A stroke occurs when blood flow to an area of the brain is suddenly cut off. The brain cells get deprived of oxygen and begin to die quickly. Having a stroke is a scary thought, but you can be mindful of your health to reduce the chances of having one.
President Nana Addo Dankwa Akufo-Addo on Thursday opened Ghana’s newest medical drone delivery base at Asante Mampong as part of his duty tour of the Ashanti region this week.
This marks the second of what will be four medical drone delivery bases that have been commissioned to help expand access to critical and life-saving medicines for people across Ghana.
Zipline, a California-based robotics company, operates the medical drone delivery service with support from Gavi, the Vaccine Alliance, the Bill & Melinda Gates Foundation, the UPS Foundation and other partners.
Researchers at EPFL have created a metallic microdevice in which they can define and tune patterns of superconductivity. Their discovery, which holds great promise for quantum technologies of the future, has just been published in Science.
In superconductors, electrons travel with no resistance. This phenomenon currently only occurs at very low temperatures. There are many practical applications, such as magnetic resonance imaging (MRI). Future technologies, however, will harness the total synchrony of electronic behavior in superconductors—a property called the phase. There is currently a race to build the world’s first quantum computer, which will use phases to perform calculations. Conventional superconductors are very robust and hard to influence, and the challenge is to find new materials in which the superconducting state can be easily manipulated in a device.
EPFL’s Laboratory of Quantum Materials (QMAT), headed by Philip Moll, has been working on a specific group of unconventional superconductors known as heavy fermion materials. The QMAT scientists, as part of a broad international collaboration between EPFL, the Max Planck Institute for Chemical Physics of Solids, the Los Alamos National Laboratory and Cornell University, made a surprising discovery about one of these materials, CeIrIn5.
Second prize is a trip to meet Dr. Aubrey de Grey! This international (short) film competition is presented by the SENS Research Foundation, the International Longevity Alliance and Heales. The winning film will be chosen by our remarkable jury. For more information on how to compete and to sign up please visit www.longevityfilmcompetition.com
A team of researchers, including Dr. David Sinclair, has recently made a new study available as a preprint prior to peer review and publication in the journal Cell.
DNA damage and the double-strand break
Two of the primary hallmarks of aging are genomic instability, which consists of damage to our DNA, and epigenetic alterations, which are the changes in gene expression that occur with aging and are harmful to normal cell function.
Circulating levels of white blood cells (WBCs) are one of the 10 variables used to quantify biological age with PhenoAge (https://michaellustgarten.com/2019/09/09/quantifying-biological-age). The reference range for WBCs is 4.5 – 11 *109 cells/L, but within that range, what’s optimal?
Several studies have reported that WBCs greater than 5 are associated with an increased all-cause mortality risk (Ahmadi-Abhari et al. 2013, Samet et al. 2005, Weijenberg et al. 1996). While observational studies are important for identifying associations with mortality risk, stronger evidence is obtained when the data from the same subjects are tracked for a time period. Perhaps the best evidence for the association between WBCs with mortality risk comes from the Baltimore Longitudinal Study on Aging (BLSA), which studied 2803 men and women over a period of 44 years (Ruggiero et al. 2007). As shown below, subjects that had circulating WBCs between 3.5 – 6 had the best survival, whereas WBCs below 3.5, between 6 – 10, and 10+ each had successively higher risk. The 0.5 point on the y-axis of the curve (survival) is defined as 50% mortality, and is the point where half of the study subjects died, whereas the remaining 50% were still alive.
A supposedly rare genetic quirk might be more common than we think, according to new research out Thursday. The study, based largely on 23andMe data, suggests that one in every 2,000 people are born with two copies of a gene from only a single parent, often with no serious health consequences.
Ordinarily, a person’s egg or sperm cells have one set of the genes that make up their chromosomes (other cells in our body have two sets). When a sperm fertilizes an egg, the resulting fertilized zygote will then have two sets of 23 chromosomes, one from each parent, making 46 chromosomes in total. If all goes well, the zygote multiplies and divides until it becomes a person, one with an even allocation of gene copies from both parents.
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.
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.
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.
