eight years confined to a small space with very little enrichment.
NATIONAL MILL DOG RESCUE
Given her difficult past, rescuers feared Lola might have a hard time adapting to rescue life. But Lola quickly proved them wrong.
“Despite everything she had experienced, Lola emerged as a happy, friendly little dog with so much love still to give,” a rescue representative told The Dodo.
A few months later, Lola met the Mullane family, and they instantly connected.
NATIONAL MILL DOG RESCUE
“From the moment they met her, Lola delighted them with her adorable little butt wiggle and radiant grin,” the representative said. “Choosing to bring her home was an easy decision for them. We were so happy to watch Lola head off to begin this next chapter of her life.”
About a year later, rescuers received an incredible update from Lola’s parents. According to a family member, Lola had been acting “funny,” lying on top of her grandpa and repeatedly nudging him, as if trying to signal that something was wrong.
Lola’s grandpa, who suffers from colon cancer, wasn’t feeling well, and he took Lola’s persistent nudges as a sign that he should go to the emergency room.
NATIONAL MILL DOG RESCUE
A few hours later, doctors confirmed that Lola’s grandpa was in kidney failure. Had he waited any longer, things could have been much worse.
“Lola may have saved his life that day,” National Mill Dog Rescue wrote in a Facebook post.
Rescuers are so proud of Lola, a dog who loves boldly, despite her years spent in solitude.
“We’re incredibly grateful for the role she has played — and continues to play — in the lives of the Mullane family,” the representative said. “They gave Lola a second chance, and in an extraordinary way, Lola was there when her family needed her most.”
ooOOoo
It has been said countless times before – dogs are beyond special. The bond they make with us humans is so beautiful, and this true story about Lola and the Mullane family is wonderful.
The Conversation Weekly podcast talked to Karl Deisseroth, a neuroscientist at Stanford University, about his journey developing optogenetics and its potential to treat a wide range of neuropsychiatric conditions. What follows is an edited transcript of the podcast.
Take us back to the early 1990s. You’re training to be a doctor and you start a rotation working with psychiatric patients. What questions about the brain did that raise for you?
Both basic neuroscience (people asking how the brain works) and clinical neuroscience (doctors trying to help people with brain disorders) have faced a very similar problem, which is the brain is quite mysterious and quite hard to study.
It’s billions of fragile, transparent, very fast-acting cells, buried within the skull and doing very complex things. We don’t have a good model for how the brain works, unlike the heart, which is very obviously a pump. We don’t actually know what the brain’s trying to do.
A lot of neuropsychiatric treatments are not as effective as they could be, and developing new ideas has been hard. The treatments we had were not grounded in a solid understanding of the cells involved. What are the cells actually doing? What are they trying to do? This was a problem that held back treatment.
When I was in psychiatry training in the early 2000s, and also as a medical student in the late 1990s, I was very much impressed with the magnitude of the challenge.
You went on to get a Ph.D. in neuroscience, and then you set up a lab at Stanford trying to understand how to control particular cells in the brain. What were the first experiments you did?
I have a background in molecular biology, and I knew how to work with genes. So I was motivated to see if we could use genetics to make a treatment or an intervention that targets one kind of cell.
Every cell has genes that tell it what to do. Different cells in the brain, just as other parts of the body, can be genetically targeted because different cells have different jobs. A cell that is a dopamine neuron has all the machinery needed to make the hormone dopamine. It uses different genes than a cell that makes the hormone serotonin, so they can be distinguished from each other.
And so the thought was maybe I could have a way of controlling just the dopamine cells or just the serotonin cells by inserting a specific gene into them. But I didn’t know what would work well, so I tried inserting different types of genes into neurons.
Some of the genes I tried were quite conventional; they were genes from mammals that I thought might affect the activity of neurons. But one was a gene from a single-celled algae – a microbe that converts light to energy. This gene coded for a light-activated protein called channelrhodopsin-2 that Peter Hegemann and Georg Nagel identified a few years earlier.
And I thought it was worth a try. It was the least likely to work, but why not try it?
And amazingly, that was the one that worked. The genes that were lower risk didn’t work, and this gene from a single-cell microbe actually did.
Walk us through what you did. You inserted the gene into rat cells, right?
I had a preparation of cultured rodent neurons in a dish – basically a 24-well plate that let me look at many different conditions at the same time in different wells of this plate. This let me test side by side the conventional mammalian genes and this gene from the algae.
So the first step was to get the genes into the cells. Then I exposed some plates of cells to light, while others I did not. I used a test to see which cells had activated.
When I looked across the cells in the screen, I found that the ones that had the algae gene and had gotten light were showing this marker of activation, whereas the others had a much lower signal. That was a really thrilling moment because it showed that this gene from a photosynthetic single-celled organism – almost as far as you can possibly be from mammals evolutionarily – was working beautifully in fragile mammalian neurons.
It was a moment of a lot of pressure and complexity, but also delight.
You went on to name your method optogenetics – the ability to control specific nerves using light in the brain – and you soon went on to using it to control living mice in various ways. What was it like in those first few years of working with live animals?
This was an experiment that was very visible and easy to understand. The right side of the brain controls the left side of the body and attention to the left side of the world. We put in a fiber optic into the right part of a mouse motor cortex – the part that controls movement – and when we flipped the switch, the mouse immediately began going left in circles.
And then as soon as we turned off the laser light, it stopped and just looked up at us, as if nothing had happened.
That, coupled with the first experiment – those were transcendent moments.
What changed in your understanding of the brain in the moment you were able to switch particular neurons on and off?
We understood that the technique would probably work to help us understand the brain better at that moment. And then we immediately started applying it to all sorts of different cells where things were mysterious – where nobody knew or couldn’t prove exactly what one cell type or another was doing in perception and cognition and action.
The general applicability became clear over the subsequent years.
Researchers are now using optogenetics in attempts to restore sight in people with visual impairment. How does that work?
In 2010, two of my colleagues in Europe were interested in delivering one of these light-activated proteins to human eye samples – specifically the retina of the eye – which worked very well.
So they did careful studies in monkeys and in people. And in 2021, just five years ago, they published a paper showing they could confer light sensitivity back to the retinas of a person who was completely blind from a neurodegenerative disease called retinitis pigmentosa.
That’s what we call direct optogenetics. It’s somewhat complicated because you have to deliver the gene and light to the person.
Karl Deisseroth, left, and his wife, Michelle Monje-Deisseroth, were at home when they were notified of his Nobel win. AP Photo/Noah Berger
And going back to your psychiatric patients, who you still see in the clinic today, how do you hope optogenetics will be able to help them?
There’s a much easier and more broadly impactful avenue that we call indirect optogenetics, which uses the knowledge that comes from studying which cells matter in a symptom and then designing medications that target those cells. This is something we’ve really lacked in neuropsychiatry for a long time.
Indirect optogenetics is making strong headway for autism and schizophrenia. There are trials that are moving to their final stages for those disorders.
My particular clinical specialty is autism, and I see the difficulties that come with irritability and anxiety in these patients. And I can see optogenetics leading to new medications that will help.
An enzyme found in the brain could help to preserve cognitive resilience with advancing age, according to research in mice, humans and cells1.
Researchers found that high levels of the enzyme are linked to low levels of inflammation in the brains of aged mice. They also showed that the enzyme boosts the growth of neurons in ageing brains. The findings were reported on 15 October in Nature Neuroscience.
The enzyme seems to act “as a compensatory cognitive-resilience mechanism”, says study co-author Amar Sahay, a neuroscientist at Massachusetts General Hospital in Boston.
“This is a fantastic, very thoughtful approach to get at what could be protecting neurons,” says Timothy Hohman, a neuroscientist and geneticist at the Vanderbilt Memory & Alzheimer’s Center in Nashville, Tennessee, who was not involved in the study. “This is a great example of how you can use a model system to get at some of these resilience mechanisms that are super challenging to study in humans.”
ooOOoo
Maybe, just maybe, the workings of the human brain is not such a mystery as it used to be.
Here in Southern Oregon I look up at the birds in the sky, some flying solo, or with a few companions, some flying in larger groups. But I never reflect on birds that migrate.
The truth, that these small animals were traveling thousands of miles across the planet, must once have seemed just as improbable.
Then, in the early 1800s, dramatic evidence emerged supporting the theory of migration. White storks began appearing in Germany with African arrows embedded in their bodies. These birds became known as pfeilstörche, or “arrow storks.” They provided compelling evidence that birds disappearing from Europe were traveling all the way to Africa and back.
Almost two centuries later, scientists are still asking the same question, but our ability to answer it has been transformed.
For most of ornithological history, scientists understood migration through brief glimpses of a bird, a specimen collected somewhere else, or the rare instance of a banded bird recovered hundreds or thousands of miles from where it had been marked. From these fragments of intelligence, scientists reconstructed journeys that took place largely beyond their view.
Today, it’s possible to see the journeys themselves, almost in real time.
A century of following birds
Bird banding was the first tool used to attempt a systematic approach to connect these fragments of information. Since the early 1900s, researchers have placed uniquely numbered metal bands on birds and hoped someone, somewhere, would encounter them again.
Over the past quarter-century or so, the tools used to determine where birds go have changed dramatically.
Tracking devices can now be carried by increasingly smaller birds, recording their movements and communicating with land-based receivers or satellites orbiting the earth. Testing stable isotopes in feathers and other tissues can reveal where a bird originated. Genetic testing can distinguish populations.
Millions of observations by bird-watchers submitted to eBird, an online database to record the birds they see, show the distribution and abundance of birds across a continent throughout the year in ways early ornithologists could scarcely have imagined.
Collectively, these methods open an extraordinary new window into migratory birds and one of nature’s most remarkable behaviors: migration.
Burrowing owls breed in the Western U.S., raising their young in burrows often taken over from ground squirrels or prairie dogs. In winter, they migrate to Southwestern states, Mexico or Central America. John Anderton/The Atlas of North America’s Migratory Birds
Discovering unknown migrations
More than 70% of North American bird species are migratory. Yet scientists have known surprisingly little about where specific populations go.
A species like the American robin may breed across thousands of miles of North America, with different breeding populations migrating to entirely different places for the winter. Birds breeding in one part of the continent may travel one route and encounter one set of environmental conditions, while members of the same species experience a completely different set of conditions along another route.
These connections between where a bird breeds and where it spends the winter is called migratory connectivity. They are critical for understanding everything from the consequences of climate change on birds to how avian pathogens and diseases spread, to a species’ basic ecology.
We are ornithologists and conservation scientists who have spent almost 15 years along with a team of contributors compiling this rapidly expanding knowledge on bird movement into The Atlas of North America’s Migratory Birds. The atlas, being published on Nov. 3, 2026, by Princeton University Press, covers the latest information on seasonal movements for nearly 600 species and combines a century of bird-banding data with eBird observations, tracking studies, stable isotope testing, genetics and other sources of information.
What emerges is a picture of migratory birds that is both more complicated and more remarkable than the simple arrows pointing between breeding and wintering ranges on a map.
Consider the yellow-billed cuckoo. These birds breed over a wide range of the eastern two-thirds of the U.S. but migrate to a relatively small wintering area in the Gran Chaco region of northern Argentina, Paraguay and southern Bolivia.
In contrast, peregrine falcons that breed in Alaska migrate almost directly south, dispersing across the Americas to wintering grounds that extend as far as southern South America.
Discoveries like these are accumulating rapidly. Collectively, they amount to a renaissance in our understanding of animal movement never before imagined.
Living masterpieces
The more clearly scientists can follow individual birds and populations across the planet, the more extraordinary these species can seem.
They navigate landscapes and respond to winds, weather, food and environmental conditions across enormous geographic scales.
The Atlas of North America’s Migratory Birds’ combines illustrations and maps to show where bird populations go when they migrate. Princeton University Press
We see these species and their migrations as among evolution’s great living masterpieces. That’s why we combined science with natural history and artist John Anderton’s extraordinary illustrations of the birds themselves. The maps allow us to see where birds travel, and the art brings the species to life.
Together, they make visible something that humans could only imagine for most of our history.
A map for conservation
North America has lost about 3 billion birds during the past half-century, and many migratory species continue to decline.
To understand why a population is declining and help save it, researchers need to understand the species’ entire annual cycle: its critical stopover habitats, wintering grounds and threats along its migration routes.
For much of the history of ornithology, scientists studied birds primarily during their breeding season. That made practical sense. Birds are conspicuous then – singing, defending territories, building nests and raising young.
But a migratory bird may spend only a few months of its life in its breeding grounds. Conditions such as weather, food availability and habitat quality encountered during migration can determine whether an individual survives to breed again.
All of this knowledge has accumulated because people value birds and have devoted enormous time and effort to understanding them.
For more than a century, thousands of bird-banders have woken up before the crack of dawn to set traps, carefully place bands on birds’ legs and release them, often knowing the chances of ever learning what happened to those individuals were exceedingly small.
More recently, tracking technology has allowed researchers to follow individual birds across continents and oceans. Those tracks exist because scientists, students, technicians and others have spent countless hours attaching and recovering tags, and contributing and sharing their data. https://www.youtube.com/embed/xfiY0tTjKxA?wmode=transparent&start=0 In this animation, Cornell’s Bird Lab traced the routes of 15 species using tracking signals. From tiny sensors to networks of humans with binoculars, efforts to understand migrations are helping to show where cruicial habitat can be preserved.
Today, millions of bird-watchers contribute observations that, thanks to advances in data science, allow us to watch migration unfold across an entire continent.
Scientists today know more about where migratory birds go, how populations are connected and what they encounter along the way than at any previous point in history. That knowledge is helping to identify where conservation efforts can make a difference for the future.
How much rain can a hurricane make, and how much do big versus small hurricanes make? – Naarah, age 8, Pittsburgh
Hurricanes can produce enormous amounts of rain, adding up to trillions of gallons of water. But the big risk isn’t their total amount – it’s how much rain falls on each location.
So, what causes that much rain, and does the size of the storm matter?
I’m an atmospheric scientist who teaches college students about weather at Georgia Tech. Let’s take a look at where a hurricane’s rainfall comes from and some of the questions about hurricanes and their rainfall that scientists are still trying to answer.
Sea surface temperatures on Oct. 6, 2026, show the very warm water in the western Gulf of Mexico, where a tropical storm grew into Hurricane Isaias the following day. Water that is over 80 degrees Fahrenheit (26.5 degrees Celsius) can fuel hurricanes. NOAA
The magic number for surface water temperature to be able to fuel a hurricane is at least 80 degrees Fahrenheit (26.5 degrees Celsius). At that temperature and above, the warm ocean water evaporates into the air, changing from liquid to vapor. As it makes that change, it provides energy to fuel the storm and also adds moisture to the atmosphere that eventually falls as rain.
Another very interesting post from The Conversation
When a hurricane moves over warm water, especially when the warm water extends many feet below the surface, the storm pulls in even more energy and moisture.
What affects hurricane size and rainfall?
This is one of the many questions about hurricanes that atmospheric scientists are working on.
The average hurricane is about 300 miles (482 kilometers) wide, but hurricanes – or typhoons, as they’re called in the western Pacific of the Northern Hemisphere – can be much bigger or smaller.
Super Typhoon Tip in 1979 grew to half the size of the lower 48 U.S. states. It had a radius of about 690 miles (1,110 kilometers), measured from the center of the storm to its outer edges, meaning it was 1,380 miles (2,222 kilometers) wide. Tropical Storm Marco’s gale-force winds in 2008, in comparison, had a radius of 11.5 miles (18.5 kilometers), meaning it was about 23 miles (37 kilometers) across – not much larger than New York City.
How the largest tropical cyclone in recorded history and the smallest compare. It’s quite a difference! NOAA
In 2025, scientists published a study showing that hurricane size appears to be influenced by how warm the ocean water is compared to its usual temperature that time of year. So, if a hurricane moves over water that is much warmer than normal, it tends to grow in size rapidly as well as growing in strength.
A recent hurricane that was very large in size was the extremely destructive Hurricane Helene in 2024. As Helene moved over water near Florida that was much warmer than normal for late September, it picked up lots of moisture that it carried all the way to the mountains of North Carolina. Several days of rain from the storm caused catastrophic flooding there.
Hurricane Andrew wasn’t very big when it made landfall on Elliott Key, Fla., near Miami, on Aug. 24, 1992, but it was powerful and extremely destructive. National Hurricane Center
A strong storm isn’t necessary for a lot of rain to fall. Tropical Storm Allison in 2001 is still one of the wettest tropical weather events in U.S. history. It caused over US$4 billion in damage in Texas alone, and it didn’t even develop into a hurricane!
So, what really leads to the highest rainfall totals?
Hurricanes that move slowly or nearly stop along their path usually cause the biggest rainfall problems because their rain keeps falling over the same location. The rain may be just as intense in a fast-moving hurricane, but it doesn’t stick around as long.
If a storm moves fast, like Hurricane Michael did in 2018 when it hit the Florida Panhandle, its winds and storm surge can make a big mess, but its rainfall totals will be lower.
Hurricane Michael passes over Mexico Beach, Fla., on Oct. 10, 2018. The storm moved quickly, so it brought less rainfall to each location compared to slow-moving Hurricane Harvey in Texas the previous year, but its wind and storm surge caused catastrophic damage. NOAA NESDIS
So, a hurricane can be large or small in size and still have a big impact, depending on how slowly it’s moving.
There is still a lot to learn about hurricanes. Some big questions involve what’s known as rapid intensification. That occurs when a tropical storm’s maximum wind speed increases quickly, by 30 knots (about 34.5 miles per hour or 55 kilometers per hour) or more within 24 hours.
When rapid intensification occurs, as happened with hurricanes Harvey, Michael and Helene before they hit land, the storm can surprise coastal residents and become catastrophic.
Hurricanes of all sizes can be dangerous, so accurate forecasting well before they reach land is crucial to help people prepare for their impacts. One very important area of research that today’s scientists – and future scientists – can work on is improving forecasting so coastal residents know what’s coming and have time to prepare.
Hello, curious kids! Do you have a question you’d like an expert to answer? Ask an adult to send your question to CuriousKidsUS@theconversation.com. Please tell us your name, age and the city where you live.
And since curiosity has no age limit – adults, let us know what you’re wondering, too. We won’t be able to answer every question, but we will do our best.
The changing weather is a frequent topic on all communication channels.
Here in Merlin, Southern Oregon, we have had weeks of drought, and what had been forecasted for early next week as rain showers has now been changed to cloudy conditions.
Have you ever taken months off training – maybe due to an injury, a new baby or crushing work deadlines – and come back convinced you were starting from zero?
Research from our team has some good news: At the cellular level, you probably weren’t.
We found that muscle and liver cells store memories fromevery training session in ways that may help improve endurance, control blood sugar levels and even slow weight regain after inactivity.
Use it or lose it? Maybe not
For most of the past century, long before fad diets and fancy workout trends took off, exercise was considered one of the most effective lifestyle changes to lower the risk of heart disease, Type 2 diabetes, several cancers and early death for people of all ages. But people typically understood exercise as something whose beneficial effects fade away over time: You use it or lose it.
When you stop training, your maximum oxygen uptake, muscle gains and insulin sensitivity drift back to where they started, often within weeks. Physical activity guidelines are built on this fact, which is why they emphasize consistency above all else.
Consistency, however, is a luxury that roughly 3 in 4 American adults aren’t able to enjoy. People can experience injuries, illness, pregnancy or jobs that limit their time for or ability to exercise. If adaptation really resets, every time you step into the gym would be as if you’ve never been there before. But that scenario doesn’t match what coaches and returning athletes typically describe: In practice, people who have trained before can get fit again faster than those who haven’t undergone similar training.
In recent years, however, scientists have started challenging the concept of “use it or lose it.” New research hints that your cells might keep a record of your training history so all of your gains are not completely lost.
More than muscle
We areexercise physiologists who study how cells remember exercise. Our lab and others have shown that the body is able to store a form of exercise memory across different organs.
To study how this exercise memory works, our team of researchers use an ON-OFF-ON exercise training protocol in mice, which involves an initial four- to eight-week training period, followed by detraining – a period of no exercise – and a second training bout. This method allows us to examine how cells form a memory of exercise, maintain a record of exercise through detraining, and recall memories of prior training when exposed again to exercise.
Using this strategy, our team found that skeletal muscle memory accelerates muscle growth. Compared to mice with no training history, mice who retrained grew bigger muscles, and the individual muscle fibers inside those muscles grew too. Larger muscle fibers meant that the working cells were themselves getting bigger, rather than the surrounding tissue.
Looking more closely at these muscle cells, we found that retrained muscle is better at matching energy production to demand – meaning, the muscles were better at drawing from energy stores when it’s needed most – and this ability persists without further exercise. This memory held even when the mice ate a high-fat diet, suggesting that prior training can still offer benefits even when diet is working against those gains.
Muscle isn’t the only body part that learns from exercise. Working muscle needs fuel, and the liver supplies it during and after training sessions.
My colleagues and I found that liver cells also store exercise memory and uses it to feed muscle more efficiently. In both mice and people who trained, stopped, then trained again, their livers released higher levels of a family of enzymes called carboxylesterases. These enzymes chop up lipids circulating in the blood, delivering fat in a form that muscle can take up and burn as it grows.
A record that outlives you
Recorded cellular memories of exercise may even be passed down to future generations.
In mice, we found that three to four weeks of maternal and paternal endurance exercise can have a lasting effect on their offspring. Compared to offspring born to sedentary parents, parental exercise granted protection against poor blood sugar levels and excess weight gain for an entire year after birth.
But there remains much to be discovered on how parents influence the health of their children and whether their lifestyle could provide a fitness advantage across generations.
Every cell remembers
Biology has traditionally granted memory to a short list of cells. Neurons store memory in the connections between them. Immune cells store memory so they can recognize pathogens faster and more strongly the next time they encounter them.
Researchers previously considered all other cells to be memoryless; a cell responds to a signal, then returns to baseline without keeping a record of that interaction. But that assumption is now coming apart.
Skin stem cells can keep a record of inflammation, allowing them to heal a new wound faster months later. Human fat cells keep a record of obesity that persists even after substantial weight loss, which may account for why you gain weight faster when switching back to a high-calorie diet – the so-called yo-yo effect.
We propose that every cell in the body remembers exercise, regardless of how little or how much someone trains. The question is how long these records are stored and whether researchers could prolong or expand each cell’s storage capacity. Better understanding of how cells learn and remember exercise, where they store memories and how those memories are preserved could help improve exercise guidelines for those who cannot exercise for prolonged or consistent periods of time.
To be clear, none of these findings are evidence for skipping the gym; nothing in our data suggests the effects of past training can substitute for present training. But there is hope that the work you put into getting in shape isn’t completely lost over time.
Somewhere, deep in your cells, there is a record waiting to be replayed the next time you lace up your running shoes, pick up a pair of dumbbells or want to fulfill a New Year’s resolution.
There were many aspects of this applied health science that surprised me, and I suspect will surprise others. It is another supporting reason why I go cycling three or four times a week.
