Lifeboat Foundation

The Standard Model of particle physics is our current best-guess on what the blue-prints for matter looks like. Of all of its predictions, none are as precise as the magnetic moment of the electron.

Not only is it precisely predicted, it’s among the most accurately measured of any particle’s properties. And while these two values are close, they don’t overlap entirely, providing tantalizing hints of new physics.

Getting closer to the exact value of the electron magnetic moment – simply put, how strongly an electron behaves like a tiny magnet – might one day unlock a greater understanding of the building blocks of physics and how they interact.

New galaxy candidates from a James Webb Space Telescope survey have astronomers shocked and thrilled.

New results show fully formed galaxies in the early Universe that could rewrite what we know about galaxies and black holes.

An updated metric for prioritizing species’ conservation that incorporates scientific uncertainty and complementarity between species, in addition to extinction risk and evolutionary distinctiveness, has been published on February 28 in the open access journal PLOS Biology, authored by Rikki Gumbs from the Zoological Society of London (ZSL), U.K., and colleagues.

In 2007, ZSL established the Evolutionarily Distinct and Globally Endangered (EDGE) metric to prioritize species for conservation based on preserving evolutionary history embodied within endangered species. The approach allocates each species a score based on the evolutionary distance, measured in millions of years, that separates a species from its closest living relatives, and its conservation status in the IUCN Red List.

EDGE has since been applied to mammals, amphibians, birds, sharks and rays, corals, and flowering plants, and is used to allocate conservation funding. To update the EDGE metric to incorporate recent advances in evolutionary biology and conservation, ZSL hosted a workshop for conservation scientists and practitioners, who reached a consensus on EDGE2—an updated metric that includes the extinction risk of closely related species and uncertainty in species’ relationships and conservation status.

Northwestern Medicine scientists have identified the cause of a genetic subtype of autism and schizophrenia that results in social deficits and seizures in mice and humans.

Scientists have discovered a key feature of this subtype is a duplicated gene that results in overactive or overexcited brain circuits. The subtype is called 16p11.2 duplication syndrome.

“We found that mice with the same genetic changes found in humans are more likely to have seizures and also have social deficits,” said lead author Marc Forrest, research assistant professor of neuroscience at Northwestern University Feinberg School of Medicine.

Rare diseases affect 6–8% of the world’s population and, although we know that small changes in the patient’s DNA are responsible for causing the majority of cases, most people wait several years before they are diagnosed and potentially treated. This hunt for an explanation is extremely distressing for the patients and their families, as well as costing healthcare systems large sums of money for medical investigations and treatments.

Background

Even for the simplest cases, where a single change in a patient’s DNA disrupts a gene and always causes the rare disease, identifying which change in the three billion base pairs in each of our genomes is a huge challenge. Prior to the completion of the human genome in 2003, we did not even know what the normal state of affairs was. Even then, the available sequencing technology limited us to only interrogating small parts of a patient’s genome, directed by intelligent guesswork, with mixed results.

Philip Ball finds out how quantum computers could transform how we make and create music.

Move over artificial intelligence, say hello to “organoid intelligence” (OI).

Life began on Earth about 3.7 billion years ago. But what if it was present in the universe even before that? It sounds strange, but this is what the Pansper…

The ability to extinguish fear memories when threats are no longer present is critical for adaptive behavior. Fear extinction represents a new learning process that eventually leads to the formation of extinction memories. Understanding the neural basis of fear extinction has considerable clinical significance as deficits in extinction learning are the hallmark of human anxiety disorders. In recent years, the dopamine (DA) system has emerged as one of the key regulators of fear extinction. In this review article, we highlight recent advances that have demonstrated the crucial role DA plays in mediating different phases of fear extinction. Emerging concepts and outstanding questions for future research are also discussed.

Learning to associate stimuli and situations with danger or safety is critical for survival and adaptive behavior. In the laboratory, these forms of learning are typically studied using Pavlovian fear conditioning and extinction. Fear conditioning is an example of associative learning in which an initially neutral stimulus such as a tone (conditioned stimulus, CS) comes to elicit fear responses after being paired in time with an aversive outcome such as a foot shock (unconditioned stimulus, US). Once the CS-US association is learned, subsequently repeated presentations of the CS in the absence of the aversive US result in a gradual decrease in conditioned fear responses, a process known as fear extinction. In the last decades, fear extinction has attracted much interest in part because deficits in extinction learning are thought to underlie human anxiety disorders, such as post-traumatic stress disorder (PTSD) and phobias (Graham and Milad, 2011; Pitman et al., 2012; Craske et al.