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Archive - Jan 3, 2018

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Cancer Researchers Investigate How Cells Communicate Using Exosomes, with Special Focus on Increased Exosome Production by Glioblastoma Cells After Chemical Stimulation

by Zehui (Lesley) Li. (The following article was authored by Zehui (Lesley) Li (photo), a PhD student in the University of Toledo College of Medicine and Life Sciences Biomedical Science Program. Lesley is studying chemical messengers between cells and how they can potentially be used to treat cancer. Lesley is doing her research in the laboratory of William Maltese, PhD, in the Department of Cancer Biology. Lesley's article first appeared in Toledo’s "The Blade" newspaper on December 31, 2017, and is reprinted here with permission. Lesley’s article from The Blade follows here): Cells are the basic structural units that are used to build all of the organs in your body. A surface membrane surrounds each cell, just as your skin surrounds you. The cell membrane controls the entry and exit of different things, including food and specific molecules that can change the rate of cell growth and division. One way that the cell membrane can bring in other molecules is within small bubble-like structures that pinch off and move inside the cell. Such bubbles are called endosomes (inside cell). Once [formed] inside the cell, each endosome can make even smaller bubbles within it. These smaller bubbles are called intraluminal vesicles (ILVs). These ILVs are so small that they can only be seen using a very high-powered microscope. Scientists have now discovered that endosomes can return to the cell surface, where they fuse back with the cell membrane and release small ILV bubbles outside the cell. Once they leave the cell, the tiny bubbles are called exosomes (outside cell). These exosomes float in your body fluid and eventually attach to other cell membranes and enter the new cell. After they move in, molecules inside of the bubbles will be released into the new cell to affect cell growth and other cell activities.

New Work Demonstrates Breakdown of Simplest, But Most Widely Used Version of “Kill the Winner” Model to Explain High Levels of Biodiversity, Presents Way to Restore Model’s Explanatory Power

There is remarkable biodiversity in all but the most extreme ecosystems on Earth. When many species are competing for the same finite resource, a theory called “competitive exclusion” suggests one species will outperform the others and drive them to extinction, limiting biodiversity. But this isn't what is actually observed in nature. Theoretical models of population dynamics have not presented a fully satisfactory explanation for what has come to be known as the “diversity paradox.” Now, researchers at the Carl R. Woese Institute for Genomic Biology at the University of Illinois at Urbana-Champaign have shed new light on this fundamental question in ecology, by improving a popular proposed scenario for diversity known as "Kill the Winner." Dr. Chi Xue and Dr. Nigel Goldenfeld (pictured together here), supported by the NASA Astrobiology Institute for Universal Biology, which Dr. Goldenfeld directs, approached the diversity paradox from the perspective of non-equilibrium statistical mechanics. Dr. Goldenfeld and Dr. Xue developed a stochastic model that accounts for multiple factors observed in ecosystems, including competition among species and simultaneous predation on the competing species. Using bacteria and their host-specific viruses as an example, the researchers showed that as the bacteria evolve defenses against the virus, the virus population also evolves to combat the bacteria. This "arms race" leads to diverse populations of both and to boom-bust cycles when a particular species dominates the ecosystem then collapses--the so-called "Kill the Winner" phenomenon. This coevolutionary arms race is sufficient to yield a possible solution to the diversity paradox.