Lifeboat Foundation: Safeguarding Humanity
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COLUMBUS, Ohio — A gravitational wave detector that’s 2.5 miles long isn’t cool. You know what’s cool? A 25-mile-long gravitational wave detector.

That’s the upshot of a series of talks given here Saturday (April 14) at the April meeting of the American Physical Society. The next generation of gravitational wave detectors will peer right up to the outer edge of the observable universe, looking for ripples in the very fabric of space-time, which Einstein predicted would occur when massive objects like black holes collide. But there are still some significant challenges standing in the way of their construction, presenters told the audience.

“The current detectors you might think are very sensitive,” Matthew Evans, a physicist at MIT, told the audience. “And that’s true, but they’re also the least sensitive detectors with which you can [possibly] detect gravitational waves.” [8 Ways You Can See Einstein’s Theory of Relativity in Real Life].

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The biotechnology sector’s fastest-growing segment, immuno-oncology, has become the hottest buzzword for investment in Asia.

The field, that uses the body’s own immune system to help fight cancer, has seen two mega acquisitions in the United States in recent months.

And Hong Kong stock exchange is now tuning into its strong future, with Hong Kong Exchanges and Clearing (HKEX) already agreeing to revamp listing rules that will fast track applications by firms linked with the sector to help more innovative drugs and medical devices developers go public as soon as early this summer, and raise much-needed development cash.

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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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Researchers at Gladstone Institutes in San Francisco report that a gene variant associated with Alzheimer’s works differently in mice and humans, and they also demonstrate how modifying this gene could potentially prevent the plaques associated with Alzheimer’s from forming and damaging the brain.

An ApoE3 gene variant is associated with Alzheimer’s disease

The gene apolipoprotein E3 (ApoE3) has a variant known as ApoE4, which is associated with the development and progress of Alzheimer’s disease. People with just one copy of the ApoE4 gene are at twice the risk as people without this gene variant. Some people even have two copies of the ApoE4 gene, which makes their risk of Alzheimer’s a staggering twelve times greater.

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