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Forget zombies or killer robots – the most likely doomsday scenario in the near future is the threat of superbugs. Bacteria are evolving resistance to our best antibiotics at an alarming rate, so developing new ones is a crucial area of study. Now, inspired by a natural molecule produced by marine microorganisms, researchers at North Carolina State University have synthesized a new compound that shows promising antibacterial properties against resistant bugs.

Decades of overuse and overprescription of antibiotics has led to more and more bacteria becoming resistant to them, and the situation is so dire that a recent report warned that they could be killing up to 10 million people a year by 2050. Worse still, the bugs seem to be on schedule, with the ECDC reporting that our last line of defense has already begun to fail in large numbers.

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https://www.engadget.com/…/3D-printed-brain-medical-imagin…/


There are almost limitless possibilities when it comes to 3D printing. Design your own color-changing jewelry? Fine. Fabricate your own drugs? No problem. Print an entire house in under 24 hours? Sure! Now, researchers have come up with a fast and easy way to print palm-sized models of individual human brains, presumably in a bid to advance scientific endeavours, but also because, well, that’s pretty neat.

In theory, creating a 3D printout of a human brain has been done before, using data from MRI and CT scans. But as MIT graduate Steven Keating found when he wanted to examine his own brain following his surgery to remove a baseball-sized tumour, it’s a slow, cumbersome process that doesn’t reveal any important areas of interest.

MRI and CT scans produce images with so much detail that objects of interest need to be isolated from surrounding tissue and converted into surface meshes in order to be printed. This involves a radiologist manually tracing the desired object onto every single image “slice” of the brain, or it can be done via automatic thresholding, where a computer converts areas that contain grayscale pixels into either solid black or solid white pixels, based on a shade of gray that is chosen to be the threshold between black and white. But since medical imaging data often contains irregularly-shaped objects and lacks clear borders, features of interest are usually over- or under-exaggerated, and details are washed out.

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I will be 85 somewhere in the mid 2050s. It seems like a mirage, an impossible thing, but the future eventually arrives regardless of whatever you or I might think about it. We all have a vision of what it is to be 85 today, informed by our interactions with elder family members, if nothing else. People at that age are greatly impacted by aging. They falter, their minds are often slowed. They are physically weak, in need of aid. Perhaps that is why we find it hard to put ourselves into that position; it isn’t a pleasant topic to think about. Four decades out into the future may as well be a science fiction novel, a far away land, a tale told to children, for all the influence it has on our present considerations. There is no weight to it.

When I am 85, there will have been next to no senescent cells in my body for going on thirty years. I bear only a small fraction of the inflammatory burden of older people of past generations. I paid for the products of companies descended from Oisin Biotechnologies and Unity Biotechnology, every few years wiping away the accumulation of senescent cells, each new approach more effective than the last. Eventually, I took one of the permanent gene therapy options, made possible by biochemical discrimination between short-term beneficial senescence and long-term harmful senescence, and then there was little need for ongoing treatments. Artificial DNA machinery floats in every cell, a backup for the normal mechanisms of apoptosis, triggered by lingering senescence.

When I am 85, the senolytic DNA machinery will be far from the only addition to my cells. I underwent a half dozen gene therapies over the years. I picked the most useful of the many more that were available, starting once the price fell into the affordable-but-painful range, after the initial frenzy of high-cost treatments subsided into business as usual. My cholesterol transport system is enhanced to attack atherosclerotic lesions, my muscle maintenance and neurogenesis operate at levels far above what was once a normal range for my age, and my mitochondria are both enhanced in operation and well-protected against damage by additional copies of mitochondrial genes backed up elsewhere in the cell. Some of these additions were rendered moot by later advances in medicine, but they get the job done.

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Earlier this month, there was a human clinical trial of the supplement MitoQ, which showed some interesting results. We thought that we would take a look at the data, and discuss the findings.


Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and efficacy of MitoQ. Twenty healthy older adults (60–79 years) with impaired endothelial function (brachial artery flow–mediated dilation 6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study.

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Research on people’s reaction to life extension is rather rare; this article discusses two such papers.


Two papers by Partridge et al [1, 2], both published in 2009, provide the somewhat rare opportunity to examine some concerns about life extension as formulated by actual people, rather than their general, more abstract forms. As highlighted in the studies, research on the public’s perception of life extension science has been very much neglected; this, in turn, has made it harder to identify the misconceptions and incorrect information fueling some common concerns about life extension and made it even harder to address those very concerns. Needless to say, the more that the public views life extension negatively, the less supportive that it will probably be, which is bad news for researchers.

The papers present the results of several interviews, conducted either in person or on the phone, aimed at understanding what ethical concerns the interviewees had about life extension and what implications they thought extended human lifespans would have for themselves and for society. The research was conducted on a sample of the Australian population only, but the issues they raised were entirely representative of a typical discussion about life extension. In both studies, the interviewees were presented with the general premise of possibly slowing down aging and the onset of age-related diseases in order to greatly extend human healthy lifespan.

We’ll be taking a look at specific claims made or sentiments expressed by different interviewees in both studies.

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Who wants to lose weight, feel great, and live a long and healthy life, and what does it take to achieve these goals? Diet and exercise are equally important in long-term health, but let’s look at what recent science is telling us about the healthiest diets.

This article will rely heavily on University of Southern California professor Valter Longo’s work because I consider it to be the gold standard for nutrition research, and his recommendations in his book The Longevity Diet are well-supported with both data and good logic. Longo is the director of the Longevity Institute at USC and the IFOM Program on Longevity and Cancer in Milan.

He comes from an area of Italy known for very long lives, and part of his research focus has been looking at similar areas around the world and why those people live so much longer than normal.

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