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

Earthquake damage to the Navy’s China Lake test base has already delayed the first test flight of these air-launched and recovered drones.

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 human cells.

The researchers combined Cas13’s antiviral activity 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.

These images, taken from 1990 to 2019, show how Hubble’s views of Saturn have gotten better over time as its cameras have improved.

Credit: NASA/Hubble #NASA #Hubble #space #science #astronomy #universe #telescope #cosmos #saturn #year #classic #ringedplanet #solarsystem

A new solar-powered system can take the salt out of ocean water. The technology can supply water for 25,000 people per day.

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.