Apostles John and Peter by Raphael, circa 1500
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FACTORIES IN ŁODŹ
Sirens roared a hoarse hunger.
The walls thudded a thick pulse,
brick crusted with centuries of soot,
the wire-paneled glass
webbed with cotton dust.
The old owners’ names, in ghost
outline over the wide wing-like gates,
were supplanted with red-lettered signs:
“Lenin Thread Manufacture,”
“Textile Works of the October Revolution.”
But for me the factories
had no names as I passed
through the black walled-in streets,
narcotic with ugliness and rhythm,
the knocking of returning shuttles:
More! More! Again! Again!
A million metal hearts
hammered my lullaby at night.
They repeated like an iron god:
I am that I am that I am.
~ Oriana
The outlines of names of the old owners (all German-sounding; perhaps some of them were Jewish) were visible because the brick was cleaner, protected from the soot by the very letters that were later ripped off when the owners got expropriated after the Communist takeover. So the banner may have said Lenin Threadworks, but high on the factory wall you could plainly read names like Goldstein or Rosenbaum.
The years in Lodz were the happiest time in my childhood. The school wasn’t yet oppressive, and I had plenty of playmates. The city was magical, alive with the rhythm of the giant factory looms. The early version of the poem had these two opening stanzas:
Like the strings of a giant piano –
the looms’ horizontal
music of massive shafts:
axis and thrust,
the surge and ebb of shuttles.
Women in gray scarves like nuns
lifted their arms in fractured time
under rows of spidery lamps.
It was a mysterious different world, whatever happened behind those “wide wing-like gates.”
Mary:
The detail you mention of the old names standing out because beneath the metal letters the brick was cleaner seems ironic — hard to erase those old capitalists!!
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WHAT HAPPENED TO THE REAL CHILDREN IN FAMOUS CHILDREN’S BOOKS
Christopher Robin
Id loved the children for years before discovering they were real. I can almost summon the magic I felt when I first saw the photographs that proved it: the little boy clad in an approximation of hunters’ skins, posing victorious. The dark-haired girl with the offset gaze, her interior expression that of a person just growing used to being looked at.
And – this is the one that really kills me – the big-eyed, dimple-chinned seven-year-old in a soft sweater and tenderly mummish haircut, clutching the teddy bear that would end up even more famous than he would.
The first: Michael Llewelyn Davies, who, along with brothers Peter, John and George, gave their names to three children (and one father) in JM Barrie’s Peter Pan. The second, Alice Liddell, whose dozy journey up the Thames with a storytelling mathematician named Charles Dodgson – later and better known as Lewis Carroll – would flower into Alice’s Adventures in Wonderland, and who served as a model for Carroll’s amateur photography. The last, Christopher Robin Milne, son of AA Milne, whose early years and nursery toys (Winnie-the-Pooh chief among them) would be written into the cosiest paradise in children’s literature, the Hundred Acre Wood.
Alice Liddell in 1858, photographed by Lewis Carroll.
I was terribly jealous of these children. Like most kids, I longed to be noticed, elevated, anointed as extraordinary for doing exactly nothing. If I couldn’t go to Neverland, I wanted at least to be written into it. I think it seemed more glamorous to me at the time (I hadn’t heard of riot grrrls yet) to inspire art than make it.
My perspective shifted as I grew. The photos of Alice – alone, in off-the-shoulder rags like a miniature Carmen, or in a kittenish line with her sisters – began to strike me as troubling. I could no longer push away the reality of the man in the room, watching the child through his camera’s eye.
I learned JM Barrie was a stranger to the Llewelyn Davies boys he met in the park, whose interest in them led to a deep connection with their family. He supported them financially after the death of their father, and became their adoptive parent after the death of their mother – and, allegedly, some business with her will. Whether or not he was ultimately a benevolent figure in their lives, there’s something unsettling about the idea of that transformation: from a stranger admiring children in a public park, to those children’s legal guardian.
And consider Christopher Robin Milne. Raised largely by a nanny then sent to boarding school at nine, to come of age in the ruthless company of peers who met him first as a sweet five-year-old in prim shorts and bobby socks, tromping through a friendly wood in the company of his stuffed animals. Milne would later describe the bullying and humiliation of those years, and his sense that his father’s fame had been won by “climbing upon my infant shoulders, that he had filched from me my good name and had left me with the empty fame of being his son”.
More and more these authors I loved, whose work I still love, began to seem like vampires, or dark puppeteers, their ungainly adult bodies lurking just outside the golden borders of a country – childhood – they can write about but never regain. Further complicating this feeling is the fact that it is, in part, that very longing, that ineffable shadow story of never-again running beneath the brightly lit adventures, that has made them so enduring.
The Children grew from this evolving fascination with both classic fantasy books and the relationship between author and child-muse. It’s the story of Guinevere and Ennis Sharpe, a brother and sister written into the pages of their distant mother’s famed portal series. The childhood she writes for them serves as a candied counterbalance to the one she’s actually giving them, of self-made enchantment and deep neglect in the Northeast Kingdom of Vermont. The narrative is split between the true story of that childhood and the adult lives of the siblings – now estranged – 20 years after their parents’ early deaths left them the sole witnesses to their shared youth and its many secrets.
The siblings have dealt in opposing ways with the fame their mother forced on them, and the world’s hungry insistence that it knows and loves them. But each has turned some part of their past into art. Guinevere has just put her name on a highly sanitized, ghostwritten memoir that presents her early life as just the kind of dreamy romp her mother’s readers have always imagined it to be. Ennis takes a thornier approach: gaining fame through large-scale installations that serve as oblique explorations of their mother’s coveted themes, and some she’d never cop to: doors and thresholds, liminal spaces, the artificiality of all tidy narratives.
Then he announces that, after two decades of silence on the subject, he will be opening a new show titled “Mother”. Fear of what, exactly, he’s planning to reveal sends Guinevere reeling back through their childhood, revisiting with fresh eyes it feral glories and hidden tragedies – and reassessing the true nature of its perilous magic.
Michael Llewelyn Davies aged 6, as Peter Pan, taken by JM Barrie in August 1906.
In creating these grownup children and the invented book series that haunts their lives, I drew first on my early, uncomplicated love of books like Peter Pan and the Chronicles of Narnia (the allegory of which flew directly over my head). But I also wrote from the experience of rereading them as an adult, a writer, a mother, as my fascination with the children behind them curdled into wariness, even pity. As I began to question the adult authors who used their names, their essence, the very fact of their existence as a tantalizing anchor for their fictions, allowing that border between life and story to become tantalizingly blurred.
It isn’t a straight line, childhood literary fame determining adult outcomes. Alice Liddell grew up and apparently thrived, marrying a rich and handsome (if not very good) cricketer, receiving an honorary degree from Columbia, and styling herself as Lady Hargreaves, despite having no claim to the title. Christopher Robin found his own place in the literary world, as a memoirist and owner of a bookshop; he even came around to a more accepting place on the subject of his namesake.
The story of the Llewelyn Davies boys had a sadder end. George was killed in action aged 21, Michael drowned with a friend at 20. Cruelly, bizarrely, a London paper saw fit to include Pan’s famous line in their coverage of the tragedy: “To die will be an awfully big adventure.”
Peter Llewelyn Davies, who maintained that “miseries” were visited upon him owing to Barrie granting his name to the Boy Who Wouldn’t Grow Up, died by suicide at 63. No clean narrative can be made of this; it’s a tragic coda to a well-loved tale.
In the final pages of Peter Pan, coming face to face again with Peter, a now grownup Wendy sends up a plea that she might be young again: “Something inside her was crying, ‘Woman, woman, let go of me.’”
The real people behind these characters make us consider the haunting inverse, which only an enchanted few can understand: the desire to escape the grip of your own child self, trapped in words and images and most of all the hearts of those who love that long-gone version of you, so much they cannot let you go.
https://www.theguardian.com/books/2026/jun/10/peter-pan-christopher-robin-alice-the-unsettling-stories-of-the-children-behind-fictions-most-enduring-tales
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WHY SILENT LETTERS?
Centuries ago, if you talked about a "knight" with a "sword," you actually pronounced the "k," the "gh," and the "w."
Many silent letters used to be spoken aloud, but spoken language evolves rapidly. Over hundreds of years, people naturally stopped pronouncing clunky or difficult consonant clusters. However, the popularization of the printing press froze English spelling in place, leaving those letters on the page as silent ghosts of Middle English pronunciation.
Other silent letters were deliberately inserted by Renaissance scholars wanting to show off their knowledge of classical languages. For example, the word "debt" originally came into English from the French "dette," and it was spelled without a "b" for centuries. But in the 1500s, academics realized the word ultimately traced back to the Latin debitum. They jammed a "b" into the English spelling to reflect its prestigious ancestry, even though no one ever pronounced it.
Scholars did the exact same thing with "doubt" (from Latin dubitare) and "receipt" (from recepta). Sometimes they even got it wrong: they added an "s" to the Old English word iland to make "island" because they mistakenly thought it came from the Latin insula.
The printing press itself introduced its own set of silent additions. Because many of the earliest printers working in England were actually from the Netherlands, they sometimes applied Dutch spelling habits to English words. The silent "h" in "ghost" and "ghastly" is a direct result of Flemish printers setting the type.
Finally, some letters are silent but highly functional. The "e" at the end of "bite" or "cape" makes no sound of its own, but it serves as a marker that tells the reader to stretch the preceding vowel. Similarly, the "u" in "guest" or "guitar" ensures the "g" is pronounced with a hard sound rather than a soft one.
Ultimately, these silent characters turn the dictionary into a fossil record. Every unpronounced letter tells a specific story about where a word came from, who printed it, or how people used to speak. ~ SepiaGlyphs, Quora
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WHAT WOULD HAPPEN IF PUTIN GOT ASSASSINATED?
As long as he remains in power, the country stays held together. Opponents get imprisoned and have little choice but to comply.
So what happens when an autocrat like Putin is suddenly removed?
Very often, the answer is chaos.
If Putin were assassinated, Russia would enter a period of profound instability almost immediately. Another strongman would attempt to seize power in much the same way Putin himself once did.
A western style democracy taking hold seems unlikely. Russians have historically preferred a strong figure at the top. When they experienced western style democracy, they elected Boris Yeltsin who projected an image of a weak Russia that the population simply could not accept.
When Putin succeeded Yeltsin, his stated goal was to restore Russia to its rightful place on the world stage, at least militarily.
~ Nexus X, Quora
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ANOTHER CAR BOMBING IN RUSSIA
Another senior Russian official has met his demise.
This time it was by a car bomb.
On June 9, 2026.
The car bombing took place in the Moscow suburb of Balashikha.
The victim of the car bombing has been identified as as Damir Davydov.
Davydov is a senior military official in Russia’s Main Missile and Artillery Directorate (GRAU). He was a fairly senior official.
According to records, he was the one in the Russian government responsible for missile and artillery ammunition supplies.
Ukraine continues its assault on high ranking Russian officials and military personnel.
Some have been killed in battle.
Others were targeted for assassination through artillery, missiles or drones.
Here are some that have met their demise during this war.
Some deaths occurred inside Russia or occupied areas, often via bombs or targeted killings. Responsibility is sometimes claimed by Ukrainian intelligence or suspected, but not always officially confirmed.
• Igor Kirillov – senior general (killed by bomb on scooter)
• Yaroslav Moskalik – senior General Staff official (car bombing)
• Fanil Sarvarov – senior General Staff official (car bombing)
• Valery Trankovsky – Russian naval captain, accused by Ukraine of war crimes; killed by bomb
• Stanislav Rzhitsky – submarine commander; shot in Russia
Other prominent pro‑war or political figures:
• Vladlen Tatarsky – pro‑war blogger; killed by bomb (2023)
• Darya Dugina – nationalist figure’s daughter; car bombing (2022)
• Illia Kyva – former Ukrainian politician aligned with Russia; shot (2023)
Ukraine is taking the war to Russia.
It is taking it to the neighborhoods and homes of Russian senior officials.
~ Brent Cooper, Quora
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RUSSIA CONSIDERS LOWERING WORKING AGE TO 12
Russia’s war has created such a severe labor shortage that a senior official is now openly suggesting filling the gap with children. The proposal would lower the legal working age from 14–15 to 12 and bring back Soviet‑style “labor camps” as summer work programs for teens. It’s being sold as voluntary, “structured” holiday work that teens supposedly want and that helps families who can’t afford long vacations, but in reality it would push 12‑ to 17‑year‑olds into the labor market to keep the wartime economy running, avoid raising the retirement age again, and dodge further mobilizing adult men in big cities.
The idea is disturbing because it rebrands child labor as “opportunity,” normalizes the language of labor camps in a country with a brutal history of them, and blurs the line between optional and pressured work for kids. The fact that it comes from a children’s rights commissioner shows how even child‑protection institutions are being pulled into wartime mobilization thinking.
More broadly, it fits a pattern: Russia is already leaning on poor, remote, minority regions and migrants to staff the army and low‑wage jobs, while reviving Soviet‑style patriotic and militarized youth culture. Now, under economic and demographic stress, the state is reaching further down the age ladder instead of changing the war policy that caused the shortage in the first place.
This is what angers me. Despite Putin taking Russia back to Stalinism with young children under 16 working in labor camps, Russians will still think their country is a paradise.
Now, what happens when all of the adults are killed in Ukraine. Will Putin recruit pre-teens/teenagers under 18 to fight?
~ Lytiek Gethers, Quora
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LABELING AN EMOTION HELPS TO CONTROL IT
The next time you're furious, don't try to calm down. Just put a name to the anger coursing through your veins.
Say "this is rage"—three words, three seconds—either out loud or silently to yourself, and you've already kept the feeling from swallowing you whole.
The technique is called affect labeling, and it works by softening the intensity of whatever's hitting you. "It turns down the volume on something that can feel really intense and overwhelming," says Lizzie Cleary, a clinical psychologist in Los Angeles. “It makes it a little bit quieter and more understandable."
Here's why such a small move does so much—and how to make it second nature.
Why addressing anger works
"Before you label an emotion, you are the emotion," says Shannon Sauer-Zavala, a clinical psychologist and mental health treatment researcher in Lexington, Ky. It's the heat in your chest, the racing thoughts, the urge to do something you'll regret. The moment you put the feeling into words, it starts to loosen its grip. “When you label an emotion, you take it outside of yourself, and it becomes something you're feeling, not something you are,” she says.
The wording matters. Psychologists generally recommend saying "This is rage" rather than "I am furious." The goal is to create distance between yourself and the emotion—to remind yourself that rage is something you're experiencing, not something you are. That split-second of separation can be powerful. It creates a brief pause between what you're feeling and what you do next. "The pause allows you to choose with intention, so the emotion isn't running the show—you are," Sauer-Zavala says.
There's a reason why that small shift can feel so powerful. When you're angry or afraid, your amygdala—the brain's threat detector—is firing. Naming the feeling pulls a different system online. "When we go through the exercise of observing, naming, labeling, and utilizing language, that tends to activate our prefrontal cortex," Cleary says, referring to the analytical, language-based part of the brain. Once that happens, the feeling starts to lose steam.
The effect shows up even in the lab. Cleary points to a study in which people with a fear of spiders were asked to approach a live tarantula. The group that was instructed to narrate their fear out loud—saying things like "this is anxiety"—got closer to the spider than those who stayed silent, demonstrating better emotional regulation in the moment. "It makes the experience just a little bit more coherent, a little bit more manageable, and helps people be a little more regulated," she says.
How to practice affect labeling
When your emotions are running strong, start by naming the dominant one: "This is rage," "this is anxiety," "this is grief."
Which one it is will determine what you do next and what you need in the moment, whether that’s comfort, a phone call, or a few deep breaths. Each emotion comes with its own pull, Sauer-Zavala says. Anger, for instance, tends to push you to set a boundary. "When you label, you can identify what the emotion is trying to tell you and act accordingly," she says. If you’re stuck on "I feel awful" after a tense exchange, you might just stew, or fire back something you'll regret. But if you land on "This is rage,” you can reflect on the fact that someone crossed a line, and pivot your focus to setting a boundary.
Make labeling your emotions a habit
Sauer-Zavala tells beginners to try labeling their big emotions just once a day for a week, rather than treating it as a lifelong project. "You don't have to become a Zen master," she says. If you’re fuming in a traffic jam, stewing after a tense meeting, or lying awake ruminating at 2 a.m., name what you’re feeling. Over time, the labels will start to reveal patterns. Cleary asks people to pay attention to which feelings keep surfacing and when—anger that flares every evening, say, or loneliness that creeps in at night. Those throughlines point to the triggers worth addressing. The more you name what you’re feeling, she says, the more you’ll learn about yourself.
https://time.com/article/2026/06/10/affect-labeling-rage-anger-emotional-regulation/?utm_source=firefox-newtab-en-us
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TO CHANGE YOUR FEELINGS, CHANGE BELIEFS
Your beliefs become a lens for viewing life. By changing the beliefs you change the expectations and emotions.
We can think of it as a chicken-and-egg thing: You have feelings—anger, anxiety, jealousy, resentment, whatever—which then stir up all kinds of thoughts. Or, no, you start thinking about what someone did, and that stirs up anger, anxiety, etc. There are both camps; many people I meet in my office tend to see emotions as the driver—I do what I do based on how I feel.
I’m in the thought camp, but it’s not just everyday thoughts. It’s something more solid, more core—faulty beliefs, assumptions, and expectations. These are what precede and then fuel the subsequent emotion. Here are 4 of the most common belief drivers:
1. I should/shouldn’t do______.
Beliefs in the form of shoulds are about rules, usually inherited from others—parents or authority figures. If you break the rule, and don’t do the "should," you likely feel guilty and/or ashamed. (Oriana: I remember a rule from the seventies: “Don’t ‘should’ on yourself.”)
2. They should/shouldn’t do_________.
It’s easy to transplant your shoulds onto others, expecting them to do what you think you should do. My boyfriend should listen and not be critical, or my boss should appreciate my working overtime. When others violate these beliefs, it stirs anger, resentment, disappointment, surprise, or some combination of them all.
3. It’s supposed to be_______.
The vacation is supposed to be fun or relaxing. The promotion is supposed to be challenging. This sounds like shoulds, but it is more about expectations, situations, and events than about people. If the expectations are not met—say, it rains the entire vacation or the promotion isn’t a challenge but a headache—you feel angry, disappointed, and depressed.
4. This is not fair; I don’t deserve______.
I don’t deserve to be criticized by my boyfriend when I’ve done nothing wrong. It’s not fair that I didn’t get that promotion after putting in all those overtime hours. Disappointment, resentment, anger, and anxiety take over.
The belief becomes the story.
Your belief now becomes the foundation for a more elaborate story. It may be about the past: My parents always favored my brother; it’s not fair; they shouldn’t have done that. Memories pile on, validating the story and fueling anger and resentment.
Or the story may be about you and your self-image: My parents favored my brother and didn’t love me because I’m unlovable; I’m a loser, and no one will ever love me; I never get a break. You now unconsciously look for evidence to support your perspective.
Or the story may be about society or the larger world: People are basically selfish and can’t be trusted, or life is out to screw me over.
Whatever your story may be, it becomes not only something you continually tell yourself but also a lens that filters everything you see, shapes the evidence you find, and sets a baseline for your emotions and attitude toward life.
So, if feelings come from beliefs, changing how you feel begins with changing the beliefs that drive them. How do you do that?
Step back from your feelings and ask which beliefs are driving your reaction.
You’re angry at your brother or feeling guilty: What’s behind this feeling? What assumptions or expectations am I making—the shoulds, the supposed tos, the not-fairs? Stepping back to reflect not only helps you get out of your emotional brain and into your rational one, but with practice you’ll diagnose the source more quickly.
What is the story you’re telling yourself?
You feel that your parents always favored your brother, or that you’ve always done a lot to support him over the years but have received little appreciation in return. You feel guilty because you never got back to your friend about coming for dinner, and you don’t follow through much.
Question the evidence.
This is where you become your own advocate or attorney. Your brother has appreciated your support and has tried to show it through actions a few times in the past. Yes, you feel guilty right now, but it is not the bigger pattern you imagine. You’re stressed and hard on yourself, but you’re generally good at following through.
Experiment with changing the story.
This is what good therapy or even a good friend can do: give you a different lens or a new perspective. Your parents weren’t favoring your sister but were simply giving her extra attention because of her disabilities. Your brother is struggling with his own issues right now, and you need to cut him some grace. You do tend to be self-critical when stressed, particularly about relationships. You need to work on your stress and self-criticism, rather than scolding yourself.
The key word here is experiment. You don’t want to create another should. Instead, adopt an attitude of curiosity. Wonder how your thoughts always drift to the same old places, assumptions, and stories. These are what shape your view of yourself, your relationships, your problems, and your view of the world.
You have the power to change how you feel. It’s just a matter of changing your mind.
https://www.psychologytoday.com/us/blog/fixing-families/202606/if-you-want-to-change-your-feelings-change-your-beliefs
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LIFE TEN THOUSAND YEARS AGO
Ten thousand years ago, the average human had no kings, currency, or permanent home. Yet they suffered almost no tooth decay and routinely lived into their 60s.
The last Ice Age had recently ended, and a rapidly warming climate was replacing endless tundras with dense forests. Socially, humans lived in egalitarian bands of 20 to 50 people. Without formal laws or standing armies, decisions were collective. People moved with the seasons, carrying their few possessions—finely crafted flint tools, bone needles, and woven baskets—between temporary camps built from wood, animal hides, and reeds.
The hunter-gatherer diet was far more diverse than that of the early farmers who would soon follow. People hunted deer, wild boar, and smaller game, while gathering hundreds of types of roots, nuts, wild fruits, and seeds. Their lack of refined sugar or heavy starches kept their dental health remarkably strong.
Without dense populations to sustain them, modern epidemics like cholera or smallpox did not exist. The main threat to life was a high infant mortality rate, with roughly a third of children dying before age five. However, those who survived the perilous early years reached adulthood with robust bone density built from constant physical activity.
By 8000 BCE, this nomadic lifestyle was already approaching its twilight. Most bands shared their camps with domesticated dogs, and in the Levant, some groups were beginning to linger in one place to harvest abundant wild wheat. At Göbekli Tepe in modern-day Turkey, hunter-gatherers were already carving 16-foot stone pillars to build monumental temples, proving that complex, organized society began long before the first crop was ever planted.
A reconstruction of a Mesolithic hunter-gatherer camp, featuring the type of temporary reed shelters commonly used during this era. ~ SepiaGlyphs, Quora
Kate Jackson:
This is an entirely romanticized and false account of the past. There's evidence in burial mounds that many died due to violence between small tribes. Disease was rife and treatments primitive, often horrific and ineffective. The past was a very scary place to live and for much of human existence to live past 18 an achievement.
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WHY SCOTLAND IS SO TREELESS
The treeless moors of the Scottish Highlands look like pristine wilderness. In reality, they are the ruins of a massive ancient forest constantly being eaten down to the ground.
This barren landscape is the result of millennia of human intervention, climate shifts, and an army of grazing animals that actively prevent trees from returning.
Thousands of years ago, much of Scotland was covered by the great Caledonian Forest, a dense woodland of Scots pine, birch, rowan, and oak. The decline of this forest began around 5,000 years ago, driven by early human settlers who cleared land for agriculture and livestock. This early human activity coincided with a natural shift toward a cooler, wetter climate, which triggered an ecological chain reaction that changed the soil itself.
As trees were felled, their roots stopped drawing water out of the earth. The frequent Scottish rains pooled in the newly cleared ground, creating waterlogged conditions perfect for sphagnum moss. Over centuries, this moss died and accumulated, forming thick layers of acidic peat. Peat bogs are hostile to tree growth; the soil lacks oxygen and nutrients, making it nearly impossible for seeds to naturally take root. Today, these "blanket bogs" cover vast stretches of the Highlands, locking the landscape into a treeless state.
Where the soil is dry enough for trees to grow, another force keeps the landscape bare: overgrazing. During the 18th and 19th centuries, the Highland Clearances replaced agricultural communities with massive flocks of sheep. At the same time, sporting estates encouraged an artificially high population of red deer. Today, millions of sheep and an estimated 400,000 red deer roam the hillsides. These animals browse almost every sapling that emerges from the soil, chewing them down before they can grow higher than a few inches.
In recent decades, significant reforestation efforts have begun across Scotland, aiming to restore the native pine woods. However, these new forests cannot survive on their own. To successfully grow a tree in the Highlands today, conservationists have to build tall, expensive fences around the planting sites to keep the deer out. Without these barriers, any natural saplings are quickly stripped bare by the local wildlife. ~ NovaPrism, Quora
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THE DARK EVENINGS OF THE 19TH CENTURY
Modern period dramas show the 19th century bathed in romantic candlelight. In reality, lighting a single ballroom for one evening cost more than a domestic servant earned in a year.
The most misrepresented aspect of daily life during the Napoleonic era is the profound darkness of the night, and the cost required to escape it. Illumination was strictly dictated by class. True beeswax candles burned brightly and cleanly, with a faint scent of honey. They were also heavily taxed and expensive. Because of this, brightly lit rooms were rare, fleeting displays of elite wealth.
The broader population relied on tallow candles. Made from rendered animal fat—usually beef or mutton—tallow was cheap but came with serious drawbacks. Tallow candles burned with a dim, yellow flame that produced heavy, greasy smoke, coating walls and ceilings in soot. They sputtered constantly and required snuffing (trimming the charred wick) every ten to fifteen minutes. If left untrimmed, the wick would curl, smoke aggressively, and become a fire hazard.
Most noticeably, tallow candles smelled rancid. They emitted a burnt-meat odor that permeated clothing and hair. Because even tallow was a significant expense for working-class households, families rarely lit an entire room. Instead, they lit a specific task. A family would huddle close to a single flame to sew, read, or repair tools, leaving the rest of the room in total blackness.
This reliance on dim, localized light dictated social schedules. Calendars were organized around the lunar cycle. Evening travel and social calls were frequently scheduled during a full moon, as navigating rutted dirt roads at night with only a weak carriage lantern risked a broken axle or an encounter with highwaymen.
Even among the upper classes, an evening without guests meant extinguishing the expensive beeswax and sitting close to the hearth, reading by the light of a single wick. ~ SepiaGlyphs, Quora
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DID ANY GERMANS KNOW FROM THE START HOW WW2 WOULD END?
General Ludwig Beck was in his office alone on September 1 1939. While the radio announced that Germany was invading Poland and people cheered, he did not rejoice. He had left a year earlier as army chief already knowing the war would end badly. For him, the first day was not a victory, but a start of a long fall.
As the German army marched fast through Poland, Beck kept watch over the supplies. He knew the country did not have enough oil, rubber or steel to wage a long war. He began meeting secretly with a few friends, discussing in dark rooms about the crash that was about to happen. They thought that those early victories were just a trap, which would later backfire.
When France fell in 1940, Beck remained worried. He told his friends that having more land made the army weaker and consumed resources at a faster rate. When in 1941 the invasion of the Soviet Union began, he was convinced that the end was near. He looked at the map and he saw the lines were getting too thin.
In his final years, Beck belonged to a secret group that planned for the day that the country would finally lose. He never altered his conviction that war was over the moment it was started. In July 1944, as a result of a failed plot to stop the leadership, he died with the same dark thoughts he had in 1939. ~Ahmed Tareen, Quora
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THE KOLA SUPERDEEP HOLE
Geologists long assumed the Earth's deep crust was entirely solid, dry, and lifeless. Instead, the Kola Superdeep Borehole revealed boiling water and intact 2-billion-year-old plankton fossils.
When Soviet scientists began the project in 1970, they were not looking for oil or gas. They were engaged in a subterranean space race to drill as far into the crust as technologically possible. By the time the drill was halted at 12,262 meters (40,230 feet), it had completely upended decades of geological assumptions.
Prior to the drilling, seismologists believed they understood the composition of the Earth's crust based on how seismic waves bounced through it. A major shift in seismic velocities at a depth of roughly 7 kilometers was universally accepted as the "Conrad discontinuity"—the point where granite gave way to denser basalt.
The drill bit reached 7 kilometers, but no basalt was found. Instead, the seismic anomaly was caused by a metamorphic transition in the granite itself. The immense heat and pressure had structurally altered the rock and caused it to heavily fracture. The "Conrad discontinuity" turned out to be a myth.
Even more surprising was what filled those deep fractures: water. Instead of perfectly solid rock, researchers discovered hot, highly mineralized water circulating freely. This water had been forced out of the crystal structures of the rock itself by the intense pressure and was trapped beneath a layer of impermeable rock closer to the surface.
The borehole also changed biological understanding of extreme environments. At a depth of 6 kilometers, inside rocks that were over 2 billion years old, researchers found 24 species of microscopic plankton fossils. These had survived perfectly intact despite the extreme pressure and temperatures.
The chemical composition of the deep crust was equally unexpected. The mud flowing out of the borehole frequently "boiled" with hydrogen gas. Huge quantities of hydrogen, helium, nitrogen, and carbon dioxide were found trapped in the deep crust, reshaping our understanding of the planet's volatile gas reserves.
Ultimately, the drill was stopped by heat. Scientists had predicted temperatures at 12 kilometers to be around 100°C (212°F). The reality was a blistering 180°C (356°F). At that temperature, the rock stopped breaking cleanly and began behaving like a plastic solid, slowly oozing back into the borehole as the drill was retracted.
The welded-shut cap of the Kola Superdeep Borehole, which remains the deepest artificial point on Earth.
~ NovaPrism, Quora
Victor Pe:
Some of my investigation, triggered because of the story of the planet Mars, seem to indicate that the Earth’s temperature differential in its interior is likely to generate a significant magnetic field for billions of years before cooling reduces that differential enough to change that. Mars being smaller, allowed it to cool significantly faster. It’s a phenomenon similar to why children shouldn’t go in hot tubs and saunas, related to surface area relative to total volume.
There is certainly reason to think that the atmosphere and the water cycle are smaller reservoirs, more susceptible to human activity disruption then the vast amount of heat in the Earth interior, which, by the way I have also learned is believed to possibly be roughly equal amounts left over heat from accretion and radioactive decay, But there is a tremendous amount of approximation and difference of opinion about everything related to the generation of our magnetic field, and the cooling rate and thresholds of protection from cosmic rays and other radiation and particles.
When I put that amount of unknown together with the criticality of the issues and then also add in the fact that because of the density of certain materials, there are certainly industrial and commercial motivations to figuring out how to extract things from very far inside the Earth and risk benefit analysis leads me to say that my own curiosity and desire to solve puzzles should really not be applied here.
Gene:
Solid rock becoming plastic … just as “solid ice” becomes plastic under hundreds of feet to allow glaciers to flow to the sea and calve.
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THE SPEED OF PROGRESS
In 1940, over 35 percent of people in the US didn't have flush toilets. In New York it was only 10 percent, and in Mississippi it was 80 percent. In 1950 it was 25 percent. In 1970, Alaska and many of the Southern states, 10 percent of the people, didn't have flush toilets. By 1990 it was virtually zero.
In 1932 only 11 percent of rural people outside of towns had electricity. It was 30 percent by 1940.
In 1930 90 percent of city dwellers had electricity and 10 percent of rural people had it. This meant that 60 percent of Americans had electricity in 1930, it was 85 percent in 1940.
The first commercial jet entered service in 1952. By 1969 we had a man on the moon.
That's how fast the world has changed. It was changing so fast, and then stalled in the late 1970’s, and nothing new except the smart phone has been invented since 1984.
Since then, technology evolved, instead of raced forward. So anyone who came of age after 1984, assumes that we always had everything.
~ Bob Wilson, Quora
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SCIENTISTS CAN PREDICT WHEN A PERSON WILL DIE
The clock is ticking on all our lives; we just don't know when it will stop.
Scientists have devised a host of tools in their attempts to gauge biological aging – not just how many birthdays a person has had, but how worn out their organs and cells are.
Many of these tools are epigenetic 'clocks', which tally chemical marks on DNA that accumulate with age and stress, but they aren't always reliable. Now, researchers have developed a new clock based on gene activity that accurately predicts lifespan and captures hallmarks of chronic disease.
That's not to say it can tell you exactly how many days you've got left before you shuffle off this mortal coil. But researchers found that their newly developed technique did pretty well at estimating how far through life a person or animal probably is.
According to the research team, the biomarker-based algorithm is going to be useful for analyzing rates of biological aging across species, including humans, and understanding when this aging speeds up or slows down.
The new clock is what's known as a transcriptomic clock: It analyzes RNA molecules that translate genes into proteins to figure out which genes are turned on and off. As this activity changes as we get older, the information can be used as a signature of aging.
One of the key innovations here was gathering a large set of data across four species – mice, rats, macaques, and humans – and then comparing aging processes between animals, and between different parts of the body.
"Aging and interventions modulate health and mortality, yet the underlying molecular mechanisms of this modulation remain unclear," write the researchers in their published paper.
"We developed multi-species, multi-tissue transcriptomic clocks of chronological age and expected mortality across more than 11,000 samples from four mammals, addressing the need for interpretable aging biomarkers that generalize across organs and species, while reflecting health status."
The team found genes associated with processes such as healthy cell division and wound repair acted as signs of slower molecular aging, while genes linked to cell death and inflammation were markers of faster aging and an older biological age.
These findings were then adapted into the new molecular clock, which was validated against other aging models and through statistical analysis.
The clock was shown to correctly assess slower or faster biological aging, as well as mortality risk. With human blood samples, it could predict time to death as well as the best epigenetic clocks.
What's more, it picked up known contributors to aging, such as chronic disease, in animal models of those diseases and tissue samples from human patients.
The researchers think this new approach could be easier to work with and more informative than epigenetic clocks, which have been around since 2013.
The genetic signs of aging were surprisingly conserved across all four species, which means they matched up to a notable degree. This consistency was shared across multiple cell types too, including muscle and blood cells.
"The same genes are associated with aging in, for example, liver and heart in rats and humans," the lead author of the study, bioinformaticist Alexander Tyshkovskiy from Harvard Medical School, told Jackie Flynn Mogensen at Scientific American.
"Even though the cells have very different functions, very different origins, they still share the same aging-related biomarkers."
That commonality suggests these biomarkers may be genuine signs of aging, though we don't know if they are contributing to aging in any way.
"The expression levels of genes that protect against and respond to cellular stress have long been known to increase with age, which is suggestive of adaptive responses, rather than causal drivers," João Pedro de Magalhães, a molecular biologist at the University of Birmingham, writes in a commentary on the study.
"It is therefore uncertain whether transcriptomic signatures drive aging, result from it or represent compensatory mechanisms."
There's not much we can do about much of the aging process, but we do several factors affect how fast our biological aging clocks tick. A healthy diet can help slow them down, while disease and pollution tend to speed them up.
One way that this new analysis tool promises to be helpful is in testing the effects of different interventions. It could be used to see how lifestyle changes or drugs were impacting biological aging, without lengthy tests or trials.
It's still an estimation tool, and wouldn't replace those tests or clinical trials in a lot of cases, but could be used for early assessments.
There's still plenty to do to develop this technique, including further testing on more diverse human populations and teasing out measurements of aging more precisely, but it looks like it could be another important resource for research into aging.
"This study reveals conserved signatures and a modular architecture of mortality regulation, providing a framework for quantifying and targeting aging of cellular subsystems across species and tissues," the researchers write.
The research has been published in Nature.
https://www.sciencealert.com/a-new-biological-clock-could-predict-when-youll-probably-die
from another source (The Guardian):
A NEW TEST CLAIMS TO TELL HOW WELL YOU’RE AGING – AND EVEN WHEN YOU’LL DIE. BUT I’D RATHER NOT KNOW
I think I’ll leave new methods to measure biological age to the Kardashians. Too much knowledge about your mortality can be bad for your health.
In the season 5 finale of The Kardashians, the family took a commercially available blood test to discover how fast their bodies were aging. It came as little surprise, given their privileged lifestyles, that the reality TV stars were said to be aging more slowly than most mortals of the same age. Khloé, then 39, found she had a biological age of 28. Cue whoops of joy and much smugness.
The Kardashians join a growing list of celebrities who have taken similar tests and then crowed about their “biological ages”. Now, there’s a new test on the block.
Chronological age is the number of candles on your birthday cake. Biological age is a measure of the health of your cells and organs. The new method, devised by Vadim Gladyshev from Harvard Medical School and colleagues, not only provides a measure of biological aging, but also a “time to death”. Who wants to hand over a sample for analysis? Definitely not me.
Researchers have been devising so-called molecular clocks to estimate biological age for more than a decade. The problem they are trying to solve is that there is no objective measure for age – humans don’t have tree rings – so researchers pick something that they can measure, that seems to change with age and that may also say something about the person’s general health.
It’s kind of like using tooth wear and tear to predict a dog’s age: you get a ballpark estimate of how old they are, as well as a vague indication of how well or otherwise the pooch is. The most famous one, known as the Horvath clock, is based on epigenetics – the pattern of chemical tags attached to DNA.
Gladyshev’s method is based on patterns of gene activity, collected from more than 4,000 people to establish how the patterns relate to age and disease, as well as looking at data from mice, rats and macaques. The researchers believe this method is more sensitive than its predecessors.
By providing a reliable measure for aging, the test could shorten the otherwise lengthy clinical trials needed to tell if anti-aging treatments work. The method could also be used to inform age-related policy. Current aging policies are based on chronological age, but the Kardashians seem to show us that some people age differently to their peers. Future policy could be adjusted to match this reality, if the tests are accurate.
For now, the test is for research purposes only. But should a spin-off version become publicly available, I still wouldn’t want it.
Based on data from vast numbers of people, tests such as this provide estimates of probability rather than definitive predictions. They cannot actually tell you the day you will die, or state with certainty what health problems you will develop. Instead, they assess how closely your molecular profile resembles others in their datasets. Then they infer your likely risk of disease or how long you might have before death based on what has happened to people with similar characteristics.
I don’t need this kind of statistical high jinks to tell me I could be aging better. I’m aged over 50. I eat biscuits. I don’t exercise as often as I should. I already know what I need to do to improve my health and prolong my life – eat fewer biscuits, exercise more – I don’t need a test to make me feel bad for not doing it.
In addition, I’m worried that a negative result could change the way I think about my future. As things stand, I feel good about getting older. I can’t be doing with anything that challenges this view, because I know how physically transformative beliefs can be.
The research of Yale University’s Becca Levy, for example, has shown that when people expect old age to be pockmarked with frailty and decline, it becomes more likely to happen. In later life, they are more likely to suffer from cardiovascular problems and memory loss.
In another study, researchers interviewed 660 people over 50 from the small town of Oxford, Ohio, about their attitudes to aging. Following up more than a quarter of a century later, Levy tallied the responses with data from the US National Death Index. Factoring in related risk factors, she found that those who had a negative view of aging died, on average, 7.5 years earlier than those who held positive beliefs about aging.
The emerging idea is that beliefs about aging don’t just stay in the mind – they can become biologically embodied. Over time, changes in behavior, stress hormone levels and immune system function can accumulate to influence physical health, aging and longevity. In this model, anything that taints the expectations we have of our own aging has the potential to influence the way that we age and, as a consequence, the timing of our death.
So, my plan is to live as healthily as I can and avoid anything that might rock my rosy view of retirement. As for tests of biological aging and mortality risk, I’ll leave those to the influencers. I’m quite happy not to keep up with the Kardashians.
https://www.theguardian.com/commentisfree/2026/jun/12/science-ageing-test-die-impressive-mortality-molecular-clock
Oriana:
Knowing when one is supposed to die (according to genetic and other tests) may actually produce a nocebo effect. That’s the opposite of the placebo effect: an improvement in health because we believe the treatment is bound to be effective. If, on the contrary, we come to believe that the treatment (medicine, supplement, certain kind of exercise, etc) is actually harmful, or has nasty side effects, we are likely to begin to feel worse — as exemplified in the Guardian article.
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MILK CONSUMPTION AND LIFE EXPECTANCY
A new study shows drinking low-fat milk — both nonfat and 1% milk — is significantly associated with less aging in adults.
Research on 5,834 U.S. adults by Brigham Young University exercise science professor Larry Tucker, Ph.D., found people who drink low-fat milk experience several years less biological aging than those who drink high-fat (2% and whole) milk.
"It was surprising how strong the difference was," Tucker said. "If you're going to drink high-fat milk, you should be aware that doing so is predictive of or related to some significant consequences."
Tucker investigated the relationship between telomere length and both milk intake frequency (daily drinkers vs. weekly drinkers or less) and milk fat content consumed (whole vs. 2% vs. 1% vs. skim). Telomeres are the nucleotide endcaps of human chromosomes. They act like a biological clock and they're extremely correlated with age; each time a cell replicates, humans lose a tiny bit of the endcaps. Therefore, the older people get, the shorter their telomeres.
And, apparently, the more high-fat milk people drink, the shorter their telomeres are, according to the new BYU study, published in Oxidative Medicine and Cellular Longevity. The study revealed that for every 1% increase in milk fat consumed (drinking 2% vs. 1% milk), telomeres were 69 base pairs shorter in the adults studied, which translated into more than four years in additional biological aging. When Tucker analyzed the extremes of milk drinkers, adults who consumed whole milk had telomeres that were a striking 145 base pairs shorter than non-fat milk drinkers.
Nearly half of the people in the study consumed milk daily and another quarter consumed milk at least weekly. Just under a third of the adults reported consuming full-fat (whole) milk and another 30 percent reported drinking 2% milk. Meanwhile, 10% consumed 1% milk and another 17% drank nonfat milk. About 13% did not drink any cow milk.
"Milk is probably the most controversial food in our country," Tucker said. "If someone asked me to put together a presentation on the value of drinking milk, I could put together a 1-hour presentation that would knock your socks off. You'd think, 'Whoa, everybody should be drinking more milk.' If someone said do the opposite, I could also do that. At the very least, the findings of this study are definitely worth pondering. Maybe there's something here that requires a little more attention."
Somewhat surprisingly, he also found that milk abstainers had shorter telomeres than adults who consumed low-fat milk.
“It's not a bad thing to drink milk," Tucker said. "You should just be more aware of what type of milk you are drinking.”
https://www.sciencedaily.com/releases/2020/01/200115120634.htm
Oriana:
It’s important to remember that this is a correlational study, so we can’t draw conclusions about causes — “Correlation does not prove causation.”
The most puzzling finding here pertains to non-drinkers of milk (“milk abstainers”) having shorter telomeres (i.e. presumably aging faster) than low-fat milk drinkers. Well, milk is very nutritious — and this goes far beyond calcium, which is easily obtained from other sources.
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FIRST VACCINE DESIGNED BY AI
Artificial intelligence has been used to develop a "fundamentally new" type of vaccine that could protect against large swathes of viruses and prevent pandemics, say researchers.
The team at the University of Cambridge say it is the first time a vaccine's key component has been designed entirely by AI and then trialed in people.
The vaccine was engineered to work on all coronaviruses which would include all Covid variants as well as viruses that currently infect animals yet have the potential to start the next pandemic.
The work is still in the early stages, but the team is already developing separate vaccines that could tackle flu and Ebola.
Vaccines teach our bodies how to spot an infection to increase our chances of fighting it off.
But some viruses are adept at changing their appearance – or mutating – so vaccines can quickly go out of date. It's why Covid and winter flu vaccines need to be regularly updated.
"We're always behind," said Prof Jonathan Heeney, from the University of Cambridge, adding "what we're trying to do is get ahead of the curve" and so far ahead they could protect against new outbreaks or pandemics.
How does it work?
Normally vaccines are designed using a current strain of a virus.
The Cambridge researchers took known genetic codes – the instruction manuals of life – from a range of coronaviruses that had been recorded by surveillance programs hunting for potential viral threats.
These genetic codes were analyzed by an artificial intelligence. It then designed a "super-antigen" that could train the immune system in such a way it gave protection against the whole family of viruses – even if they mutated or a new infection jumped from animals to people.
Antigens are the critical components of vaccines as this is what the immune system learns to attack.
Heeney said this was the first time an antigen designed by AI had been trialed in people. He said the technology was "surprising all of us" and it was "amazing what we can do with it for the good of humanity".
Heeney told BBC News: "This is about making vaccines that protect us, not just from today's viruses, but protect us from what can cause the next outbreak or disease.
"This is a fundamental shift in how we prepare for pandemics."
The trials, in 39 people, were designed to assess if such vaccines were safe. A second study – involving around 200 people – will give a greater understanding of how well it is training the immune system.
The findings detailed in the Journal of Infection said the impact on the immune system was "modest", but they are still generating excitement.
Prof Saul Faust, who performed some of the trials at the University of Southampton, said the AI design "definitely has potential" and was "really exciting".
He told the BBC: "What's really interesting is the technology is an awful lot better at designing vaccines for potential pandemics when viruses are changing."
The Cambridge team are already performing animal research on universal seasonal flu vaccines that would not need to be adapted every year and an H5N1-bird flu vaccine, in case the virus that is currently devastating bird populations became a human pandemic.
They are also looking at a vaccine for viral hemorrhagic fevers, which would include Ebola species.
The current outbreak in the Democratic Republic Congo is being caused by a species that does not have a vaccine developed for it yet.
Prof Andy Pollard, the director of the Oxford Vaccine Group, was not involved in the study, but said this approach was generating compelling evidence in animal research.
"It's fascinating data and people wouldn't have predicted they'd be able to generate these immune responses," he told BBC News.
The real test, he says, is what happens in the human trials as our immune systems are different than laboratory mice as ours have been shaped by years of infections.
More broadly he said artificial intelligence was going to be a "game changer" for vaccine research and that AI tools had the potential to predict how the immune system would respond to a vaccine making development much faster and would "save lives".
Prof Marian Knight, scientific director for National Institute for Health and Care Research, said: "The remarkable success of this AI-designed 'super-antigen' trial marks a pivotal leap forward in our ability to deliver broad, lasting viral protection."
Science Minister Lord Vallance said: "Another British science success story, this is a great example of how we can bring our research expertise together with AI to deliver new treatments.
"With the first human trials showing positive results, this work could help speed up the roll out vaccines to benefit people all over the world for the long-term."
https://www.bbc.com/news/articles/crrpggegwe0o
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CANCER SPREADS MORE IN MIDDLE AGE THAN IN OLD AGE
Melanoma may be most dangerous in middle age, as cancer briefly gains the upper hand against the immune system before losing it again in extreme old age.
Summary:
Melanoma may not become steadily more dangerous with age as scientists once assumed. In a surprising discovery, researchers found that cancer spread was lowest in young mice, surged in middle-aged mice, and then dropped again in very old mice. The key appears to be a special type of immune cell that helps keep cancer dormant and prevents it from spreading.
Researchers discovered that melanoma spread peaked in middle-aged mice and declined in very old mice, revealing an unexpected age-related pattern.
Cancer becomes more common with age and is often harder to treat in older adults. Yet most cancer studies in mice do not reflect that reality. Fewer than 10% of mouse experiments use aged animals, with researchers typically relying on mice that roughly correspond to humans in their early 20s.
That gap may help explain why many cancer therapies that perform well in laboratory studies ultimately fail in human clinical trials.
New findings from Fox Chase Cancer Center, presented at the American Association for Cancer Research annual meeting, suggest that melanoma does not behave the same way throughout the aging process. Researchers found that cancer spread was lowest in young mice, reached its highest level in middle aged mice, and then declined again in very old mice.
"The vast majority of studies are done in these very young mice that have a healthy and intact immune system," said Mitchell Fane, PhD, a cancer biologist who specializes in aging and cancer, and lead investigator of the study. “Right now, it's easy to personalize care for someone who's young and fit, who's potentially not going to experience as many toxicities; understanding how therapies affect older patients would give us more and better treatment options.”
Immune Cells May Hold the Key
The researchers believe a specialized group of immune cells known as gamma delta (γδ) T cells may help explain the surprising pattern.
These cells act as an early defense system, helping prevent cancer from spreading throughout the body. Young mice and very old mice had higher levels of these protective immune cells, and their tumors were more likely to remain dormant or spread less aggressively.
Middle aged mice told a different story. They had fewer γδ T cells, and melanoma was much more likely to spread to organs such as the lungs and liver.
The team also discovered that melanoma cells can actively weaken the immune system as animals age. In middle aged mice, the cancer released molecules that suppressed or exhausted γδ T cells. As those defenses weakened, previously dormant cancer cells were able to become active and spread more aggressively.
Additional experiments reinforced the importance of these immune cells. When researchers removed γδ T cells from young and very old mice, melanoma spread increased significantly.
Conversely, blocking the signals that suppress immune activity restored protection and reduced cancer spread in middle aged mice, although the same effect was not seen in the younger or older groups.
Why Researchers Need More Aged Mouse Models
One reason aging studies remain uncommon is practical. Young mice are easier and less expensive to obtain, while aged mice require long term care and breeding. Researchers must typically wait 18 to 24 months before mice reach an age suitable for aging research.
To address that challenge, Fane and colleague Yash Chabra, PhD, both Assistant Professors in the Cancer Signaling and Microenvironment Research Program, helped establish an aged mouse facility at Fox Chase Cancer Center.
The goal is to make older animal models more accessible and encourage scientists to test whether their findings hold true across different stages of life.
"Now we have a facility with established aged mouse colonies, which lowers the cost and time barriers to aging research," he said. "It allows us to tell colleagues, 'Your model is interesting, why not test it in aged mice?'"
Rethinking the Link Between Cancer and Aging
Understanding how aging affects cancer could lead to more effective treatments for older adults. Fane's laboratory is particularly interested in the observation that the relationship between age and cancer does not appear to follow a simple straight line.
Although cancer risk generally rises with age, rates unexpectedly decline among people over 80 to 85 years old.
"While risk increases steadily as people age, it abruptly decreases after ages 80-85," said Fane. "We want to explain the mechanism of why very old patients are getting less cancer, but middle-aged patients are getting more."
The new findings suggest that changes in the immune system over the course of aging may play an important role in determining when cancer is most likely to spread. They also highlight the importance of including older animals in cancer research to better reflect the patients most affected by the disease.
https://www.sciencedaily.com/releases/2026/05/260530053422.htm
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SCIENTISTS DISCOVER A HIDDEN CAUSE OF AGING CELLS THAT CAN BE REVERSED
Summary:
Researchers discovered that declining levels of phosphatidylcholine may be a major cause of age-related mitochondrial dysfunction and loss of cellular energy. Remarkably, boosting this nutrient restored more youthful mitochondrial performance in aging organisms, suggesting some aspects of aging can be slowed or reversed.
A simple nutrient may help turn back the clock on aging cells by restoring the powerhouses that keep them running.
As people grow older, their cells gradually become less efficient at producing energy and responding to changing demands. Scientists have long known that mitochondria, often called the cell's powerhouses, play a central role in this decline. Now, researchers at the Leibniz Institute on Aging (FLI) in Jena, Germany, have identified an important contributor to the process: a membrane lipid known as phosphatidylcholine.
Their findings show that lower levels of phosphatidylcholine reduce the flexibility of mitochondria, accelerating age-related deterioration. The researchers also found that supplying phosphatidylcholine through diet helped restore mitochondrial function in aging laboratory organisms. The results suggest that some aspects of biological aging may be more adjustable than previously believed.
Why Mitochondria Matter in Aging
One of the biggest questions in aging research is why people tend to lose energy and vitality over time.
Mitochondria are best known for generating the energy cells need to function, but scientists now understand that they do much more. These structures also help coordinate communication within cells, support adaptation to changing conditions, and regulate many processes essential for life. They provide the energy needed for movement, growth, and tissue repair.
Although mitochondrial performance is known to decline with age, the reasons behind this gradual deterioration have remained unclear.
A Key Role for Membrane Lipids
For many years, researchers suspected that genetic damage inside mitochondria was the primary cause of their decline. However, a new study published in Nature Communications points to another important factor.
The international research team, led by Dr. Maria Ermolaeva of FLI, found that disruptions in the mitochondrial network are linked to changes in membrane composition. At the center of the discovery is phosphatidylcholine, one of the most abundant lipids found in biological membranes.
Phosphatidylcholine helps membranes remain flexible and able to reorganize when needed. This flexibility is especially important for mitochondrial fusion, a process in which individual mitochondria join together to form interconnected networks.
These networks allow cells to share and distribute vital components, including energy molecules, metabolic products, DNA, and signaling compounds. By remaining connected, mitochondria can balance resources and replace damaged parts more effectively.
The researchers discovered that phosphatidylcholine production naturally decreases with age. As levels fall, mitochondrial membranes become increasingly fragmented and dysfunctional.
When the team disabled genes involved in phosphatidylcholine production in young worms, the mitochondria quickly began to resemble those typically seen in much older animals. Even more striking, feeding the worms phosphatidylcholine or its precursor, choline, restored a more youthful mitochondrial structure within just two days.
"We were surprised ourselves by how strongly this molecule influences the structure, connectivity, and function of mitochondria," explains Dr. Tetiana Poliezhaieva, the study's first author.
How Aging Disrupts Cellular Energy Networks
What may seem like a small biochemical change can have widespread effects throughout the cell.
Under healthy conditions, mitochondria form a highly dynamic network that adjusts continuously to changing energy needs. As aging progresses, that network becomes less stable and less efficient.
"You can imagine the whole system as a finely branched power grid that becomes increasingly damaged with age: connections break down and currents stall," explains Dr. Maria Ermolaeva, the study's lead author.
"Although energy production continues, it becomes less efficient and sustainable, and energy can no longer be distributed flexibly."
As a result, cells lose what scientists call metabolic plasticity, their ability to rapidly adapt to shifting energy demands. This adaptability is important not only for individual cells but also for tissues and entire organ systems. Reduced metabolic flexibility has increasingly been recognized as a hallmark of aging and is also associated with diseases such as diabetes.
From Worms to Human Data
To investigate the mechanisms involved, the researchers combined several different approaches.
The study included experiments in the nematode Caenorhabditis elegans, investigations using human cell cultures, and analysis of extensive clinical datasets. The team examined proteomic and lipidomic profiles, genetic variation, gene activity, and metabolic function across different stages of human aging.
By integrating these datasets, the researchers were able to connect molecular changes observed in laboratory models with patterns found in humans. Experimental validation and whole-body analyses in worms helped reveal a direct link between gradual molecular alterations and broader aging processes.
New Clues About How Aging Unfolds
The results suggest that mitochondrial aging is driven not only by accumulated genetic damage but also by age-related changes in lipid production.
This expands current understanding of why mitochondria become less effective over time and highlights membrane lipid dynamics as another important factor in the aging process.
The study also revealed that aging may occur in distinct stages rather than as one continuous process. According to the data, cells first experience a decline in stress resistance and disruptions in protein homeostasis, the system responsible for maintaining protein stability. Metabolic changes follow, with epigenetic alterations appearing later.
Researchers also observed sex-specific differences in lipid metabolism. Human metabolomic data showed the most pronounced relative decline in phosphatidylcholine levels among women around the time of menopause.
"This observation is particularly noteworthy, as it coincides with a time when many women report a significant decline in energy levels and the onset of persistent fatigue," adds Dr. Ermolaeva.
Can Diet Help Slow Cellular Aging?
Perhaps the most significant finding was that some age-related mitochondrial changes appeared reversible.
When phosphatidylcholine levels were increased in older C. elegans, mitochondrial networks became more stable and energy production improved. The results indicate that targeted metabolic interventions may help preserve cellular function and extend the period of healthy aging.
"Our work shows that both mitochondrial aging and broader systemic aging are, at least in part, modifiable. If we understand the underlying processes, we may be able to take targeted countermeasures," summarizes Dr. Ermolaeva.
Additional research will be needed to determine whether these findings can lead to therapies for humans. However, the role of nutrition is particularly intriguing, as certain dietary supplements may help support cellular health later in life.
The researchers note that phosphatidylcholine supplementation remained effective even when introduced during middle or advanced age. Overall, the findings shift attention away from the idea that aging is solely an irreversible decline and toward the possibility that some aspects of the process can be influenced, opening new avenues for promoting healthy aging.
https://www.sciencedaily.com/releases/2026/06/260610003119.htm
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ending on beauty:
B FLAT
A black hole hums as it spins,
astrophysicists announced. It sings
one melancholy note, B flat —
many octaves too low for the human ear.
Perhaps that primordial B flat
is a greeting to other black holes,
singing each to each
across the black mother void —
a prelude to the yet undetected
birth song of stars being born
in their black-hole nests —
and not just the anthem
of everything leaving everything —
galaxies rushing off
to more important places;
a lover quickly walking away.
~ Oriana
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