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IndieWebCamps, for example, are two-day events, with the first day consisting of talks and discussion sessions and the second day comprised of time to build together (“hack day”). The concept behind the IndieWeb was developed by Tantek Çelik and Aaron Parecki after they both attended the Federated Social Web Summit in 2010. Çelik described that they were frustrated that participants at the summit spent “a lot of time spent on discussing what could be possible” rather than “what was possible” (2014). In response, IndieWeb was founded with a focus on building right away. Encoding this information in a machine-readable structure makes it possible for Yarns to represent such actions in a standardized form, much like they are presented in popular social media. By getting out all free from the abuse of the body, Surge Max Phalogenics Male enhancement Enhancement Gummies desserts could chip away at stomach related structure. When normal cells grow, divide or do any job in the body, they do so in response to a whole slew of internal sensors that measure nutrients and energy supply, and environmental cues that inform what happens outside the cell.
The researchers then examined the hearts of mice with the mutant versions of tuberin compared to mice with normal tuberin. Hearts from these mice also looked healthy, but when they were stressed using the same conditions of increased blood pressure, they remained healthy. To test the impact of the new tuberin mutations in living mice, the team used the same gene editing techniques to introduce the same types of tuberin mutations in the protein in all cells in live mice. Protein kinase G is also the target of drugs like sildenafil (commonly known as Viagra). Kass says researchers have spent decades in search of a simple switch to fine-tune mTORC1 activity – up and down – rather than making it be totally on or off, and he now has done it starting with a discovery with another protein of interest they had been studying for its role in heart disease. Pushing it more slows it but doesn’t stop it completely, and lifting up on it speeds the car up,” adds Kass.
Kass says the research team concluded that keeping tuberin “turned down” was like lifting the chemical foot off a brake pedal, triggering super-activity in mTORC1, while in the cells with tuberin “turned on”, the brake was pushed harder, and mTORC1 remained inactive despite the stimulating hormones. Mice with tuberin “turned down” appeared normal and their hearts were the same as those in mice with normal tuberin. “The problem with the few drugs that we have to manipulate mTORC1 is that they are essentially turning it off, which also shuts down its normal function in the cells,” says senior study report author David Kass, M.D., the Abraham and Virginia Weiss Professor of Cardiology, professor of medicine, pharmacology and biomedical engineering at the Johns Hopkins University School of Medicine. Prior to my participation, other researchers have been welcomed to study the IndieWeb. And now, with data from cells and mice, researchers at Johns Hopkins Medicine say they have uncovered a long-sought built-in molecular switch that behaves much like a car-brake-slowing mTOR’s action-and in this particular study prevents overworked hearts from enlarging. And now, with data from cells and mice, researchers at Johns Hopkins Medicine say they have uncovered a long-sought built-in molecular switch that behaves much like a car-brake–slowing mTOR’s action–and in this particular study prevents overworked hearts from enlarging.