Lifeboat Foundation: Safeguarding Humanity
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Blog – Page 8722

Do you really want to live forever?

My mission is to drastically improve your life by helping you break bad habits, build and keep new healthy habits to make you the best version of yourself. I read the books and do all the research and share my findings with you!

This video is “Day 0” of RAADFest 2019 in Las Vegas. I discuss various topics and will do my best at RAADFest to interview longevity experts like Bill Faloon, James Strole, Bernadeane, Liz Parrish, Dr. Aubrey de Grey, Dr. Bill Andrews, Dr. Ed Park, Dr. Duncan Ross, Ben Goertzel and hopefully many more. I’ll bring you all the major updates from RAADFest!

Continue reading “RAADFest Roundup Day 0, 2019, Las Vegas” | >

Many of the world’s most common or deadly human pathogens are RNA-based viruses—Ebola, Zika and flu, for example—and most have no FDA-approved treatments. A team led by researchers at the Broad Institute of MIT and Harvard has now turned a CRISPR RNA-cutting enzyme into an antiviral that can be programmed to detect and destroy RNA-based viruses in human cells.

Researchers have previously adapted the Cas13 enzyme as a tool to cut and edit human RNA and as a diagnostic to detect the presence of viruses, bacteria, or other targets. This study is one of the first to harness Cas13, or any CRISPR system, as an antiviral in cultured .

The researchers combined Cas13’s with its diagnostic capability to create a single system that may one day be used to both diagnose and treat a viral infection, including infections caused by new and emerging viruses. Their system, called CARVER (Cas13-Assisted Restriction of Viral Expression and Readout), is described today in Molecular Cell.

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Aim: Aging in humans is associated with a 10–40-fold greater incidence of sudden cardiac death from malignant tachyarrhythmia. We have reported that thiol oxidation of ryanodine receptors (RyR2s) by mitochondria-derived reactive oxygen species (mito-ROS) contributes to defective Ca2+ homeostasis in cardiomyocytes (CMs) from aging rabbit hearts. However, mechanisms responsible for the increase in mito-ROS in the aging heart remain poorly understood. Here we test the hypothesis that age-associated decrease in autophagy is a major contributor to enhanced mito-ROS production and thereby pro-arrhythmic disturbances in Ca2+ homeostasis.

Methods and Results: Ventricular tissues from aged rabbits displayed significant downregulation of proteins involved in mitochondrial autophagy compared with tissues from young controls. Blocking autophagy with chloroquine increased total ROS production in primary rabbit CMs and mito-ROS production in HL-1 CMs. Furthermore, chloroquine treatment of HL-1 cells depolarized mitochondrial membrane potential (Δψm) to 50% that of controls. Blocking autophagy significantly increased oxidation of RyR2, resulting in enhanced propensity to pro-arrhythmic spontaneous Ca2+ release under β-adrenergic stimulation. Aberrant Ca2+ release was abolished by treatment with the mito-ROS scavenger mito-TEMPO. Importantly, the autophagy enhancer Torin1 and ATG7 overexpression reduced the rate of mito-ROS production and restored both Δψm and defective Ca2+ handling in CMs derived from aged rabbit hearts.

Conclusion: Decreased autophagy is a major cause of increased mito-ROS production in the aging heart. Our data suggest that promoting autophagy may reduce pathologic mito-ROS during normal aging and reduce pro-arrhythmic spontaneous Ca2+ release via oxidized RyR2s.

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Back in January, we were joined by Dr. Aubrey de Grey, Dr. Amutha Boominathan, Dr. Matthew O’Conner, and Michael Rae from the SENS Research Foundation for a webinar discussion panel focused on MitoSENS, the mitochondrial repair program. During the webinar, a number of points were discussed, and the Lifespan Heroes in the audience got to ask the researchers questions about MitoSENS and about the work of the SENS Foundation in general.

In 2015, the MitoSENS team raised funding on Lifespan.io to launch a study testing if they could create mitochondrial DNA copies in the cell nucleus, and they were successful in doing so as a result of the funds they received. In October 2019, the MitoSENS team launched a new follow-up project called MitoMouse, which aims to bring its mitochondrial repair therapy to mammals as a proof of concept on the road to translation to human use.

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Modern research and technology have completed the quest of Juan Ponce de Leon. We have found the fountain of youth. Instead of some remote island, it is everywhere around us in the food that we eat and the beverages we drink. A variety of edibles have been indicated above. They all contain the youth restoring chemical known as NAD+. Including them in your diet is one of the best health decisions you can make today.

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Many of us are fascinated by our various computing devices — our smartphones, our smart watches, and an ever-growing array of smart devices. What we sometimes forget is that we are biological creatures (at least, until The Singularity), and that even though biology as a discipline has been around much longer than computing, biology may yet supersede it.

If the 20th century was the era of computers, the 21st century may be the era of biology. And the two may even merge. Hello, synthetic biology and biological computing!

Last week SynBioBeta hosted The Global Synthetic Biology Summit, “where tech meets bio and bio meets tech.” People were urged to attend “to see how synthetic biology is disrupting consumer products, food, agriculture, medicine, chemicals, materials, and more.”

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