The laws of physics that concern heat and work could gain a firmer mathematical footing thanks to “gauge theory”, which already helps us understand quantum fields
Ladder-type oligothiophenes are an important class of sulfur-containing π-conjugated molecules. Because their fused, ladder-like structures can support efficient electronic interactions, they are widely studied as core motifs for organic semiconductors, organic field-effect transistors, flexible electronics and related molecular materials.
In molecular electronics, however, simply connecting rings together is not enough. The electronic properties of these molecules depend strongly on how the thiophene rings are fused and how sulfur atoms are oriented along the molecular framework. Some arrangements produce highly conjugated systems, while others introduce cross-conjugated segments that can alter the band gap and molecular packing.
Although interest in such mixed conjugated/cross-conjugated molecular systems is growing, a general method for systematically constructing regioisomeric ladder-type oligothiophenes with precise control over thiophene ring orientation has not been well established.
DZNE researchers have uncovered a mechanism that determines why a neuron usually forms a single, long extension called an “axon”—a phenomenon that is fundamental to how our brain functions. Contrary to the common view that external cues drive axon formation, the team of scientists concluded that its growth originates primarily inside the cell. Their work, based on cell cultures and published in the journal Nature with collaborators from other institutions in Germany, Austria and Japan, reveals how a neuron’s structure is remodeled to generate the axon.
Neurons in the brain and spinal cord form a vast network in which each cell receives many inputs but sends output through only a single, long extension: the axon. “If our neurons had multiple axons, this would cause chaos in the brain,” says Frank Bradke, a neurobiologist and research group leader at DZNE. “Nature has therefore found a clever way to make sure that neurons generate only one axon. This applies not only to humans, but across the entire animal kingdom. So, we’re dealing with very fundamental processes that shape the wiring of the brain and nervous system.”
Researchers at Karolinska Institutet in Sweden and Kyoto University in Japan have identified new subgroups of the blood cancer acute myeloid leukemia. The study, published in the journal Nature, shows that changes in the regulation of genes within cells can help explain variation in the disease and influence prognosis and treatment choices.
Acute myeloid leukemia (AML) is an aggressive form of blood cancer in which immature blood cells grow uncontrollably. Despite extensive knowledge of the genetic alterations underlying the disease, it is still difficult to fully understand why patients develop different disease courses. In this study, the researchers analyzed so-called epigenetics—how genes are regulated without changes to the DNA sequence.
Anxiety disorders affect more than 300 million people globally. Several brain regions have been linked to anxiety, but how these regions connect has been poorly understood. By exploring these connections, scientists at St. Jude Children’s Research Hospital revealed that epinephrine-producing C1 neurons in mice modulate fear and anxiety. They found that while the activity of these neurons was normally temporarily elevated in times of stress, prolonged activation led to heightened anxiety that could last many days. Inhibition of C1 neurons reduced anxiety-like behaviors, suggesting these neurons may be worth exploring as therapeutic targets for anxiety disorders. The findings were published today in Neuron.
Anxiety helps us prepare for future threats, but when it is excessive or persistent, it can significantly affect quality of life. Medications exist to alleviate symptoms but can have off-target effects that might discourage long-term use. By identifying C1 neurons as novel modulators of fear and anxiety, Lindsay Schwarz, Ph.D., Department of Developmental Neurobiology, is hopeful that these cells could serve as a new therapeutic target for anxiety-related disorders.
“C1 neurons appear to promote anxiety without directly affecting autonomic functions,” Schwarz said. “This suggests they may be a better target than broadly affecting signaling across the entire brain and body.”
I’ve been playing with local AI models; AI you can run on your own computer for years now. Each year it gets better and better. Similar to the online cloud-based frontier models (you know them). I won’t go into all the advantages of running open source models on your own local hardware, the reasons are somewhat obvious.
Spielberg’s Disclosure Day reopened a question I’ve carried since childhood: what happens when humanity learns it was never alone?