Even before a tumor in the pancreas becomes discernible, an activated cancer gene actively remodels its future environment and creates an inflammatory and immune-defensive microenvironment in which the carcinoma can grow. This has been shown by an international research team led by Ulm University in a pioneering study. The scientists’ study opens up new possibilities for developing personalized intervention strategies—before a difficult-to-treat tumor even develops.
It is one of the most aggressive forms of cancer: Pancreatic cancer is usually diagnosed late because it initially causes no symptoms and therefore goes unnoticed. In addition, it is highly metastasizing. Once pancreatic cancer is finally identified, a cure is often no longer possible.
A research team from the Institute of Molecular Oncology and Stem Cell Biology (IMOS) at Ulm University, together with national and international partners, has made a ground-breaking discovery that could pave the way for a much earlier diagnosis: The oncogene KRAS —the main driver of pancreatic cancer—creates its own environment, providing best growth conditions for the carcinoma and in which immune defense T-cells cannot penetrate. The results of the study have now been published in the journal Molecular Cancer.
An exploration of the concept of artificially manipulated star clusters and how it might constitute a technosignature.
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Arad Soffer, Aishwarya Bhosale, Carien M. Niessen, Chen Luxenburg, Matthias Rübsam (Universität zu Köln) and colleagues identify spectrin as a central component of epithelial cortical actomyosin networks to control cortex mechanics and signaling.
Cell shape and fate are tightly linked, yet how the cortical cytoskeleton integrates regulation of shape and fate remains unclear. Using the multilayered epidermis as a paradigm for cell shape–guided changes in differentiation, we identify spectrin as an essential organizer of the actomyosin cortex to integrate transitions in cell shape with spatial organization of signaling. Loss of αII-spectrin (Sptan1) in mouse epidermis altered cell shape in all layers and impaired differentiation and barrier formation. High-resolution imaging and laser ablation revealed that E-cadherin organizes gradients of cortical actin and spectrin into layer-specific submembranous networks with discrete structural and mechanical properties that coordinate cell shape and fate. This layer-specific organization dissipates tension and, in upper layers, retains activated growth factor receptor EGFR and the calcium channel TRPV3 at the membrane to induce terminal differentiation. Together, these findings reveal how polarized organization of the cortical cytoskeleton directs transitions in cell shape and cell fate at the tissue scale necessary to establish epithelial barriers.
Danish nuclear technology company Copenhagen Atomics has completed two years of continuous operation of a molten salt pump and test loop at its facilities in Copenhagen. The system has been running without issues under high-temperature molten salt conditions, marking one of the longest continuous durability tests of its kind worldwide, it said. ;
Dashiell Hammett mentioned Sam Spade’s jutting chin in the opening sentence of his novel, “The Maltese Falcon.” Spade’s chin was among the facial features Hammett used to describe his fictional detective’s appearance, but starting with that distinctive chin was—at least from an evolutionary perspective—an unintentional redundancy, since every chin is distinctive in the sense that humans are the only primates to possess that physical characteristic.
Chimpanzees, humans’ closest living relatives, do not have a chin. Neither did Neanderthals, Denisovans, or any other extinct human species. Humans, it turns out, have a unique capacity to “take it on the chin” because we’re uniquely in possession of that physical feature. That exclusive nature makes the chin well suited for identifying Homo sapiens in the fossil record.
In simplest terms, a chin is a bony projection of the lower jaw. So why is it there? How and why did it evolve?
