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 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.
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.
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.
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.
A surprising MIT study published in Nature at the end of 2016 helped to spur interest in the possibility that light flickering at the frequency of a particular gamma-band brain rhythm could produce meaningful therapeutic effects for people with Alzheimer’s disease. In a new review paper in the Journal of Internal Medicine, the lab that led those studies takes stock of what a growing number of scientists worldwide have been finding out since then in dozens of clinical and lab benchtop studies.
Brain rhythms (also called brain “waves” or “oscillations”) arise from the synchronized network activity of brain cells and circuits as they coordinate to enable brain functions such as perception or cognition. Lower-range gamma-frequency rhythms, those around 40 cycles a second, or hertz (Hz), are particularly important for memory processes, and MIT’s research has shown that they are also associated with specific changes at the cellular and molecular level. The 2016 study and many others since then have produced evidence, initially in animals and more recently in humans, that various noninvasive means of enhancing the power and synchrony of 40Hz gamma rhythms helps to reduce Alzheimer’s pathology and its consequences.
“What started in 2016 with optogenetic and visual stimulation in mice has expanded to a multitude of stimulation paradigms, a wide range of human clinical studies with promising results, and is narrowing in on the mechanisms underlying this phenomenon,” write the authors including Li-Huei Tsai, Picower Professor in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT.
A new study reports that measurable brain changes — such as altered functional connectivity, synaptic activity, or metabolic patterns — can appear up to seven years before amyloid-beta plaques become detectable in Alzheimer’s disease. These early alterations may serve as preclinical biomarkers, enabling earlier diagnosis and opening a critical window for intervention before irreversible neurodegeneration occurs. The findings suggest that Alzheimer’s pathology begins years before plaque formation and support shifting detection and treatment strategies to this pre-plaque stage.
A new study suggests that Alzheimer’s disease may be detected by brain imaging more than seven years earlier than previously assumed. Researchers from the Department of Psychology at the University of Oslo led the study, published in Nature Neuroscience.
The study suggests that the gold standard for imaging in Alzheimer’s disease (amyloid-PET) has not been sensitive enough to detect early brain processes associated with the disease, such as the accumulation of amyloid plaques in the brain. The researchers found signs of Alzheimer’s at least seven years before plaques become visible.
“We found that structural changes in the brain occur many years before high levels of plaque are seen on PET scans, which is the brain scan currently used to identify the earliest signs of Alzheimer’s disease,” says James Michael Roe.
Fibrinogen, the abundant plasma protein best known for forming blood clots, may play a second and far less benign role during SARS-CoV-2 infection: acting as a molecular bridge that simultaneously hides the virus from neutralizing antibodies and delivers it to the cells lining blood vessels.
That is the hypothesis put forward by Saroj Kumar Panda (Department of Chemistry and Biochemistry, University of Texas at Arlington), Shashi Singh, and Parth Sarthi Sen Gupta (School of Biosciences and Bioengineering, D Y Patil International University, Pune) in a Viewpoint article published in ACS Pharmacology & Translational Science.
The proposal offers a single mechanistic explanation for two features of COVID-19 that have long been treated as separate problems: the virus’s ability to evade immunity and the vascular damage, microclotting and inflammation that characterize severe disease and long COVID.