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Our morning routine could be appended to something like “breakfast, stretching, sit on a medical examiner, shower, then commute.” If we are speaking seriously, we don’t always get to our morning stretches, but a quick medical exam could be on the morning agenda. We would wager that a portion of our readers are poised for that exam as they read this article. The examiner could come in the form of a toilet seat. This IoT throne is the next device you didn’t know you needed because it can take measurements to detect signs of heart failure every time you take a load off.

Tracking heart failure is not just one test, it is a buttload of tests. Continuous monitoring is difficult although tools exist for each test. It is unreasonable to expect all the at-risk people to sit at a blood pressure machine, inside a ballistocardiograph, with an oximeter on their fingers three times per day. Getting people to browse Hackaday on their phones after lunch is less of a struggle. When the robots overthrow us, this will definitely be held against us.

We are not sure if this particular hardware will be open-source, probably not, but there is a lesson here about putting sensors where people will use them. Despite the low rank on the glamorous scale, from a UX point of view, it is ingenious. How can we flush out our own projects to make them usable? After all, if you build a badass morning alarm, but it tries to kill you, it will need some work and if you make a gorgeous clock with the numbers all messed up …okay, we dig that particular one for different reasons.

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The United States should devote substantially more resources to nuclear fusion research and build an ambitious prototype fusion power plant, according to a new report.

The report is the work of the National Academies of Sciences, Engineering, and Medicine. Its conclusion: it’s more important than ever for the U.S. and the world to explore roads to practical fusion power.

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The Longevity Therapeutics Summit was focused on therapeutics that target aging, rather than basic research or theory.


This was the first year for the Longevity Therapeutics Summit in San Francisco, California. Ably organized by Hanson Wade, with John Lewis, CEO of Oisín Biotechnologies, as program chair, the conference focused on senolytics for senescent cell clearance, big data and AI in finding new drugs (“in silico” testing), delivery systems for therapeutics like senolytics, TORC1 drugs, and biomarkers of aging, and the challenges of clinical trial development and FDA approval.

The conference featured a smorgasbord of cutting-edge longevity research, and, as the name implies, the general focus was on therapeutics that target aging, rather than basic research or theory.

Ned David, CEO of Unity Biotechnology, kicked off the conference with a talk about the company’s latest research on senolytics, which clear away senescent (“zombie”) cells, which secrete harmful chemicals that can cause neighboring cells to also become senescent. Unity has made the news recently with an extension request for its clinical trial of its first-in-class senolytics for osteoarthritis. Its preliminary Phase 1 clinical trial results were deemed “safe,” a major step in obtaining FDA approval, and the full results will be available later this year or in 2020.

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An MIT-led research team has developed a drug capsule that could be used to deliver oral doses of insulin, potentially replacing the injections that people with type 1 diabetes have to give themselves every day. About the size of a blueberry, the capsule contains a small needle made of compressed insulin, which is injected after the capsule reaches the stomach. In tests in animals, the researchers showed that they could deliver enough insulin to lower blood sugar to levels comparable to those produced by injections given through skin. They also demonstrated that the device can be adapted to deliver other protein drugs.


Capsule that releases insulin in the stomach could replace injections for patients with type 1 diabetes.

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In the life-threatening condition known as sepsis, the body responds to infection by inducing widespread biochemical changes that make the situation worse, some of which can lead to a severe decline in blood pressure. Several molecular factors that alter the constriction of blood vessels are involved in this decline, including nitric oxide, prostaglandins and oxidants such as hydrogen peroxide. In 2010, kynurenine — a metabolic product of the amino acid tryptophan — was identified as another factor that causes blood vessels to widen during sepsis. Writing in Nature, Stanley et al. (who work in the same laboratory as the researchers who identified kynurenine) now say that they got the wrong culprit.


Nine years ago, the compound kynurenine was reported to be responsible for the dilation of blood vessels during a potentially fatal inflammatory condition. New evidence has now identified the true culprit. A re-evaluation of a factor involved in vasodilation.

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Most people have at some point echoed Macbeth’s complaint about the loss of “sleep that knits up the ravelled sleeve of care”. Sleep disorders, such as obstructive sleep apnoea (when breathing temporarily stops, causing both sleep disruption and lack of oxygen in blood) and sleep deprivation, have been associated with an increased risk of atherosclerosis and its harmful cardiovascular effects,. Atherosclerosis is characterized by the formation of ‘plaques’ in arteries, as white blood cells enter the artery wall, take up cholesterol and other substances from the blood and trigger an inflammatory response. However, the mechanisms linking sleep disruption and atherosclerosis have been largely unknown. Writing in Nature, McAlpine et al. show that persistent sleep disruption causes the brain to signal the bone marrow to increase the production of white blood cells.

McAlpine et al. studied mice that were prone to developing atherosclerosis. The authors induced sleep fragmentation by moving a bar intermittently across the bottom of the animals’ cages during their sleep period (Fig. 1), and compared these animals with animals that slept normally. They found that mice with sleep fragmentation had more-severe atherosclerosis, which was paralleled by increases in the production of white blood cells in the bone marrow and in the numbers of monocytes and neutrophils — two types of white blood cell — in the blood. These effects were absent if the bar was moved when the mice were fully awake. Stress activates the sympathetic nervous system (which is associated with the ‘fight-or-flight’ response), and such activation increases the production of white blood cells and atherosclerosis in other experimental settings. However, the authors did not find evidence for a role of sympathetic activation in their setting.

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