Lifeboat Foundation

When CRISPR-Cas9 is used to edit genomes, off-target DNA damage is more common than previously thought.

A GREAT deal rides on the accuracy of the gene-editing tool known as CRISPR-Cas9. Since its discovery in 2012 it has become popular for tinkering with genomes of all kinds, thanks to its ability to make editing cheap and easy. Firms such as CRISPR Therapeutics, Intellia Therapeutics and Editas Medicine have been built on the idea that it could be used to develop treatments for human diseases. Editas, based in Cambridge, Massachusetts, announced this year that it would work on five new human medicines over the next five years.

In China the technology is already in clinical use. In Hangzhou Cancer Hospital, for example, CRISPR-Cas9 is being employed to engineer immune-system cells removed from patients with cancer of the oesophagus. The hope is that when the engineered cells are returned to a patient’s body, the editing will have improved their ability to attack tumours. More studies involving human beings are expected in other countries for the treatment of beta-thalassaemia, a blood disorder, and Leber’s congenital amaurosis, a form of blindness. Further ahead, there is hope that CRISPR-Cas9 will help treat diseases such as AIDS, cystic fibrosis, Huntington’s chorea and Duchenne muscular dystrophy.

Continue reading “The safety of CRISPR-Cas9 gene editing is being debated” »

Scientists like Dan Carlson are in high demand, thanks to recently discovered tools that enable them to tweak the DNA of all kinds of organisms.

A Chinese artificial intelligence (AI) system has beaten a team of elite doctors in a tumour diagnosis competition.

Vivli, which spun out of a policy think tank at Harvard University–affiliated Brigham and Women’s Hospital in Boston, is part of a push to encourage drug developers to share trial data—even negative results, findings that show a treatment has no benefit. Companies seeking U.S. regulatory approval for a drug, as well as investigators funded by the National Institutes of Health, must post limited, summary results on ClinicalTrials.gov. But many researchers and policy analysts believe sharing detailed raw data on individual patients, stripped of identifying information, would be valuable. Researchers could confirm that a drug works, look for side effects, or explore new questions.

Vivli aims to ease sharing of anonymized clinical studies.

They’re so toxic they can rip your skin apart on contact. But that virulence is what makes them perfect candidates for a new wave of antibiotics.

Researchers have created the fastest man-made rotor in the world, which they believe will help them study quantum mechanics.

At more than 60 billion revolutions per minute, this machine is more than 100,000 times faster than a high-speed dental drill.

Continue reading “World’s fastest man-made spinning object could help study quantum mechanics” »

http://undoing-aging.org/videos/doug-ethell-presenting-at-undoing-aging-2018

Btw: the facebook event page for Undoing Aging 2019 is already up fb.com/events/2044104465916196/

Mitochondrial dysfunction is associated with many mitochondrial diseases, most of which are the result of dysfunctional mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS accounts for the generation of most of the cellular adenosine triphosphate (ATP) in a cell. The OXPHOS function largely depends on the coordinated expression of the proteins encoded by both nuclear and mitochondrial genomes. The human mitochondrial genome encodes for 13 polypeptides of the OXPHOS, and the nuclear genome encodes the remaining more than 85 polypeptides required for the assembly of OXPHOS system. Mitochondrial DNA (mtDNA) depletion impairs OXPHOS that leads to mtDNA depletion syndromes (MDSs)^{1, 2}. The MDSs are a heterogeneous group of disorders, characterized by low mtDNA levels in specific tissues. In different target organs, mtDNA depletion leads to specific pathological changes. MDS results from the genetic defects in the nuclear-encoded genes that participate in mtDNA replication, and mitochondrial nucleotide metabolism and nucleotide salvage pathway^{1, 4,5,6,7,8,9,10}. mtDNA depletion is also implicated in other human diseases such as mitochondrial diseases, cardiovascular^{11, 12}, diabetes^13,14,15, age-associated neurological disorders^16,17,18, and cancer^{19,20,21,22,23,24,25}.

A general decline in mitochondrial function has been extensively reported during aging^{26,27,28,29,30,31,32,33}. Furthermore, mitochondrial dysfunction is known to be a driving force underlying age-related human diseases^{16,17,18, 34,35,36}. A mouse that carries elevated mtDNA mutation is also shown to present signs of premature aging^{37, 38}. In addition to mutations in mtDNA, studies also suggest a decrease in mtDNA content and mitochondrial number with age^{27, 29, 32, 33, 39}. Notably, there is an age-related mtDNA depletion in a number of tissues^40,41,42. mtDNA depletion is also frequently observed among women with premature ovarian aging⁴³. Low mtDNA copy number is linked to frailty and, for a multiethnic population, is a predictor of all-cause mortality⁴⁴. A recent study revealed that humans on an average lose about four copies of mtDNA every ten years. This study also identified an association of decrease in mtDNA copy number with age-related physiological parameters³⁹.

To help define the role of mtDNA depletion in aging and various diseases, we created an inducible mouse expressing, in the polymerase domain of POLG1, a dominant-negative (DN) mutation that induces depletion of mtDNA in the whole animal. Interestingly, skin wrinkles and visual hair loss were among the earliest and most predominant phenotypic changes observed in these mice. In the present study, we demonstrate that mtDNA depletion-induced phenotypic changes can be reversed by restoration of mitochondrial function upon repletion of mtDNA.

Not long ago, getting a virus was about the worst thing computer users could expect in terms of system vulnerability. But in our current age of hyper-connectedness and the emerging Internet of Things, that’s no longer the case. With connectivity, a new principle has emerged, one of universal concern to those who work in the area of systems control, like João Hespanha, a professor in the departments of Electrical and Computer Engineering, and Mechanical Engineering at UC Santa Barbara. That law says, essentially, that the more complex and connected a system is, the more susceptible it is to disruptive cyber-attacks.

“It is about something much different than your regular computer virus,” Hespanha said. “It is more about cyber physical systems—systems in which computers are connected to physical elements. That could be robots, drones, smart appliances, or infrastructure systems such as those used to distribute energy and water.”

In a paper titled “Distributed Estimation of Power System Oscillation Modes under Attacks on GPS Clocks,” published this month in the journal IEEE Transactions on Instrumentation and Measurement, Hespanha and co-author Yongqiang Wang (a former UCSB postdoctoral research and now a faculty member at Clemson University) suggest a new method for protecting the increasingly complex and connected power grid from attack.

Continue reading “Team suggests a way to protect autonomous grids from potentially crippling GPS spoofing attacks” »