Lifeboat Foundation

The experiment raises major safety concerns for gene-edited babies.

In the last few years, most of the data such as books, videos, pictures, medical and even the genetic information of humans are moving toward digital formats. Laptops, tablets, smartphones and wearable devices are the major source of this digital data transformation and are becoming the core part of our daily life. As a result of this transformation, we are becoming the soft target of various types of cybercrimes. Digital forensic investigation provides the way to recover lost or purposefully deleted or hidden files from a suspect’s device. However, current man power and government resources are not enough to investigate the cybercrimes. Unfortunately, existing digital investigation procedures and practices require huge interaction with humans; as a result it slows down the process with the pace digital crimes are committed. Machine learning (ML) is the branch of science that has governs from the field of AI. This advance technology uses the explicit programming to depict the human-like behaviour. Machine learning combined with automation in digital investigation process at different stages of investigation has significant potential to aid digital investigators. This chapter aims at providing the research in machine learning-based digital forensic investigation, identifies the gaps, addresses the challenges and open issues in this field.

Sending a handful of people certainly could serve as a proof of concept analogous to America’s Spanish and Portuguese outposts in the early 1500’s, or the English and Dutch settlements in the early 1600’s. In these instances the populations measured in the dozens and would not have amounted to a lasting European presence had they not been followed by thousands of new settlers over the next few decades. But, given our more advanced technology, our level of medicine, the idea that humans could have equipment that will utilize the Martian environment to produce food, air, and other consumables, and the certainty that settlers will not be at war with the Martian equivalent of the Aztecs or Incas—couldn’t a Martian settlement survive long term with just a low number of colonists?

The answer is no—not if the goal is a permanent human presence. Not if the goal is to provide our species with some kind of extinction insurance against planetary disaster on Earth, such as a mega-volcanic eruption, nuclear war, or some other existential threat. Mars setters can use technology to get air and food from the Mars environment, but early European explorers in the New World had access to one natural resource that mid-21st century Mars colonists will not be able to manufacture: a human gene pool.

If we really want Martian colonies, we can’t send just a few Adams and Eves. We can’t set-up a Martian Jamestown of 100 people. Long-term survival will depend on the genetic diversity of a large gene pool, and this means the Elon Musk plan of sending thousands might be the only colonization plan that could work.

Why does this happen?

To put things as simply as possible, the root cause of all aging is a loss of energy on the cellular level, and there are basically two major theories for why this occurs. One says cellular energy decline is the result of accumulated cellular and mitochondrial damage. In other words, it’s the result of wear and tear on a cellular level. The other theory speculates that it is the result of genetic programming, with some genes getting overexpressed while others get underexpressed as we age.

These two theories of cellular energy decline aren’t in competition with one another. They just look at the problem from two different vantage points. The reality is these “causes” are interrelated. Gene overexpression and underexpression can cause cellular damage. Cellular damage can impair gene expressions.

A new study is the first to quantify the proportion of differences in sensitivity that can be explained by genetic factors.

Two people with beta thalassaemia and one with sickle cell disease no longer require blood transfusions, which are normally used to treat severe forms of these inherited diseases, after their bone marrow stem cells were gene-edited with CRISPR.

Result of the ongoing trial, which is the first to use CRISPR to treat inherited genetic disorders, were announced today at a virtual meeting of the European Hematology Association.

“We have a researcher who was removed by the RCMP from the highest security laboratory that Canada has for reasons that government is unwilling to disclose. The intelligence remains secret. But what we know is that before she was removed, she sent one of the deadliest viruses on Earth, and multiple varieties of it to maximize the genetic diversity and maximize what experimenters in China could do with it, to a laboratory in China that does dangerous gain of function experiments. And that has links to the Chinese military.”

Gain of function experiments are when a natural pathogen is taken into the lab, made to mutate, and then assessed to see if it has become more deadly or infectious.

Most countries, including Canada, don’t do these kinds of experiments — because they’re considered too dangerous, Attaran said.

Continue reading “Canadian scientist sent deadly viruses to Wuhan lab months before RCMP asked to investigate” »

A team of scientists from the Wellcome Sanger Institute, the Francis Crick Institute, and EMBL-EBI has created a comprehensive structural variation atlas for a geographically diverse set of human genomes and recovered sequences missing from the human reference sequence. Among the 126,018 structural variations discovered by the team were medically-important genes in Oceanian populations that were inherited from Denisovans, a sister group to Neanderthals.

Good talk, not just about NAD. Q&A just before 35 minutes. A lot of epigenetics here.

David A. Sinclair, Ph.D., A.O. is a Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School. He is best known for his work on understanding why we age and how to slow its effects. He obtained his Ph.D. in Molecular Genetics at the University of New South Wales, Sydney in 1995. He worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente where he co discovered a cause of aging for yeast as well as the role of Sir2 in epigenetic changes driven by genome instability. In 1999 he was recruited to Harvard Medical School where he has been teaching aging biology and translational medicine for aging for the past 16 years. His research has been primarily focused on the sirtuins, protein-modifying enzymes that respond to changing NAD+ levels and to caloric restriction (CR) with associated interests in chromatin, energy metabolism, mitochondria, learning and memory, neurodegeneration, and cancer. The Sinclair lab was the first one to identify a role for NAD+ biosynthesis in regulation of lifespan and first showed that sirtuins are involved in CR in mammals. They first identified small molecules that activate SIRT1 such as resveratrol and studied how they improve metabolic function using a combination of genetic, enzymological, biophysical and pharmacological approaches. They recently showed that natural and synthetic activators require SIRT1 to mediate the in vivo effects in muscle and identified a structured activation domain. They demonstrated that miscommunication between the mitochondrial and nuclear genomes is a cause of age-related physiological decline and that relocalization of chromatin factors in response to DNA breaks may be a cause of aging.