A small-molecule drug proves its mettle in the treatment of spinal muscular atrophy, a disease amenable to intervention at the pre-mRNA level.
“AI will most likely lead to the end of the world, but in the meantime there will be great companies created.” — Sam Altman, OpenAI CEO
I used to think that was dark humor.
This week, I stopped laughing — and cancelled my ChatGPT subscription.
Not because of the technology. Because of the values.
On February 27, Anthropic refused to give the Pentagon unrestricted access to its AI for mass surveillance and autonomous killer weapons. Within hours, OpenAI’s Sam Altman swooped in and took the deal.
One company held the line. The other sprinted to cross it.
“Our system provides a pathway towards a fast, scalable tool for measuring real-time brain activity in synthetic tissue cultures that replicate human brain tissue,” Associate Professor Simpson said.
If successful, this brain-on-chip technology could help evaluate the effectiveness of treatments for neurological diseases, including Alzheimer’s, schizophrenia, epilepsy and anxiety, in the laboratory before moving into expensive and complex human trials.
NYU researchers have found a way to use light to control how microscopic particles assemble into crystals, effectively turning illumination into a tool for shaping matter. By adding light-sensitive molecules to a liquid filled with tiny particles, they can adjust how strongly the particles attract or repel one another simply by changing the light’s intensity or pattern. This allows them to trigger crystals to form, dissolve, or even be reshaped in real time.
Isomorphic Labs has developed a drug-protein interaction model which surpasses the previous tech in this area. Yet the model is proprietary, so no one knows how it was designed and trained and why it works so well!
Isomorphic Lab’s proprietary drug-discovery model is a major advance, but scientists developing open-source tools are left guessing how to achieve similar results.
Breast cancer destroyed by a plant compound.
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, characterized by the poorest prognosis, and poses a significant threat to women’s health. In this study, we identified two novel prieurianin-type limonoids extracted from Munronia henryi, one of which, named DHL-11, exhibited antitumor activity against TNBC cells. DHL-11 suppressed cell proliferation and migration, induced G2/M cell cycle arrest and apoptosis, and effectively increased the accumulation of reactive oxygen species (ROS) and cellular DNA damage in TNBC cells. Mechanistically, we found that DHL-11 binds to the non-catalytic pocket of IMPDH2 and disrupts the interaction between IMPDH2 and FANCI, leading to the degradation of the IMPDH2 protein. The decrease of IMPDH2 protein reduced guanine synthesis, increased ROS levels, and induced DNA damage.