Lifeboat Foundation

Human appetites have transformed the tomato — DNA and all. After centuries of breeding, what was once a South American berry roughly the size of a pea now takes all sorts of shapes and sizes, from cherry-like to hefty heirloom fruit.

Today, scientists are teasing out how these physical changes show up at the level of genes — work that could guide modern efforts to tweak the tomato, says Howard Hughes Medical Institute Investigator Zachary Lippman.

He and colleagues have now identified long-concealed hidden mutations within the genomes of 100 types of tomato, including an orange-berried wild plant from the Galapagos Islands and varieties typically processed into ketchup and sauce.

Chimeric antigen receptor (CAR) T cells have transformed the treatment of refractory blood cancers. These genetically engineered immune cells seek out and destroy cancer cells with precision. Now, scientists at Memorial Sloan Kettering are deploying them against other diseases, including those caused by senescence, a chronic “alarm state” in tissues. The scope of such ailments is vast and includes debilitating conditions, such as fibrotic liver disease, atherosclerosis, and diabetes.

Key to the success of CAR T cell therapy has been finding a good target. The first US Food and Drug Administration-approved CAR T cells target a molecule on the surface of blood cancers called CD19. It is present on cancer cells but few other normal cells, so side effects are limited.

Taking their cue from this prior work, a team of investigators including Scott Lowe, Chair of the Cancer Biology and Genetics Program in the Sloan Kettering Institute, and Michel Sadelain, Director of the Center for Cell Engineering at MSK, along with their trainees Corina Amor, Judith Feucht, and Josef Leibold, sought to identify a target on senescent cells. These cells no longer divide, but they actively send “help me” signals to the immune system.

A human embryo editing experiment gone wrong has scientists warning against treading into the field altogether.

To understand the role of a single gene in early human development, a team of scientists at the London-based Francis Crick Institute removed it from a set of 18 donated embryos. Even though the embryos were destroyed after just 14 days, that was enough time for the single edit to transform into “major unintended edits,” OneZero reports.

Human gene editing is a taboo topic — the birth of two genetically modified babies in 2018 proved incredibly controversial, and editing embryos beyond experimentation is not allowed in the U.S. The scientists in London conducted short-term research on a set of 25 donated embryos, using the CRISPR technique to remove a gene from 18 of them. An analysis later revealed 10 of those edited embryos looked normal, but that the other eight revealed “abnormalities across a particular chromosome,” OneZero writes. Of them, “four contained inadvertent deletions or additions of DNA directly adjacent to the edited gene,” OneZero continues.

Back in 2005, Drs. Irina and Michael Conboy showed that joining the circulatory systems of young and old mice together in a procedure called parabiosis could rejuvenate aged tissues and reverse some aspects of aging in old mice.

Following this discovery, many researchers concluded that there must be something special in young blood that was able to spur rejuvenation in aged animals, and various companies have been trying to find out what. Indeed, we recently reported that researchers were apparently successful in halving the epigenetic age of old rats by treating them with Elixir, a proprietary mix of pro-youthful factors normally found in young blood.

However, a question still remains: was the rejuvenation the result of there being something beneficial in the young blood, or is it more a case of dilution of the harmful factors present in old blood?

Chemical process called ELAST allows labeling probes to infuse more quickly, and makes samples tough enough for repeated handling.

When there’s a vexing problem to be solved, people sometimes offer metaphorical advice such as “stretching the mind” or engaging in “flexible” thinking, but in confronting a problem facing many biomedical research labs, a team of MIT researchers has engineered a solution that is much more literal. To make imaging cells and molecules in brain and other large tissues easier while also making samples tough enough for years of handling in the lab, they have come up with a chemical process that makes tissue stretchable, compressible, and pretty much indestructible.

“ELAST” technology, described in a new paper in Nature Methods, provides scientists a very fast way to fluorescently label cells, proteins, genetic material, and other molecules within brains, kidneys, lungs, hearts, and other organs. That’s because when such tissues can be stretched out or squished down thin, labeling probes can infuse them far more rapidly. Several demonstrations in the paper show that even after repeated expansions or compressions to speed up labeling, tissues snap back to their original form unaltered except for the new labels.

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.