While investigating a mysterious radiation signal unlike any seen before, astronomers may have uncovered a rare pair of binary supermassive black holes with a truly monstrous appetite.
Certain cells in the brain create a nurturing environment, enhancing the health and resilience of their neighbors, while others promote stress and damage. Using spatial transcriptomics and AI, researchers at Stanford’s Knight Initiative for Brain Resilience discovered these interactions playing out across the lifespan—suggesting local cellular interactions may significantly influence brain aging and resilience.
A new study was published in Nature in an article titled, “Spatial transcriptomic clocks reveal cell proximity effects in brain aging.”
“What was exciting to us was finding that some cells have a pro-aging effect on neighboring cells while others appear to have a rejuvenating effect on their neighbors,” said Anne Brunet, the Michele and Timothy Barakett Endowed Professor in Stanford’s department of genetics and co-senior investigator of the new study.
The field “touches on all the questions that humanity has asked since it was walking on this planet,” says Moshe Szyf, a professor of pharmacology at McGill University. “How much of our destiny is predetermined? How much of it do we control?”
For some people, the concept that we can carry a legacy of trauma makes sense because it validates their sense that they are more than the sum of their experiences.
“If you feel you have been affected by a very traumatic, difficult, life-altering experience that your mother or father has had, there’s something to that,” says Rachel Yehuda, professor of psychiatry and neuroscience of trauma at Mount Sinai in New York. Her research points to a small epigenetic “signal” that a life-altering experience “doesn’t just die with you,” she says. “It has a life of its own afterwards in some form.”
New research suggests we’ve misunderstood how the building blocks of life on Earth came together. See what scientists found.
A breakthrough in understanding how a single-cell parasite makes ergosterol (its version of cholesterol) could lead to more effective drugs for human leishmaniasis, a parasitic disease that afflicts about 1 million people and kills about 30,000 people around the world every year.
The findings, reported in Nature Communications, also solve a decades-long scientific puzzle that’s prevented drugmakers from successfully using azole antifungal drugs to treat visceral leishmaniasis, or VL.
About 30 years ago, scientists discovered the two species of single-cell parasites that cause VL, Leishmania donovani and Leishmania infantum, made the same lipid sterol, called ergosterol, as fungi proven susceptible to azoles antifungals. These azoles antifungals target a crucial enzyme for sterol biosynthesis, called CYP51.
A new type of norovirus is causing a very high number of cases in countries like England, just as a large trial of an mRNA vaccine is starting up.
If you’ve heard of two of the brain’s chemical neurotransmitters, it’s probably dopamine and serotonin. Never mind that glutamate and GABA do most of the work—it’s the thrill of dopamine as the “pleasure chemical” and serotonin as a tender mood-stabilizer that attract all the headlines.
Of course, the headlines mostly get it wrong. Dopamine’s role in shaping behavior goes way beyond simple concepts like “pleasure” or even “reward”. And the fact that it takes weeks or months for serotonin-boosting SSRI antidepressants to work suggests that it’s not actually the immediate jump in serotonin levels that drum out the doldrums of depression, but some still-mysterious shift in downstream brain circuits.
A new study from Stanford’s Wu Tsai Neurosciences Institute reveals yet another new facet of these mood-managing molecules. The research, published November 25, 2024 in Nature, demonstrates for the first time exactly how dopamine and serotonin work together—or more precisely, in opposition—to shape our behavior.
Algorithm finds the optimal transducer location to focus ultrasound through the skull onto a target in the brain.
It’s time to recalibrate the navigation systems on ships, airplanes, and (given the time of year) Santa’s sleigh: the position of the magnetic North Pole is officially being changed, continuing its shift away from Canada and towards Siberia.
Experts from the US National Oceanic and Atmospheric Administration (NOAA) and the British Geological Survey (BGS) have joined forces – as they do every five years – to produce a new, more accurate World Magnetic Model (WMM).
While the geographical North Pole stays fixed in place (at the very summit of the Earth’s rotational axis), the WMM pinpoints the magnetic North Pole – where Earth’s magnetic field points straight down, a perfectly vertical magnetic field.
Each year, flu causes hundreds of thousands of deaths and millions of hospitalizations worldwide. Although the best way to protect against serious illness is annual vaccination, the influenza vaccine’s effectiveness is far from perfect. In the past decade, CDC estimates of flu vaccine effectiveness have ranged from a low of 19% to a high of 48%, spurring calls for development of more effective flu vaccines. Now, NIH-funded researchers at the Stanford University School of Medicine have taken a new approach to crafting flu vaccines that resulted, both in mice and human tonsil tissue, in a more broadly protective immune response compared to currently available flu vaccines. The studies were led by Mark M. Davis, Ph.D., and the findings appeared in Science.
The trouble with current vaccines
Currently, flu vaccines are formulated annually to contain up to four strains of human influenza virus that are predicted to circulate widely in the coming season. For example, the 2024–2025 seasonal flu vaccine contains two strains of the influenza viurs A subtype and one of influenza virus B subtype. Each virus strain includes a viral protein called hemagglutinin (HA) that the virus uses to attach to and enter human cells. The immune system recognizes and responds to components of a virus or a vaccine—the antigens—by generating protective antibodies and T cells. On exposure to the flu virus, a subset of flu-specific T cells, called CD4+ helper T cells, provides signals to generate and activate antibody-producing B cells. Ideally, a swarm of HA-matched antibodies is produced following vaccination and will protect the vaccinated person from infection by flu virus strains represented in that year’s vaccine.
