Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical

Almost a year ago, we were told by our governments and healthcare professionals that a two-week shutdown of the economy would “flatten the curve.”

The Chinese Coronavirus (COVID-19) hit American shores — officially, anyway, there is significant evidence that it arrived earlier — in late January 2020. The American public was then told that a two-week shutdown of the economy would “flatten the curve,” relieving the pressure on hospital intensive care units and saving lives in the long run.

The average American, including conservatives, being people of good faith, complied, thinking that this was a common-sense measure that would save lives in the wake of a new and mysterious pandemic.

But two things quickly happened: First, the goalposts moved. No longer was it enough to “flatten the curve.” Now we were to be locked down until there was a cure.

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Researchers at Osaka City University use quantum superposition states and Bayesian inference to create a quantum algorithm, easily executable on quantum computers, that accurately and directly calculates energy differences between the electronic ground and excited spin states of molecular systems in polynomial time.

Understanding how the natural world works enables us to mimic it for the benefit of humankind. Think of how much we rely on batteries. At the core is understanding molecular structures and the behavior of electrons within them. Calculating the energy differences between a molecule’s electronic ground and excited spin states helps us understand how to better use that molecule in a variety of chemical, biomedical and industrial applications. We have made much progress in molecules with closed-shell systems, in which electrons are paired up and stable. Open-shell systems, on the other hand, are less stable and their underlying electronic behavior is complex, and thus more difficult to understand. They have unpaired electrons in their ground state, which cause their energy to vary due to the intrinsic nature of electron spins, and makes measurements difficult, especially as the molecules increase in size and complexity.

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Synthetic cannabidiol, better known as CBD, has been shown for the first time to kill the bacteria responsible for gonorrhea, meningitis and legionnaires disease.

The between The University of Queensland and Botanix Pharmaceuticals Limited could lead to the first new class of for in 60 years.

The UQ Institute for Molecular Bioscience’s Associate Professor Mark Blaskovich said CBD—the main nonpsychoactive component of cannabis—can penetrate and kill a wide range of bacteria including Neisseria gonorrhoeae, which causes gonorrhea.

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McMaster researchers have developed a new form of cultivated meat using a method that promises more natural flavor and texture than other alternatives to traditional meat from animals.

Researchers Ravi Selvaganapathy and Alireza Shahin-Shamsabadi, both of the university’s School of Biomedical Engineering, have devised a way to make by stacking of cultivated muscle and grown together in a lab setting. The technique is adapted from a method used to grow tissue for human transplants.

The sheets of living cells, each about the thickness of a sheet of printer paper, are first grown in culture and then concentrated on growth plates before being peeled off and stacked or folded together. The sheets naturally bond to one another before the cells die.

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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.

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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.

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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 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 (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 , just like in the in the brains of patients with Alzheimer’s disease.”

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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 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 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.

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