Lifeboat Foundation

The ancient Egyptians mummified an abundance of cats during the Late Period (664 — 332 BC). The overlapping morphology and sizes of developing wildcats and domestic cats confounds the identity of mummified cat species. Genetic analyses should support mummy identification and was conducted on two long bones and a mandible of three cats that were mummified by the ancient Egyptians. The mummy DNA was extracted in a dedicated ancient DNA laboratory at the University of California – Davis, then directly sequencing between 246 and 402 bp of the mtDNA control region from each bone. When compared to a dataset of wildcats (Felis silvestris silvestris, F. s. tristrami, and F. chaus) as well as a previously published worldwide dataset of modern domestic cat samples, including Egypt, the DNA evidence suggests the three mummies represent common contemporary domestic cat mitotypes prevalent in modern Egypt and the Middle East. Divergence estimates date the origin of the mummies’ mitotypes to between two and 7.5 thousand years prior to their mummification, likely prior to or during Egyptian Predyanstic and Early Dynastic Periods. These data are the first genetic evidence supporting that the ancient Egyptians used domesticated cats, F. s. catus, for votive mummies, and likely implies cats were domesticated prior to extensive mummification of cats.

Keywords: ancient DNA, Felis silvestris catus, mitochondrial, control region, domestication.

Ancient Egyptian culture is well known for its reverence and mummification of cats (Ginsburg, et al., 1991). Cats featured in early Egyptian art and skeletal remains from c. 4000 BC, has led scholars to conclude that our current feline companions might have been domesticated in Egypt (Baldwin, 1975, Ginsburg, et al., 1991, Linseele, et al., 2007). However, the first documentation of wildcat taming, the precursor to domestication, is an archeological finding in Cyprus of a potential wildcat buried with a human, dating to approximately 9500 years ago (Vigne, et al., 2004), implying prior to the Predynastic Period in Egypt. Recent genetic studies have suggested that the origins of cat domestication occurred in the adjacent Near Eastern sites (Driscoll, et al., 2007, Lipinski, et al., 2008) as domestic cats have derived mitotypes from regional wildcats and the genetic diversity of modern domestic cats is highest within these regions.

Weird, right?

The team’s critical insight was to construct a “viral language” of sorts, based purely on its genetic sequences. This language, if given sufficient examples, can then be analyzed using NLP techniques to predict how changes to its genome alter its interaction with our immune system. That is, using artificial language techniques, it may be possible to hunt down key areas in a viral genome that, when mutated, allow it to escape roaming antibodies.

It’s a seriously kooky idea. Yet when tested on some of our greatest viral foes, like influenza (the seasonal flu), HIV, and SARS-CoV-2, the algorithm was able to discern critical mutations that “transform” each virus just enough to escape the grasp of our immune surveillance system.

AI — Artificial Intelligence, lots of potential for good, but also a threat to the world.

From biological machines to superintelligence.

The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. But this doesn’t only affect the individual, it also creates a significant burden on public healthcare. And yet, research efforts into the biological processes and biomarkers that define muscle aging have not yet defined the underlying causes.

Now, a team of scientists from lab of Johan Auwerx at EPFL’s School of Life Sciences looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. They have discovered protein aggregates that deposit in skeletal muscles during natural aging, and that blocking this can prevent the detrimental features of muscle aging. The study is published in Cell Reports.

“During age-associated muscle diseases, such as inclusion body myositis (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles,” explains Auwerx. “The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease.”

NRF2 is just one of thousands of critical proteins in the cell, but it is one that we now know a lot about. Once any molecule achieves a certain level of celebrity status, it tends to acquire a groupie following in the supplement market. Today, we have all manner of NRF enhancers, releasers, activators and synergizers ready to arrive on your doorstep at the click of a button. But what could any of these things possibly do for us, and how much is too much of a good thing?

At the risk of overstating the obvious, if a little extra NRF2 is good for every cell in your body, and every cell in your body is good, then NRF2 must be good for your body. The weak link in that argument, however, is that all cells are not good. Nobody wants harmful bacterial cells to flourish, and nobody wants cancer cells to flourish. A paper recently published in Nature now suggests that inhibiting NRF2 can block the migration and invasion of non-small-cell lung cancer cells through the body. If anyone is going to derive benefit from NRF2, they may need to be smart about it.

The main reason NRF2, or Nuclear factor-erythroid 2-related factor 2, is so highly sought, is because it is a key transcriptional regulator of several antioxidant and anti-inflammatory enzymes. Unfortunately, as the authors above have revealed, it also moonlights as an activator of the Rho-ROCK pathway, which promotes actin filamentation and movement of cells. The researchers were able to block this activity of NRF2 by giving an inhibitor known as brusatol.

A legally blind 78-year old man has regained his sight after being the inaugural patient to receive a promising new type of corneal implant, Israel Hayom has reported. Developed by a company called CorNeat, the KPro is the first implant that can be integrated directly into the eye wall to replace scarred or deformed corneas with no donor tissue. Immediately after the surgery, the patient was able to recognize family members and read numbers on an eye chart.

The corona is the clear layer that covers and protects the front portion of the eye. It can degenerate or scar for various reasons, including diseases like pseudophakic bullous keratopathy, kerotoconus and trauma.

Imagine going to a surgeon to have a diseased or injured organ switched out for a fully functional, laboratory-grown replacement. This remains science fiction and not reality because researchers today struggle to organize cells into the complex 3D arrangements that our bodies can master on their own.

There are two major hurdles to overcome on the road to laboratory-grown organs and tissues. The first is to use a biologically compatible 3D scaffold in which cells can grow. The second is to decorate that scaffold with biochemical messages in the correct configuration to trigger the formation of the desired organ or tissue.

In a major step toward transforming this hope into reality, researchers at the University of Washington have developed a technique to modify naturally occurring biological polymers with protein-based biochemical messages that affect cell behavior. Their approach, published the week of Jan. 18 in the Proceedings of the National Academy of Sciences, uses a near-infrared laser to trigger chemical adhesion of protein messages to a scaffold made from biological polymers such as collagen, a connective tissue found throughout our bodies.

Biologists balk at any talk of ‘goals’ or ‘intentions’ — but a bold new research agenda has put agency back on the table.

Animal immune systems depend on white blood cells called macrophages that devour and engulf invaders. The cells pursue with determination and gusto: under a microscope you can watch a blob-like macrophage chase a bacterium across the slide, switching course this way and that as its prey tries to escape through an obstacle course of red blood cells, before it finally catches the rogue microbe and gobbles it up.

But hang on: isn’t this an absurdly anthropomorphic way of describing a biological process? Single cells don’t have minds of their own – so surely they don’t have goals, determination, gusto? When we attribute aims and purposes to these primitive organisms, aren’t we just succumbing to an illusion?

Continue reading “The biological research putting purpose back into life” »

In a new study, German scientists have restored the ability to walk in mice that had been paralyzed after a complete spinal cord injury. The team created a “designer” signaling protein and injected it into the animals’ brains, stimulating their nerve cells to regenerate and share the recipe to make the protein.

Spinal cord injuries are among the most debilitating. Damaged nerve fibers (axons) may no longer be able to transmit signals between the brain and muscles, often resulting in paralysis to the lower limbs. Worse still, these axons cannot regenerate.

Previous studies have shown promise in restoring some limb function through spinal stimulation therapy, or by bypassing the injury site altogether. Other promising research in similar areas has involved using compounds that restore balance to the inhibitory/excitatory signals in the neurons of partially paralyzed mice, and transplanting regenerating nose nerve cells into the spines of injured dogs.