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Petter Törnberg: Algorithmic Tyranny & Digital Modernity
What do Facebook, Google, and TikTok see when they look at you? And more importantly, what do they miss?
I recorded this conversation with Petter Törnberg almost a year ago. It has aged into something closer to a warning.
Törnberg is Assistant Professor of Computational Social Science at the University of Amsterdam and co-author of Seeing Like a Platform: An Inquiry into the Condition of Digital Modernity. His claim is straightforward and uncomfortable: platforms have become the new eyes of power. Industrial modernity ruled from the top down and you could see it. Digital modernity rules through #algorithms you cannot see at all, and it is no less total for being invisible.
Algorithms do not reflect society. They rebuild it. Politics, culture, and your own sense of who you are.
We got into:
Why algorithmic tyranny does not need a tyrant. Why self-organization so often smuggles in a new hierarchy rather than dissolving the old one. Decentralization as camouflage. Whether #AI becomes the ultimate platform of platforms, the layer that sits above and swallows all the others. What is actually left for citizens, activists, and policymakers who want to push back.
Scientists Discover a Bizarre New Way Life Can Make DNA… Without DNA
To replicate information, life usually has fairly straightforward ways of doing things.
To copy DNA, you generally use DNA as a template. To make RNA, cells generally use DNA as a template, while RNA in turn provides the instructions for making proteins.
But now a bacterium has revealed a different path, and it’s deeply surprising.
Micron’s TakeorPay Memory Contracts Lock In $100B, No Cancellation Clause
Micron’s customers have put up $22 billion in cash deposits and financial commitments to secure guaranteed memory supply through 2030, under contracts that require payment whether or not they take delivery. Fourteen of the first sixteen agreements lock in roughly $100 billion in minimum revenue. Micron’s own new capacity won’t ship until mid-2027 at the earliest, meaning buyers are financing a factory they won’t benefit from for years.
Take-or-pay memory contracts have become the price of admission to guaranteed AI memory supply, and the terms favor the seller more than most buyers seem to be pricing in. Micron disclosed that customers across data center, consumer, and automotive segments have committed $22 billion in cash deposits and related financial commitments under 16 strategic capacity agreements, according to The Globe and Mail’s coverage of CEO Sanjay Mehrotra’s comments. Fourteen of those sixteen deals add up to roughly $100 billion in contracted minimum revenue over their terms.
Micron’s CFO Mark Murphy has been precise about the structure: roughly $18 billion of the $22 billion is cash, the rest letters of credit, and none of it counts as prepaid revenue, since it returns to customers on a schedule weighted toward the back half of the contract term, according to Futurum’s analysis of the Q3 earnings call. Most agreements run five years, from calendar 2026 through late 2030, with automotive deals typically three years. Take-or-pay memory contracts require the customer to buy a set volume at agreed pricing regardless of whether they ultimately need it, and the biggest deals carry a price floor that holds for the full term.
Active supermassive black holes may help form massive planets
A popular myth about black holes is that they act like giant cosmic vacuum cleaners, sucking in everything around them. But Wladimir Lyra’s research found a new mechanism around supermassive black holes that is more like a cosmic nursery, giving birth to planets more massive than Jupiter.
“We’re finding objects that are a thousand times the mass of the Earth, but built of pure dust,” Lyra said. “And not only that, but also some of these objects are approaching the mass of the sun.”
Lyra, an associate professor of astronomy at New Mexico State University, began this line of research as a postdoctoral fellow collaborating with Barry McKernan, Saavik Ford and Mordecai-Mark Mac Low at the American Museum of Natural History in 2010.
Silent Strep A infections may explain immunity gained by adulthood
Exposure to Streptococcus pyogenes (Strep A) that causes mild or no symptoms can trigger the body’s immune response and naturally build protection, potentially solving a nearly 100-year-old mystery of immunity.
New Griffith University research, with the help of clinical scientists from the Murdoch Children’s Research Institute (MCRI), investigated how immunity developed over time as infection rates declined with age, suggesting progressive immune protection. The paper “Subclinical exposure to Streptococcus pyogenes drives the development of long-lived homologous immunity” has been published in Nature Communications.
Strep A is a common bacterium that can cause painful tonsillitis and impetigo in young children and teenagers. If untreated, it can lead to rheumatic fever, rheumatic heart disease and kidney disease, conditions for which First Nations peoples in Australia suffer some of the highest reported rates in the world.
Noncircadian BMAL1YAP activity amplifies persistent inflammation in aged epidermis Aging
Researchers have identified a cellular “aging switch” driving age-related skin decline and chronic inflammation, centered on the interaction between two proteins, BMAL1 and YAP. While these proteins independently maintain cellular structure in youth, age-related tissue stiffening and the immune signaling protein Interleukin-17 (IL-17) cause them to alter their behavior, binding to new DNA regions to aggressively activate inflammatory genes and impair wound healing. In a study published in Nature Aging, experiments on mice demonstrated that temporarily blocking IL-17 suppressed this BMAL1-YAP inflammatory pathway and significantly reversed visible signs of skin aging, highlighting a promising new therapeutic target for treating age-related epidermal deterioration in humans.
Chronic inflammation is a hallmark of aging, yet the underlying molecular mechanisms are incompletely understood. Here the authors show that, in the skin, BMAL1 and YAP cooperate at enhancers to maintain epidermal homeostasis. During aging, this cooperation is increased at inflammatory enhancers, driven by age-associated changes in the microenvironment, promoting epidermal inflammation.
