Researchers at Johns Hopkins have discovered how to block a molecular switch that triggers brain damage caused by the lack of oxygen during a stroke. The Hopkins study, conducted on mice, is believed to be the first to demonstrate that a protein on the surface of nerve cells called the EP1 receptor is the switch, and that a specific compound, known as ONO-8713, turns it off.
The finding holds promise for the development of effective alternatives to anti-inflammatory drugs called COX inhibitors, which have potentially lethal side effects that limit their use, says Sylvain Doré, Ph.D., an associate professor in the departments of Anesthesiology and Critical Care Medicine and Neuroscience at The Johns Hopkins University School of Medicine. Doré is senior author of the paper, published in the January issue of Toxicological Sciences. "Our work has shifted the focus from drugs that inhibit COX-2 to drugs that block the EP1 receptor," Doré said.
Receptors are protein-docking sites on cells into which "signaling" molecules such as nerve chemicals or hormones insert themselves. This binding activates the receptor, which transfers the signal into the cell to produce a specific response.
Eric Vohr | EurekAlert!
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The BMBF-funded OWICELLS project was successfully completed with a final presentation at the BMW plant in Munich. The presentation demonstrated a Li-Fi communication with a mobile robot, while the robot carried out usual production processes (welding, moving and testing parts) in a 5x5m² production cell. The robust, optical wireless transmission is based on spatial diversity; in other words, data is sent and received simultaneously by several LEDs and several photodiodes. The system can transmit data at more than 100 Mbit/s and five milliseconds latency.
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19.06.2018 | Physics and Astronomy