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Disruption of the regulator for G protein signaling 14 (RGS14) knockout (KO) in mice extends their lifespan and has multiple beneficial effects related to healthful aging, that is, protection from obesity, as reflected by reduced white adipose tissue, protection against cold exposure, and improved metabolism. The observed beneficial effects were mediated by improved mitochondrial function. But most importantly, the main mechanism responsible for the salutary properties of the RGS14 KO involved an increase in brown adipose tissue (BAT), which was confirmed by surgical BAT removal and transplantation to wild‐type (WT) mice, a surgical simulation of a molecular knockout. This technique reversed the phenotype of the RGS14 KO and WT, resulting in loss of the improved metabolism and protection against cold exposure in RGS14 KO and conferring this protection to the WT BAT recipients. Another mechanism mediating the salutary features in the RGS14 KO was increased SIRT3. This mechanism was confirmed in the RGS14 X SIRT3 double KO, which no longer demonstrated improved metabolism and protection against cold exposure. Loss of function of the Caenorhabditis elegans RGS‐14 homolog confirmed the evolutionary conservation of this mechanism. Thus, disruption of RGS14 is a model of healthful aging, as it not only enhances lifespan, but also protects against obesity and cold exposure and improves metabolism with a key mechanism of increased BAT, which, when removed, eliminates the features of healthful aging.

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A clinical-grade retinal implant made of human #embryonic stem cell (#hESC)–derived RPE grown on a synthetic substrate has been developed by Kashani and team. The progressive binding disease that causes loss of the retinal pigment epithelium (RPE) of the eye is known as #Non-neovascular age-related macular degeneration (#NNAMD). Currently there are only preventative measures that can be taken but there is no effective treatment. Some preventative measures include quitting smoking and the use of specific nutritional supplements to reduce the risk of developing NNAMD. The implant was not only shown to be safe in a first-in-human phase 1 clinical trial in five patients with advanced NNAMD, but also well tolerated. Plausible therapeutic effects on visual clarity were reported in the experimental results, indicating that this approach may be beneficial for treating retinal disorders involving #RPE loss.

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Scientists could be one step closer to a solution to atherosclerosis by preventing the buildup of plaques that clog the arteries and lead to strokes and heart attacks.

What is atherosclerosis?

Atherosclerosis is the accumulation of cholesterol-containing plaques in the walls of arteries; this causes them to narrow, leading to reduced blood flow, higher blood pressure, and an increased risk of a heart attack or stroke. Atherosclerosis is the number one cause of death globally, and, by far, the highest risk factor for this disease is aging, although there are lifestyle factors, such as poor diet, smoking, obesity, and being sedentary.

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ESA’s Mars Express orbiter is getting a major software upgrade that will extend its service life for years to come. On Sunday, the space agency uploaded the update into the veteran deep space probe’s computers where it will remain stored in memory until a scheduled restart on April 16. If successful, it will take some of the burden off the aging gyroscopes used to keep the unmanned spacecraft’s vital high-gain radio antenna pointed at Earth.

As anyone who regularly uses digital devices can tell you, software updates are a way of life. It turns out that Mars orbiting spacecraft are no exception, with aging electronics that need new instructions to deal with worn out components after years of heavy use.

Mars Express is one of the oldest still-functioning missions to the Red Planet. Launched on June 2, 2003 atop a Soyuz-FG rocket from the Baikonur Cosmodrome, the orbiter arrived at Mars on December 25 of that year. Since then, it has spent 14 years revolving about Mars taking photographs and gathering a mountain of scientific data to send back to mission control in Darmstadt, Germany.

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This is a fairly common response to the discussion of extending healthy human lifespans. The idea that fear of dying is the only thing that motivates the advocates, supporters, and scientists working on rejuvenation biotechnology and ending age-related diseases.


These days, war is not really portrayed in a very good light. When we think about war, we think about genocide, mass murder, and slaughter, and we call for an end to it. The popular sentiment is that war is bad and we should just do away with it. However, once upon a time, things were rather different, and soldiers fighting wars were not seen as victims of mindless violence. Losing your life in battle was considered glorious and noble, and your family would be proud of you for fighting in the name of your country, your God, or whatever. People who were afraid of dying and refused to fight were regarded as cowards, most certainly not as pacifists of a strong moral fiber, and were possibly executed; being a conscientious objector was not yet a thing, and human rights weren’t either.

This is sheer madness to us, but back in the day, it was entirely normal. Most of us will probably think people must have been crazy to let themselves be fooled into believing such nonsense, but that’s the power of propaganda for you.

The modern age of pro-death propaganda

However, the story is not completely over even today. This may be because of past glorification of death, stale ideas about the “circle of life”, a widespread coping mechanism, or a combination of the three, but at least in certain circumstances, being afraid of death is still seen as a sign of cowardice and sometimes also inferiority.

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It’s time to rethink the quest to control aging, death, and disease—and the fear of mortality that fuels it.

I went to medical school, at least in part, to get to know death and perhaps to make my peace with it. So did many of my doctor friends, as I would find out. One day—usually when you’re young, though sometimes later—the thought hits you: You really are going to die. That moment is shocking, frightening, terrible. You try to pretend it hasn’t happened (it’s only a thought, after all), and you go about your business, worrying about this or that, until the day you put your hand to your neck—in the shower, say—and … What is that? Those hard lumps that you know, at first touch, should not be there? But there they are, and they mean death. Your death, and you can’t pretend anymore.

I never wanted to be surprised that way, and I thought that if I became a doctor and saw a lot of death, I might get used to it; it wouldn’t surprise me, and I could learn to live with it. My strategy worked pretty well. Over the decades, from all my patients, I learned that I would be well until I got sick and that although I could do some things to delay the inevitable a bit, whatever control I had was limited. I learned that I had to live as if I would die tomorrow and at the same time as if I would live forever. Meanwhile, I watched as what had been called “medical care”—that is, treating the sick—turned into “health care,” keeping people healthy, at an ever-rising cost.

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Kazan, Russia, April 23–25.


23–25 April 2018 in Kazan (Russia) will be a biogerontological conference with the following main topics:

- Epigenetic mechanisms of aging

- Genomics, metabolomics, proteomics of longevity in humans and animals.

- Environment and aging

- Biomarkers of biological age

- Pharmacological interventions in aging.

- Mechanisms of regeneration.

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