IN A NUTSHELL 🔍 The ARC-AGI-2 test challenges AI models to identify visual patterns and adapt to new problems. 💡 Unlike its predecessor, ARC-AGI-2 emphasizes efficiency, assessing both problem-solving ability and resource use. 📉 Many top AI models, including OpenAI’s o1-pro, scored around 1% on the test, highlighting current limitations. 🏆 The Arc Prize 2025
🧬 What keeps your cells from dividing at the wrong time? In this video, we dive into the world of Cyclin-Dependent Kinases (CDKs) — the master regulators of the cell cycle.
📌 Here’s what you’ll learn:
What CDKs are and how they function.
The role of cyclins in activating CDKs.
Key cell cycle checkpoints (G1, G2, M)
How CDK-cyclin complexes regulate progression through each phase.
Driven by genetic and environmental factors, aging is a physiological process responsible for age-related degenerative changes in the body, cognitive decline, and impaired overall wellbeing. Notably, premature aging as well as the emergence of progeroid syndromes have posed concerns regarding chronic health conditions and comorbidities in the aging population. Accelerated telomere attrition is also implicated in metabolic dysfunction and the development of metabolic disorders. Impaired metabolic homeostasis arises secondary to age-related increases in the synthesis of free radicals, decreased oxidative capacity, impaired antioxidant defense, and disrupted energy metabolism. In particular, several cellular and molecular mechanisms of aging have been identified to decipher the influence of premature aging on metabolic diseases. These include defective DNA repair, telomere attrition, epigenetic alterations, and dysregulation of nutrient-sensing pathways. The role of telomere attrition premature aging in the pathogenesis of metabolic diseases has been largely attributed to pro-inflammatory states that promote telomere shortening, genetic mutations in the telomerase reverse transcriptase, epigenetic alteration, oxidative stress, and mitochondrial dysfunctions. Nonetheless, the therapeutic interventions focus on restoring the length of telomeres and may include treatment approaches to restore telomerase enzyme activity, promote alternative lengthening of telomeres, counter oxidative stress, and decrease the concentration of pro-inflammatory cytokines. Given the significance and robust potential of delaying telomere attrition in age-related metabolic diseases, this review aimed to explore the molecular and cellular mechanisms of aging underlying premature telomere attrition and metabolic diseases, assimilating evidence from both human and animal studies.
Aging is defined as a physiological phenomenon driven by genetic and biological processes, which are related to the lifespan of an individual and are associated with all age-related pathologies (Li et al., 2021). The aging process increases the susceptibility of individuals to factors leading to death as they grow older. Aging is a complex multifactorial phenomenon that involves the simultaneous interaction between various factors at different levels of functional organization. The role of genetic and environmental factors is represented by the heterogenous aging phenotype across different individuals, hence, these factors influence the lifespan of an individual via the process of aging (Jayanthi et al., 2010). With the deterioration of physiological functions critical to the survival and fertility of humans, the process of aging is known to relate to the notion of natural selection (Gilbert, 2000).
Chronic pain—or pain that lasts at least three months—is closely intertwined with depression. Individuals living with pain’s persistent symptoms may be up to four times more likely to experience depression, research shows.
Almost 30% of people worldwide suffer from a chronic pain condition such as low back pain and migraines, and one in three of these patients also report co-existing pain conditions.
Now, a new study published in Science Advances shows that a person’s risk of depression increases alongside the number of places in the body in which they experience pain. Furthermore, inflammatory markers such as C-reactive protein (a protein produced by the liver in response to inflammation) help explain the association between pain and depression.
Imagine a Slushee composed of ammonia and water encased in a hard shell of water ice. Now picture these ice-encrusted slushballs, dubbed “mushballs,” raining down like hailstones during a thunderstorm, illuminated by intense flashes of lightning.
Planetary scientists at the University of California, Berkeley, now say that hailstorms of mushballs accompanied by fierce lightning actually exist on Jupiter. In fact, mushball hailstorms may occur on all gaseous planets in the galaxy, including our solar system’s other giant planets, Saturn, Uranus and Neptune.
The idea of mushballs was initially put forth in 2020 to explain nonuniformities in the distribution of ammonia gas in Jupiter’s upper atmosphere that were detected both by NASA’s Juno mission and by radio telescopes on Earth.
Altman’s playful response to Meta’s AI ambitions: ok fine maybe we’ll do a social app.
Sam Altman’s OpenAI has recently starting woking on an internal prototype social network to rival Elon Musk’s X.
A paper published in 2024 theorizes that time may have existed before the Big Bang, but we’re still not entirely sure.
Scientists precisely removed a gold nanocluster’s core atom and outer electron, revealing how spin state affects catalytic activity without structural loss.
A research team at the Institute for Basic Science (IBS) has identified a previously unknown enzyme, SIRT2, that plays a key role in memory loss associated with Alzheimer’s disease (AD). The study, led by Director C Justin LEE, of the IBS Center for Cognition and Sociality, provides critical insights into how astrocytes contribute to cognitive decline by producing excessive amounts of the inhibitory neurotransmitter GABA.
Astrocytes, once thought to only support neurons, are now known to actively influence brain function. In Alzheimer’s disease, astrocytes become reactive, meaning they change their behavior in response to the presence of amyloid-beta (Aβ) plaques, a hallmark of the disease. While astrocytes attempt to clear these plaques, this process triggers a harmful chain reaction. First, they uptake them via autophagy (Kim and Chun, 2024) and degrade them by the urea cycle (Ju et al, 2022), as discovered in previous research. However, this breakdown results in the overproduction of GABA, which dampens brain activity and leads to memory impairment. Additionally, this pathway generates hydrogen peroxide (H2O2), a toxic byproduct that causes further neuronal death and neurodegeneration.
